Surgical treatment of acquired heart defects.

Aortic aneurysm. Aortic dissection. Modern

methods of treatment.

1 History of Heart Valve Surgery

Unfavorable prognosis of patients with severe and worsening heart valve disease can be
successfully reversed by cardiac surgery. This idea was first put forward over a century ago by
Sir Lauder Brunton, who was confronted with the ineffectiveness of treatment modalities for
rheumatic mitral stenosis, which was very common at the time. In 1902 he published an article in
Lancet where he suggested the enlargement of the stenotic mitral orifice by surgical procedure.
This audacious concept was brought into practice on 20 May 1923 when Elliot Carr Cutler
performed in Boston the first operation of mitral stenosis on a 12-year-old girl [2, 3]. He
dissected the stenotic mitral orifice by means of a transventriculary-introduced tenotom.
Following this successful operation, however, the next five patients died from surgically created
mitral incompetence, and Cutler did not continue performing these operations.
Twenty-five years later, Charles Philamore Bailey, 10 June 1948 in Philadelphia, and
Dwight Emary Harken, on 16 June 1948 in Boston, performed independently the first successful
mitral commissurolyses (preceded by several unsuccessful attempts since 1945). In Europe
Russell Claude Baron Brock of Wimbledon performed his first successful mitral commissurolysis
on 16 September 1948 in London.
The possibility to operate using cardiopulmonary bypass inside the heart chambers
enabled performance, under direct visual control, of not only open mitral commissurotomies but
also valve repairs and later valve replacement.The 1960 is the year of the first artificial valves
implantations.
Nina Braunwald and Andrew Morrow in Bethesda implanted a polyurethane heart valve
of their own design into the mitral orifice on 10 March and the other one on 11 March 1960. In
regards to only short survival of their patients literature attributes the priority to Albert Starr from
Portland who implanted a ball cage valve into the mitral position on 21 September 1960 followed
by a longterm survival of the patient .
The first aortic valve replacement into the subcoronary position was performed by
Dwight Harken in Boston on 10 March 1960. Robert Cartwright (Pittsburg) carried out the first
combined aortic and mitral valve replacement on 1 November 1961 and Albert Starr the fi rst
simultaneous aortic, mitral, and tricuspid valve replacement on 21 February 1963. Soon after the
first mechanical heart valve implantations, the era of biological valves in human cardiac surgery
was launched. Donald Nixon Ross (London) performed the first subcoronary implantation of the
aortic allograft on 24 July 1962. Two months later, he was followed by the second pioneer of
allograft surgery, Sir Brian Gerald Barratt-Boyes (Auckland, New Zealand). The pioneering work
of Alain Frederick Carpentier on the research and development of the porcine aortic valve
xenograft resulted in the first human implantation into the aortic position in Paris in 1965
(together with Jean-Paul Binet). In 1967 Carpentier (together with Charles Dubost) implanted a
stented xenograft into the mitral position. Also in 1967 Donald Ross used for the first time the
patient’s pulmonary valve as an autograft for aortic valve replacement and reconstructed the
pulmonary outflow tract with an allograft.
In 1968 Hugh Bentall and Anthony DeBono reported the surgical treatment of the
annuloaortic ectasia. They replaced the aortic valve with a mechanical Starr-Edwards valve
mounted on a
Teflon (DuPont, Wilmington, Del.) vascular
graft. The coronary ostia were anastomosed to
the graft, which then replaced the ascending
aorta (inclusion technique).The
expansion of reconstructive mitral valve
surgery owes much to Alain Carpentier (Paris)
who, since the 1980s, has 17 History of Heart
Valve Surgery been the leading promoter
of valve-sparing procedures on the mitral
valve. Aortic valve-sparing surgery in
patients with aortic incompetence
has, contrary to this, attracted the growing
interest of cardiac surgeons only in the past
decade. The contributions of Sir Magdi
Yacoub (London) and Tirone David (Toronto) in this field are fundamental. Techniques of aortic
valve reconstruction surgery have been adopted at the majority of cardiac surgery units, and
current progress has been influenced primarily by Hans Joachim Schafers (Homburg) and
Gebrine El Khoury (Brussels).

Surgical Anatomy of the Heart Valves

Introduction

The human heart, after a faultless completion of embryonic development, is an

exquisitely designed pumping organ equipped with two working units. Four cardiac valves are
indispensable components of this entity. Morphology of the cardiac valves merits admiration for
its integration of subtle construction with perfect functionality and durability. Not only the valve
architecture itself, but also the space-saving valves’ interrelation in the heart center, and spiral
wedging of the outfl ow tracts and great vessels, is a technically brilliant and compact solution.
Perfect knowledge of the close relationship between the heart valves and other heart components
is essential for both cardiac surgeons and cardiologists. Four cardiac valves are situated in the
right-sided heart chambers (tricuspid and pulmonary) and the left-sided heart chambers (mitral
and aortic). Morphologically the valves are divided into two atrioventricular (mitral and
tricuspid) and two semilunar (aortic and pulmonary) valves. The valves have, under normal
circumstances, their typical localization and relationship to the central fibrous skeleton,
conduction system, and coronary vessels (Figs. 2.1, 2.2).

Aortic Valve
The aortic valve situated in the left ventricular outflow tract consists of the complex of
three semilunar cusps and their adjacent sinuses of Valsalva. Terminology of the sinuses is
derived
left coronary cusp

right cusp
| anterior cusp

right coronary cusp

 n
o
nseptal leaflet
-
posterior leaflet
c
oronary cusp anterior leaflet

anterior leaflet

posterior leaflet

Fig. 1 Terminology of the valve cusps and leafl ets. P pulmonary, A aortic, Mmitral, Ttricuspid
 from the respective arising coronary arteries, i.e., left, right, and non-coronary (Figs. 2.3,
2.4). Th e aortic cusps coapt against each other in t he center of the aortic orifice during diastole.
The cusps display a mild thickening at the midpoint of its edge (nodulus Arantii), whereas near
the commissure they are thinner or even contain small fenestrations.The aortic valve does not
have an anatomically defined annulus. The line of cusp insertion is crown-shaped with the
highest points at the connection of the cusps (commissures) and the lowest points (nadir) in the
middle between them (Fig. 2.5). The zone between the aortic root with bulging sinuses of
Valsalva and the straight tubular ascending aorta is called the sinotubular junction. Aortic
diameters at the level of aortic valve insertion (“annulus,” ventriculoarterial junction) are
important dimensions that characterize normal aortic root geometry and its pathological
anomalies. The aortic valve is located in the center of the heart close to other cardiac cavities.
The non-coronary and left coronary cusps are directly connected to both fibrous trigones of the
heart skeleton and in this way also to the anterior mitral leafl et. Th e triangular area below the
right/non-coronary cusp commissure adjoins to the atrioventricular septum and the course of the
bundle of His.

Mitral Valve
The mitral valve is a bileaflet atrioventricular valve between the left atrium and the left
ventricle. The valve itself consists of the larger anterior (aortic, septal) leaflet and smaller
posterior (mural, ventricular) leafl et (Figs. 2.6, 2.7). Clinical terminology divides both leaflets
into respective thirds that are differentiated by small indentations (namelythe posterior leafl et;
Fig. 2.8). Both leafl ets join together in the commissural areas. A sufficiently large zone of
coaptation is necessary for proper competence of the valve. Normal function of the valve depends
not only on the morphology of the leafl ets but also on the other components: the mitral annulus;
the chordae; the papillary muscles; and the left ventricular geometry. Both mitral leaflets are
connected by numerous chordae to both papillary muscles (anterolateral and posteromedial). The
chordae of the first order are attached at the free margin of the leaflet, whereas the second-order
chordae insert into the ventricular surface of the leaflet a short distance from the free edge. The
chordae originating from the basal portion of the posterior leaflet are anchored directly to the left
ventricular trabeculae (third-order chordae). The portion of the mitral annulus corresponding with
the base of the anterior mitral leaflet is fixated within the fibrous heart skeleton and thus directly
connects to the aortic valve (aortico-mitral continuity; Figs. 2.9, 2.10). The closely adjacent
course of the circumflex artery is also of clinical relevance [1-3].
Fig.2 Mitral valve. A1-A3 anterior leafl et, P1-P3 posterior leafl et,ALC anterolateral commissure, PMC posteromedial
commissure, AL antero lateral papillary muscle, PM posteromedial papillary muscle

Tricuspid Valve
The tricuspid valve is between the right atrium and the right ventricle (Fig. 2.11). It
consists of the anterior, posterior, and septal leaflets. The anterior leaflet is the largest leafl et,
with eventual indentations. It is connected by the chordae to the medial and anterior papillary
muscle. The posterior leafl et is the smallest leafl et and is connected to the anterior and posterior
papillary muscles. The septal leaflt is slightly larger and its chordae are anchored to the posterior
andseptal papillary muscles. Close to the septal leaflet and the anteroseptal commissure (the
triangle of Koch,

Fig. 3 Topographic interrelations of the tricuspid valve to adjacent structures. 1 atrioventricular

node, 2 aortic valve, 3 right coronary artery, 4 coronary sinus, 5 inferior vena cava

which is delineated by the septal leafl et annulus, the coronary sinus, and the tendon of Todaro)
there is the atrioventricular node of the conduction system and the penetration of the bundle of
His through the right fi brous trigone (Fig. 2.12). The area of the anteroseptal commissure is close
to the aortic valve and the posterior leafl et annulus lies very close to the mid-portion of the right
coronary artery.
Pulmonary Valve
Th e pulmonary valve is a tricuspid semilunar valve in the right ventricular outflow tract
(Figs. 2.13, 2.14). The morphology of the sinuses and cusps is similar to that of the aortic valve;
the pulmonary valve is, however, thinner. There are neither coronary ostia nor a fi brous
continuity with the tricuspid valve (Fig. 2.15). The pulmonary valve cusps are usually termed the
right, left, and anterior (non-septal) cusps.

Overview of the Valve Replacement Devices

Introduction

Severely diseased heart valves that cause signifi cant valvular disease, not amenable to
repair due to extensive calcification, infection, or congenital malformation, have to be replaced
by artifi cial or biological heart valves. Artificial heart valves (mechanical valves, prostheses) are
constructed from plastic materials, titanium or metallic alloys with the sewing ring from various
fabrics. In biological valves the valve itself is mostly a biological tissue from other animal
species (xenograft) that is mounted on a stent equipped with a sewing ring (bioprosthesis). Less
frequent options are the allografts (homografts) and autografts that are implanted without a stent
or sewing ring. Hemodynamically, the most important parameter of both mechanical valves and
bioprostheses is their effective orifice area (EOA; Fig. 3.3). Effective orifice area has to be
differentiated from geometric orifice area (GOA). Geometric orifice area is the whole inner area
of the valve including the area occupied by the opened discs or leaflets, struts, and other
mechanisms of the valve.

Fig. 4. GOA, COA, and EOA of bileaflet valves (left column), tilting monodiscs (center column),
and bioprostheses (right column)

The aim is to implant a valve large enough to avoid hemodynamically significant patient-
prosthesis mismatch (PPM).
Mechanical bileaflet valves have gained popularity since the mid-1980s and currently are
the most frequently implanted valves in the world. There are a variety of bileaflet heart valves
available. The best-known and most implanted mechanical bileafl et valve is the St. Jude Medical
(SJM) valve (Fig. 5.). In 1994 a CarboMedics universal valve, Orbis, was launched, enabling
implantation of the same valve either to the aortic or mitral position Two other bileafl et valves
are the ATS Medical (since 1992), standard type and AP type (advanced performance) for small
annuli , and OnX (since 1996), with different rings. An interesting feature of the OnX valve is
that the pyrolytic carbon ring overtops the sewing ring and thereby prevents tissue from
overgrowing into the valve mechanism. Bileaflet valve Medtronic Advantage has, since 2003, a
modification for supraannular implantation named Medtronic Advantage Supra.

Fig. 5 Bileaflet valve St. Jude Medical

The rationale for development of biological valves was to reduce the risk of serious
complications related to the mechanical heart valves (thrombosis, embolism, bleeding
complications due to anticoagulation therapy). The most frequently implanted tissue valves are
xenografts manufactured as bioprostheses, whereas allografts and autografts are being implanted
less often.

Fig.6 Bioprosthesis Sorin-Soprano

 Aortic Valve Surgery

Hemodynamically significant aortic valve disease - both stenosis and regurgitation,

regardless of its etiology - can be treated surgically. Adult patients with aortic stenosis require
valve replacement with either mechanical or tissue valves. In patients with aortic regurgitation
the valve can in some instances be repaired. Aortic stenosis in infancy and childhood is usually
not operated but treated with percutaneous balloon valvuloplasty. Balloon valvuloplasty of the
aortic valve may, however, be chosen for elderly and polymorbid patients who would not tolerate
cardiac surgery. Th e fi rst balloon dilation of a calcifi ed aortic valve was performed by Alain
Cribier in Rouen in 1985. Th e increase in stenotic aortic valve area is followed by immediate
decrease of afterload, decrease of the left ventricular fi lling pressure, decrease of pulmonary
hypertension, and improvement of left ventricular ejection fraction. Formerly, the clinical
improvement was only temporary due to early restenosis and therefore this method was only
seldom employed. Continuous technological and procedural refi nement has led to improvement
of midterm results and to a certain renaissance of balloon valvuloplasty. It is beginning to be
performed as a palliative alternative to valve replacement in elderly and comorbid patients
contraindicated for surgery and also in patients with critical aortic stenosis who require vital
major extracardiac surgery. Th e procedure can be repeated upon restenosis. Hemodynamically
signifi cant aortic valve disease - both stenosis and regurgitation, regardless of its etiology - can
be treated surgically. Adult patients with aortic stenosis require valve replacement with either
mechanical or tissue valves. In patients with aortic regurgitation the valve can in some instances
be repaired. Aortic stenosis in infancy and childhood is usually not operated but treated with
percutaneous balloon valvuloplasty. Balloon valvuloplasty of the aortic valve may, however, be
chosen for elderly and polymorbid patients who would not tolerate cardiac surgery. Th e fi rst
balloon dilation of a calcifi ed aortic valve was performed by Alain Cribier in Rouen in 1985. Th
e increase in stenotic aortic valve area is followed by immediate decrease of afterload, decrease
of the left ventricular fi lling pressure, decrease of pulmonary hypertension, and improvement of
left ventricular ejection fraction. Formerly, the clinical mprovement was only temporary due to
early restenosis and therefore this method was only seldom employed. Continuous technological
and procedural refi nement has led to improvement of midterm results and to a certain
renaissance of balloon valvuloplasty. It is beginning to be performed as a palliative alternative to
valve replacement in elderly and comorbid patients contraindicated for surgery and also in
patients with critical aortic stenosis who require vital major extracardiac surgery. The procedure
can be repeated upon restenosis.
Fig. 7 ed aortic stenosis. a Degenerative etiology. b Rheumatic etiology

Indications for Surgery

In deciding whether the patient with aortic stenosis should be operated, one has to take
into consideration:
1. If the patient is symptomatic or asymptomatic
2. What the degree of severity of the aortic stenosis is
3. Whether there is an isolated aortic valve procedure
planned or a combined procedure [coronary artery bypass
graft (CABG), mitral valve procedure, etc.]
4. What the left ventricular function and dimensions are
5. What the comorbidities are
Clinical symptoms of severe aortic stenosis present in a well-known triad: (a) dyspnea;
(b) angina; and (c) syncope. Parameters of severe aortic stenosis are: (a) orifi ce area <0.5
cm2/m2 (the updated U.S. and European guidelines recommend the value of 0.6 cm2/m2, which,
however, includes a lot of asymptomatic patients); (b) mean gradient >40 mmHg; and (c)
maximum flow velocity (Vmax) on aortic valve Vmax >4 m/s. Gradients are signifi cantly
influenced by the cardiac output and therefore the aortic valve orifice area should be taken into
consideration in preference. Symptomatic severe aortic stenosis is a straightforward indication for
surgery. More difficult is the decision making in symptomatic aortic stenosis with low ejection
fraction (EF <35%) and low gradient (mean gradient <30 mmHg) simultaneously. In these
patients the myocardial contractile reserve has to be tested, usually by means of dobutamine
stress echocardiography.
Fig. 8 Aortic valve prosthesis after placement of all sutures before running down into the aortic
annulus

Aortic Regurgitation
Aortic regurgitation is characterized by reverse fl ow from the aorta to the left ventricle
during diastole. In pure or predominant regurgitation disease of the aortic valve, the left ventricle
complies for a long time with the volume and pressure overload due to compensatory
mechanisms. The pathological condition results in eccentric left ventricular dilation and
hypertrophy with corresponding increase in dimensions and volume (both end-diastolic and end-
systolic). Further progression of the valve disease, however, leads to the failure of compensatory
mechanisms. The left ventricular end-systolic volume continues to increase without accordant
changes of the already high end-diastolic volume. As a result, the left ventricular EF decreases,
whereas the left ventricular end-diastolic pressure, left atrial pressure, and pulmonary pressure
increase. Clinical manifestations are fatigue, inefficiency, and dyspnea. Angina may also be
present,caused by high demands of the hypertrophic myocardium in combination with coronary
hypoperfusion from low aortic diastolic pressure and high left ventricular end -diastolic pressure.
The symptoms (shortness of breath, fatigue, angina,palpitations) often appear very late and
sometimes. Aortic Valve Surgery when the systolic dysfunction is already irreversible; thus,
aortic regurgitation is not called an insidious disease for no reason, because many patients stay
asymptomatic with already severe left ventricular impairment. If only the onset of advanced
clinical symptoms triggers the diagnostic process, confirming poor EF and large left ventricular
dimensions,the indication for surgery is a late one with high operative risk and dubious long-term
results.Operations for aortic regurgitation are less frequent than those for aortic stenosis,
accounting for about 20% of all aortic valve operations.

Etiology of Aortic Regurgitation

Aortic regurgitation may be caused by isolated cusp involvement,dilation of the aortic
annulus, the sinuses of Valsalva,the sinotubular junction, or a combination of two or more
coinciding pathological factors.Pathological changes of the aortic cusps causing valve
regurgitation may be congenital (a unicuspid or more frequently a bicuspid aortic valve) or
acquired. Infective endocarditis is the frequent cause of acquired valve regurgitation,either in its
active phase (Figs. 5.45-5.47) or after healing of the infection (Fig. 5.48). Other etiological
causes are rheumatic or degenerative sclerotic calcifi ed (Fig. 5.49) involvement of the cusps
leading predominantly to their retraction. A prolapse of one or more cusps may occur (Fig. 5.50)
as well as damage to the cusps from turbulent blood fl ow in subvalvular aortic stenosis (see Fig.
5.9). Aortic regurgitation occasionally in rheumatoid arthritis, ankylosing spondylitis, systemic
lupus erythematosus, and Takayasu’s disease (Fig. 5.51). In childhood aortic regurgitation may
also result from an isolated right-cusp prolapse caused bya the loss of morphological support due
to the subaortic ventricular septal defect (Fig. 5.52).Dilation of the aortic annulus leading to the
central regurgitation is often accompanied by dilation of the sinuses of Valsalva and of the
sinotubular junction, thus forming the clinical entity of annulo-aortic ectasia.

Indications for Surgery

Aortic regurgitation is an insidious valve disease because even asymptomatic patients may
already have severe aortic regurgitation and advanced left ventricular dysfunction. Indication
therefore has to diff erentiate between symptomatic and asymptomatic patients. Symptomatic
patients with severe aortic regurgitation are defi nitely indicated for surgery [3, 4]. Th e criteria
for severe aortic regurgitation are as follows:
1. Regurgitation volume >60 ml/contraction
2. Regurgitation fraction >50%
3. Regurgitation orifi ce area >0.3 cm2
4. Vena contracta >6 mm
5. Holodiastolic reverse fl ow in the descending aorta
6. Undelayed equivalent contrast opacifi cation of the left ventricle at aortography
Asymptomatic patients with severe aortic regurgitation are also indicated for surgery provided
their EF is <50% and/or at the left ventricular end-diastolic dimension (LVEDD) >75 mm and the
left ventricular end-systolic dimension (LVESD) >55 mm. Constant improvement of operative
results and, simultaneously, the evidence of unsatisfactory long-term results of operation in
patients with already grossly enlarged left ventricle have infl uenced the decision making in the
way the cut-off value for indication for surgery has been lowered recently to an LVEDD of 70
mm and an LVESD of 50 mm. Simultaneous surgical procedure at the ascending aorta during
aortic valve operation is generally indicated if the diameter of the ascending aorta reaches 50-55
mm. In bicuspid aortic valve and Marfan syndrome the operation is already indicated if the aortic
diameter exceeds 45-50 mm. Th e indexed parameters should again be used, preferably with the
cut-off value of 25 mm/m2 for the patients with Marfan syndrome or bicuspid aortic valve.
Prolapse of the right aortic cusp in subaortic ventricular septal Defect

Mitral Valve Replacement

Th e approaches to the mitral valve have already been described. Mitral valve replacement is
optimally started by a short incision at the base of the anterior mitral leafl et at the 12 o’clock
position (from surgeon’s view; Fig. 6.11). It is advisable to place immediately a pledgeted
mattress stitch into the mitral annulus at the point of incision. Th is stitch helps to pull the
annulus into the operative fi eld. Th e whole anterior leafl et is then circumcised as far as the
commissures (Fig. 6.12) and its chordae are divided at the tip of the papillary muscles. Th e
posterior mitral leafl et should be left in, as recommended by Lillehei in 1964. Preservation of
ventriculo-annular continuity through the retained leafl et, its chordae, and the papillary muscles
is benefi cial for maintenance of original left ventricular geometry. It helps to prevent acute left
ventricular dilation, which may occur namely in severely impaired left ventricles after complete
mitral valve excision and longer ischemic heart arrest. Decrease of left ventricular ejection
fraction after mitral valve excision is also less should the posterior mitral leafl et be preserved. Th
is strategy is recommended in mitral stenosis whenever the morphology of the valve allows it. It
is, however, even more important in mitral regurgitation unsuitable for repair
Rheumatic mitral stenosis with fused commissures with a dilated, severely impaired left
ventricle. Preservation of the posterior leafl et also reduces the risk of a rare but mostly fatal left
ventricular rupture. In order to prevent left ventricular dilation and to maximize the protection of
ventricular architecture, also the part of the anterior mitral leafl et with its chordae can be
preserved (Fig. 6.13). A variety of other techniques and modifi cations have been described
focused on partial anterior leafl et preservation, for example, fi xation of the annulus to the
papillary muscles by artifi cial chordae. The mechanical valve or bioprosthesis is fi xated to the
mitral annulus most safely by pledgeted mattress stitches (Figs. 6.14-6.16). In cases of well-
accessible fi rm-tissue annulus, a continuous stitch may be used for valve implantation. Th is
technique is somewhat faster. Bileafl et heart valve should be positioned antianatomically in
order to achieve optimal hemodynamics. Th e slit between the two leafl ets should be orientated
perpendicular to the original zone of coaptation of the anterior and posterior mitral leafl ets (Fig.
6.15). Patient-prosthesis mismatch may exist also in mitral valve replacement. Mild mismatch
occurs if the indexed eff ective orifi ce area is within the range of 0.9 to 1.2 cm2/m2 and severe
mismatch is defi ned by an eff ective orifi ce area index of less than 0.9 cm2/m2. Severe patient-
prosthesis mismatch results in higher operative mortality, worse longterm outcome, and lesser
decrease of pulmonary hypertension. The eff ort to implant a valve that is large enough is justifi
ed in small mitral annuli (rheumatic mitral stenosis with small left ventricle). On the other hand,
in very large mitral annuli (mitral incompetence) the implantation of a valve bigger than 31 mm
is useless. A mild undersizing
 St. Jude Medical valve seated in the mitral annulus in antianatomical orientation before tying of the sutures
is reasonable and prevents the risk of disc collision with the myocardium in case of postoperative
decrease of the left ventricular diameter. A proper placement of the stitches in the mitral annulus
is very important at mitral valve replacement. The stitch must pass through the annulus only or
through the narrow junction of the annulus and myocardium. The stitch must never pass through
the myocardium. If the stitch grossly bites the myocardium, it will cut through the fragile
myocardium during the tying (Fig. 6.17). Such a lesion may lead to intramyocardial hematoma or
subepicardial hematoma in the atrioventricular groove, which will subsequently perforate in the
course of operation or soon after operation. This is one of the causal mechanisms of the most
feared complication of mitral valve replacement: left ventricular rupture . Another cause of left
ventricular rupture is an overly radical - and left untreated - excision of the calcifi cations that
grow into the annulus and the myocardium . Excessive annular calcifi cations at the base of the
posterior leafl et (Fig. 6.18) can be widely excised and the area reinforced by suture with use of a
pericardial patch or pledgeted stitches . In the opinion of the present authors, this procedure is too
risky, and instead of it, a safer, faster, and easier implantation of the valve into the posterior
mitral leafl et should be preferred, with leaving the calcifi cations in situ (Fig. 6.19). Besides
these two elementary reasons for left ventricular rupture in the area of the atrioventricular groove
(type-I rupture), an occurrence of this complication after forceful implantation of an overly large
valve prosthesis has also been published. Myocardial injury or even endocardial discontinuation
can also happen during reoperation for dysfunction of the implanted mitral valve due to
aggressive explantation of the valve from the mitral annulus (the tips of the scissors or the lancet
have to follow closely the edge of the sewing ring and point centrally below the valve and not
perpendicular to the plane of its orifi ce). Left ventricular rupture types II and III are localized
distally to the atrioventricular groove. Th is results from myocardial injury caused most often by
a surgical tool. It may occur from the cut of the scissors tips during valve excision under poor
visibility conditions (Fig. 6.20; the thickened chordae have to be cut precisely with the scissors
tips under perfect visual control). Endocardial and myocardial lesions can also be caused by
pressure of the sharp metallic suction device (Fig. 6.21; it is advisable to use a round-tipped glass
suction device and forbid suction by the assistant, who has an obstructed view of the operative fi
eld). Similarly, the strut of the bioprosthetic stent can get buried in the myocardium and cause a
deep lesion (Fig. 6.22; pushing of the stent into the ventricle during the tying has to be avoided
and countertraction of the stitch has to be used instead). All these mechanisms can cause either a
complete tear or a partial lesion fi rst followed by intramyocardial and later subepicardial
hematoma, which can end in perforation even after several hours. Left ventricular rupture is a
rare but highly lethal complication (65-80%); therefore, all abovementioned risk factors for its
occurrence during mitral valve replacement have to be kept in mind. Surgical management of the
rupture is potentially possible but very diffi cult and often unsuccessful due to the inability to
localize its origin and treat the precise pathway of the rupture (pledgeted stitches, pericardial
patch, glue, etc.). Chance for salvage of the patient is higher if the complication manifests when
the cardiopulmonary bypass is still instituted than at the end of the operation or even at the
intensive care unit in the moment of rupture of subpericardial hematoma. Some authors therefore
recommend gentle lifting of the heart and inspection of the posterior left ventricular wall and the
area of atrioventricular groove at every mitral valve replacement before disconnecting the
cardiopulmonary bypass.

Mitral Regurgitation
Surgical procedures for mitral regurgitation are the second most frequent valve operations.
Regurgitant fl ow from the left ventricle into the left atrium causes volume overload of the left
ventricle. Th is volume overload in the long-term course leads to left ventricular dilation and
hypertrophy, dilation of the left atrium with onset of atrial fi brillation, and, without treatment, to
a signifi cant impairment of the left ventricular ejection fraction. Th e fi rst clinical symptoms are
weakness, fatigue, palpitation, and exertional dyspnea. The majority of mitral regurgitation cases
can be treated by valve repair. In recent years a signifi cant shift toward much earlier indications
for operation, even in asymptomatic patients, has been witnessed, supported by excellent early
and long-term results of mitral repairs and, on the other hand, worse early and uncertain long-
term outcome in cases of delayed surgery.

Etiology of Mitral Regurgitation

Degenerative disease is the most common cause of mitral regurgitation. Th is involves
myxomatous degeneration (Barlow’s disease with leafl ets billowing into the left atrium, floppy
mitral valve), fi broelastic leafl ets degeneration leading to their prolapse (Fig. 6.23), leafl ets
prolapse caused by rupture or elongation of the chordae, mitral regurgitation in Marfan and
Ehlers-Danlos syndromes, and also annular calcifi cations (Fig. 6.18) and sclerotic changes of the
leafl ets. Mitral regurgitation caused by degenerative etiology is in most cases amenable to valve
repair. Ischemic etiology is the second most common cause of mitral regurgitation. In ischemic
mitral regurgitation the valve itself is not altered morphologically, but its incompetence results
from dysfunction of the ischemic left ventricular myocardium (remodelation, akinesis,
dyskinesis, papillary muscles displacement; Fig. 6.24) . Ischemic mitral regurgitation can be
almost always resolved by annuloplasty ring implantation. Rare papillary muscle rupture (Fig.
6.25) in acute myocardial infarction leads to acute mitral regurgitation, which necessitates acute
surgery, i.e., repair or replacement of the mitral valve. Third in order of incidence is the
functional (secondary, non-organic) mitral regurgitation in which the valve again is not altered
but regurgitation develops from annular dilation and left ventricular remodelation with
displacement of papillary muscles (dilated left ventricle due to dilated cardiomyopathy or aortic
valve disease, mainly aortic regurgitation). In functional mitral regurgitation the left ventricular
systolic function used to be signifi cantly impaired. Th e majority of these functional
regurgitations can be treated by annuloplasty ring implantation. Infective endocarditis, either
active (Fig. 6.26) or healed (Fig. 6.27), can lead to mitral regurgitation due to infective
destruction of the valve (leafl et defects, periannular abscesses, chordae ruptures). Infective mitral
regurgitation in acute endocarditis where fulminant and uncured infection
Excised mitral valve (deteriorated from Barlow’s disease) after healing of infective endocarditis (defect in the
anterior leafl et)
process destroyed the valve leafl ets requires valve replacement. If the infection is restricted (e.g.,
to a portion of the posterior leafl et only) or had caused the perforation, valve repair may be
considered (partial posterior leafl et resection, closure of the leafl et perforation with a pericardial
patch). Mitral regurgitation after healed endocarditis can sometimes also be treated by a
valvesparing procedure. Rheumatic etiology of mitral regurgitation is rare in developed countries
and may be encountered in the elderly population only. On the other hand, in developing
countries it is still very common mainly in young girls and women. Rheumatic mitral
regurgitation is usually not very suitable for valve repair, because it is associated mostly with
valvular stenosis and advanced rheumatic dystrophy of the leafl ets, their commissures, and
chordae (Fig. 6.28). Moreover, the ongoing rheumatic process impacts negatively in the long
term on the result of the valve repair, which is, due to the nature of rheumatic involvement,
scarcely ideal even at the surgery. The commonest type of congenital mitral regurgitation is the
cleft of the anterior mitral leafl et in atrioventricular septal defect (Fig. 6.29). Th e easiest
treatment is suture of the cleft. In adulthood the complete form of the atrioventricular septal
defect is not to be met as a subject of primary operation, but sometimes reoperations for steno-
incompetence of the mitral valve are required after previous surgical corrections of a complete or
incomplete form in childhood. Such findings usually end up with mitral valve replacement. An
iatrogenic lesion of the mitral valve during balloon mitral valvuloplasty is one of the rare causes
of acute mitral regurgitation (Fig. 6.30). It happens when the pressure of the infl ated balloon
does not cause the desired loosening of the fused commissures but tears the valve in the place of
least resistance, usually across the anterior leafl et. Acute surgery is inevitable. A rheumatic
diseased valve with disrupted leafl et has to be replaced by a mechanical prosthesis or
bioprosthesis.

Indications for Surgery

Surgical treatment of mitral regurgitation should be offered to patients early, i.e., before
development of irreversible left ventricular dysfunction and dilation, left atrial dilation,
pulmonary hypertension, onset of atrial fi brillation, and fi nally, tricuspidalization of mitral valve
disease. Patients with severe mitral regurgitation who are symptomatic are unequivocally
indicated for surgery. Hemodynamically severe mitral regurgitation is determined by
regurgitation volume (RV) >50 ml, regurgitation fraction >50 %, eff ective regurgitation orifi ce
(ERO) >0.4 cm2, vena contracta >6-7 mm, and by impaired left ventricular functional parameters
(EF <60% and end- systolic left ventricular diameter, LVESD, >40-45 mm). The onset of atrial fi
brillation and development of pulmonary hypertension (systolic pulmonary pressure >50 mmHg)
are the signs of long-term presence of signifi cant mitral regurgitation. In cases of ischemic mitral
regurgitation, the indication criteria for surgery are stricter. Mitral valve repair should be
performed as an adjunct to coronary bypass grafting in already mild to moderate ischemic mitral
regurgitation, i.e., provided that RV is >30 ml and ERO >0.2 cm2. Th ese strict criteria need not
be applied - and often even should not be - in patients with signifi cant comorbidities and in those
over 75 years. Except for increased operative risk, the quality of life would remain unaff ected,
keeping in mind that mitral regurgitation is only mild to moderate and overall life expectancy
shorter. Indications for surgery are not easy to identify in symptomatic patients with chronic
mitral regurgitation and poor left ventricular function (EF <30 %). In general, mitral valve repair
should be performed if there is evidence of contractile reserve. Current progress in myocardial
protection and perioperative care has infl uenced the indication criteria. Patients with severe
mitral regurgitation and low ejection fraction who would have been formerly rejected for surgery
are currently operated with acceptable outcome. If the decision remains controversial, the left
ventricular end-diastolic diameter (LVEDD) also has to be taken into account. The surgery can be
recommended at LVEDD below 65 mm. Operative risk rapidly increases when dimensions
exceed 65 mm, and at LVEDD of 85 mm the surgery is no longer indicated. Th ese patients with
poor ejection fraction, large ventricular dimensions, and no contractile reserve are amenable to
medical therapy only or could be considered candidates for heart transplantation. Asymptomatic
patients with severe mitral regurgitation are followed-up by echocardiography. Surgery is indi
cated when the fi rst signs of the left ventricular impairment appear (EF <60%, LVESD >45
mm,) ERO >40 mm2, at the onset of atrial fi brillation or pulmonary hypertension (at-rest
pulmonary systolic pressure >50 mmHg).

Mitral Valve Repair

Perfect performance of the mitral valve depends on correct function and coordination of all
components of the mitral valve complex (i.e., mitral annulus, mitral leafl ets, chordae, papillary
muscles, and left ventricular myocardium). The mitral leafl ets have to coapt along the whole line
of closure in a safe coaptation zone of several millimeters in height (Fig. 6.31). A lesion of
whichever mitral valve component can lead to severe regurgitation based on the loss of
coaptation of the mitral leafl ets. Morphological classifi cation of mitral regurgitation has been
mentioned previously (i.e., degenerative, ischemic, functional, rheumatic, congenital, and
iatrogenic types). For surgery there is important functional classifi cation into three basic types
according to Carpentier. Type I is characterized by normal leafl et mobility (Fig. 6.32).
Regurgitation results from loss of coaptation due to annular dilation, left ventricular dysfunction,
or occasional perforation of a leafl et. In type II there is mitral leafl et prolapse caused by
elongation or rupture of the chordae or papillary muscles (Fig. 6.33). Type III is characterized by
restricted motion of the leafl ets caused by shortening of the chordae in rheumatic disease (Fig.
6.34) or by traction of the chordae due to ischemic left ventricular remodelation. A prerequisite of
successful surgery is proper preoperative echocardiographic analysis of the regurgitation
mechanisms. Selection of the repair technique is based on knowledge of the regurgitation
etiology, pathomorphology fi ndings, and functional type of the regurgitation. Th e eff ect of the
repair should be durable and simultaneously the valve must not become stenotic. Th e main
principle to be pursued in all repair techniques is achievement of safe and wide coaptation of the
mitral leafl ets. Th e eff ect of the accomplished repair has to be proved by peroperative
echocardiography after weaning off cardiopulmonary bypass.

Annuloplasty Procedures
Chronic hemodynamically signifi cant mitral regurgitations existing over a long time display one
common feature: dilation of the mitral annulus. Th e dilation does not develop symmetrically
along the whole annular circumference but only in the area of the posterior leafl et and both
commissures. Annular length of the area belonging to the anterior leafl et remains unaltered (Fig.
6.35). Th is finding determines the philosophy of annuloplasty ring implantations as well as other
repair techniques. Annuloplasty rings are being implanted in a manner to reduce the dilated
portion of the annulus only. Th e mattress sutures in the area of the posterior leafl et and both
commissures take wider bites along the annulus but are passed through the ring in narrower
intervals (Fig. 6.36). In this way the annular circumference can be plicated and intentionally
reduced. Annuloplasty rings are very eff ective in most Carpentier type-I mitral regurgitations A
variety of annuloplasty rings have been designed and marketed (Fig. 6.37). Th ey are rigid (e.g.,
Carpentier-Edwards, St. Jude Medical Rigid Saddle, AnuloFlo-Carbo- Medics), semifl exible
(e.g., Carpentier-Edwards Physio,
St. Jude Medical Sequin, Sorin MEMO3D), and fl exible (e.g., Medtronic-Duran, Sorin-Sovering,
Anulo Flex- Carbo Medics, ATS Simulus FLX-O). Some rings are designed without the anterior
leafl et portion (resembling horizontal fi gure of C, e.g., Colvin-Galloway, Cosgrove-Edwards,
ATS Simulus FLX-C, or AorTech MRS) or this portion can be either used or trimmed off (St.
Jude Medical Tailor, AnuloFlex-CarboMedics) . All rings are biocompatible, and some of them
are even carbofi m coated (Sorin-Sovering) or produced from polytetrafl uoroethylene (PTFE;
Jostra).
Principle of implantation of annuloplasty ring. Mattress sutures placed in the area of posterior leafl et take wider
bites than their intervals in annuloplasty ring

There is a possibility to implant a new adjustable annuloplasty ring, St. Jude Medical Attune. Th
is ring off ers symmetrical adjustability by pulling both purse-string-suture ends equally or
asymmetrical adjustability by pulling one purse-string-suture end more than the other (Fig. 6.38).
Very similar adjustable rings, such as Puig-Massana-Shiley and St. Jude Medical BiFlex, were
used in the 1980s. The GeoForm ring is geometrically designed to treat mitral regurgitation
caused by the enlargement of the left ventricle. Anteroposterior distance of the mitral annulus is
reduced and the P2 zone is elevated in the ring. A novel annuloplasty ring design, Myxo-ETlogix
(Edwards), is also aimed at prevention of systolic anterior motion (SAM) in patients with
myxomatous leafl et degeneration (Barlow’s disease). Th is ring has a signifi cantly longer
anteroposterior diameter and saddle-like elevation in the area of P2. The proper size of the ring is
decided upon by measuring the distance between the two commissures marked with the fi rst two
mattress sutures (Fig. 6.39). In ischemic and secondary mitral regurgitation, a sole annuloplasty
ring implantation is an adequate procedure (Figs. 6.40, 6.41). The effect of the annuloplasty lies
not only in reduction of the dilated annular portion but also in true remodelation of the almost
circular dilated mitral annulus into its correct original “kidney-shaped” appearance. Th is brings
the two leafl ets closer together and thereby enables restoration of their proper coaptation.
Annuloplasty rings are also being implanted after complex reconstructive repairs of the mitral
valve to prevent any later redilation of the annulus and reoccurrence of mitral regurgitation. Some
authors recommend securing each mitral repair by annuloplasty ring implantation
Adjustable annuloplasty ring St. Jude Medical-Attune
and Puig-Massana-Shiley (top)
A result similar to that achieved by fl exible C-ring implantation can be obtained by a
semicircular annuloplasty according to Burr et al. With this technique running sutures are passed
through the posterior leafl et from the commissures toward the midpoint of P2 (Fig. 6.42).
Tightening of the sutures leads to reduction of the dilated annular portion (Fig. 6.43). It is
advisable to use company ring sizers (usually 26 mm for women and 28 mm for men) to facilitate
proper degree of tightening. This suture annuloplasty technique is simple, fast and inexpensive,
preserves fl exibility of the annulus, and durability of the result is comparable to that of ring
implantations. Reduction of dilated mitral annulus as a treatment of mitral regurgitation was
published in 1958 by Kay et al., who coined the term “annular plication”; however, the method
published by Wooler et al. in 1962 has become more popular and widely used. The principle of
the Wooler repair involves shortening of the annulus at both commissures and adjacent portions
of the posterior leafl et (Figs. 6.44, 6.45). It is a very fast and simple annuloplasty
(commissuroplasty) that can resolve not only regurgitation located in the commissural area but
also central regurgitation from mitral annulus dilation, because it also brings the leafl ets closer
together. Nonetheless, implantation of the annuloplasty ring seems currently to be a more proper
way of treatment for these cases, because it guarantees postoperatively long-term prevention of
redilation of the annulus; therefore, use of the Wooler repair is presently justifi ed in occasional
situations only (long duration of cardiopulmonary bypass in complex procedures, elderly patients,
diffi cult exposure of mitral valve due to deep chest, in reoperations, etc.).

Leafl et and Chordae Procedures

Besides the abovementioned classic and relatively easy mitral valve repair techniques, also more
demanding procedures are being performed at the mitral leafl ets and chordae. Annuloplasty ring
implantation is, however, usually added as a final step also in these techniques. Prolapse of one or
both mitral leafl ets from degenerative etiology (Carpentier classifi cation type II) is the
commonest situation that requires such procedure. Prolapse occurs most often at the posterior
leafl et, predominantly at the middle portion (P2; Figs. 6.23, 6.46). Quadrangular or triangular
resection of the posterior leafl et is the treatment of choice that can be accomplished irrespective
of the actual cause of prolapse (elongated or ruptured chordae, excessive leafl et tissue, or a
combination of both). Th e prolapsing portion of the posterior leafl et is cut off , the remaining
portions (P1 and P3) are sutured together, and long-term durability of the repair eff ect is secured
by annuloplasty ring implantation (prevention of annular redilation; Fig. 6.47). If too much
excessive tissue remains, even after quadrangular leafl et resection, and its height exceeds 1.5 cm,
sliding plasty is indicated. With this method the leafl et resection is extended periannularly and
cuneiform areas of the excessive leafl et tissue are excised (Fig. 6.48). Sliding plasty is
considered to be prevention of occurrence of SAM, i.e., collapsing of the anterior mitral leafl et
into the left ventricular outfl ow tract in systole. Since their publication by Carpentier in the mid-
1980s, both techniques have been popular. In 2006 Calafi ore et al. published a new concept
regarding how to treat the excess of posterior leafl et tissue and named it “ posterior leafl et
longitudinal plication”. The principle is very simple and lies in shortening of

Placement of sutures at repair. (According to Burr et al. [66])

the posterior leafl et height by several mattress sutures led through the annulus and prolapsing
portion of the posterior leafl et (Fig. 6.49). Despite limited experience, the technique seems to be
promising in the prevention of SAM. While the classic concept of mitral repair is based on some
reduction in the area of posterior leafl et, a diff erent, more conservative approach has recently
been advocated by Perier et al. In their strategy “respect rather than resect” they try to save the
patient’s prolapsing posterior leafl et tissue as much as possible and to transform it, by means of
PTFE chordae, into a smooth vertical buttress. Similarly, Tabata et al. suggest remodeling of the
excessive posterior leafl et tissue by one or more sutures, which would pull in the prolapsing edge
beneath the body of the posterior leafl et (Figs. 6.50, 6.51). The occurrence of SAM after mitral
valve repair is a serious perioperative complication that causes left ventricular outfl ow tract
obstruction and also mitral regurgitation (Fig. 6.52). Incidence of this troublesome situation after
mitral valve repair is reported usually in 5% of cases. Numerous authors claim to not have
encountered this complication, although others report its incidence as up to 10%. Controversy
exists regarding the origin of SAM, thus refl ecting the diversity of potential causes. The main
risk factors for SAM are: (a) excessive amount of leafl et tissue; (b) an overly large posterior leafl
et left; (c) small annulo plasty ring; (d) left ventricular hypertrophy; (e) interventricular septal
hypertrophy; and (f ) hyperkinetic circulation. The danger is increased if several potential risk
factors are present simultaneously. Most authors emphasize the role of an excessive amount of
posterior leafl et tissue left. Th e height of the posterior leafl et should not exceed 1.5 cm;
otherwise, performing a sliding plasty is recommended. In small and hypertrophic left ventricle
also preservation of excessive anterior leafl et tissue may increase the risk of SAM. In such
situations Quigley in 2005 recommended performance of anterior leafl et reduction by a
semilunar excision parallel to the annulus of the anterior leafl et. Systolic anterior motion after
mitral valve repair occurs predominantly as a result of the disparity between the excessive area of
leafl et tissue left compared with the size of the left ventricle and width of the left ventricular
outfl ow tract, as well as a small-size annuloplasty ring implantation (Fig. 6.52). As a rule, testing
of the completed repair on an arrested heart demonstrates excellent leafl et coaptation; however,
peroperative transesophageal echocardiography on a beating heart reveals SAM causing pressure
gradient in the left ventricular outfl ow tract, and simultaneously the presence of mitral
regurgitation. Management remains always problematic and individual. Th e principal decision
concerns the necessity of mitral valve surgical reintervention. This decision can be facilitated by
several tests, which may lead to cessation of SAM. The most important test is volume expansion
(i.e., increase of preload). Th e patient’s hypovolemia has to be excluded. Th e eff ect of volume
expansion can be forecasted by a quick maneuver performed by partial compression of the
ascending aorta by clamp or fi ngers. In this way, during several systoles the increased preload
leads to cessation of both SAM and mitral regurgitation. If cessation of SAM is achieved, the
volume expansion is continued together with administration of small doses of beta--blockers to
suppress the left ventricular hypercontractility. In this case surgical reintervention on the mitral
valve is not deemed necessary. Postoperatively, volume expansion and beta-blocker
administration are continued, hypovolemia has to be strictly avoided, and repeated
echocardiography controls are performed. If, however, SAM persists in the operating room
despite the testing maneuvers, surgical intervention has to be undertaken. Th e easiest solution is
Alfi eri edge-to-edge repair (see below), provided, however, the initial mitral procedure did not
already result in a signifi cant mitral annulus “undersizing” (borderline mitral orifi ce area). If the
cause of SAM is clearly detected, its correction may be attempted at the reintervention;
otherwise, namely after a time-consuming primary complex mitral valve repair, fast mitral valve
replacement is the safest alternative compared with an uncertain and long repair correction.
Failure in attempting repair correction will result in further reintervention (valve replacement),
and the total of three cardiopulmonary bypass periods may have a deleterious impact. Procedures
for anterior leafl et prolapse are more diffi cult than for posterior leafl et prolapse. Isolated
anterior leaflet prolapse occurs rarely compared with isolated posterior leafl et prolapse. Anterior
leafl et prolapse is usually part of bilateral leafl et prolapse. In bilateral leafl et prolapse a
relatively new Alfi eri repair can be performed. With this technique the incompetent mitral orifi
ce is transformed into two competent orifi ces by suturing the midpoints of the anterior and
posterior leafl ets together (“double-orifi ce” or “edge-to-edge” repair). It is important to place
the sutures at some distance from the edge of the leafl ets to shorten their length and to secure a
suffi cient zone of coaptation of newly created orifi ces (Fig. 6.53). Suturing is performed with
over-and-over sutures or, in the case of thin leafl ets, with pledgeted mattress sutures. It is an
extremely simple and fast technique, but it is still controversial, having both supporters and
opponents. A classic and still used method in anterior leafl et prolapse is triangular resection,
which is performed by cutting off a narrow triangle from the most prolapsing portion of the
anterior leafl et (Fig. 6.54). Occasionally, the excessive area of the anterior leafl et can be
reduced by suture plication of the anterior leafl et edge as described by Fundaro et al. (Fig. 6.55) .
Elongated chordae of the anterior and posterior leaflets can be shortened by their insertion into
the papillary muscles (Fig. 6.56). Ruptured and recently also the elongated chordae are being
replaced by artifi cial chordae from PTFE sutures (Figs. 6.57, 6.58). They can also be excised and
replaced by transposition of the nearest thick secondary chord. Sometimes the secondary chordae
retract the midportion of the anterior leafl et (“ seagull-sign” deformation of the anterior leafl et
on echocardiography examination) and thereby worsen the degree of mitral regurgitation. Their
resection, as a part of mitral valve repair, improves the anterior leafl et mobility toward the
coaptation zone (Fig. 6.59). In some cases of mitral regurgitation caused by ischemic left
ventricular remodelation, it has been recommended to suture together both heads of papillary
muscles by a pledgeted mattress stitch (sandwich plasty). Reapproximation of the anterior and
posterior papillary muscles reduces tethering and improves the leafl et coaptation . Rheumatic
mitral valve disease results in Carpentier type-III mitral regurgitation characterized by shortening
and retraction of chordae and papillary muscles. Should

a Rupture of primary chord of anterior mitral leafl et. b Placement of polytetrafl uoroethylene (PTFE) suture into the
papillary muscle (artifi cial chord)
valve-sparing surgery be attempted (in spite of mitral valve replacement) dissection of the fused
commissures, liberation of the thickened, fused, and shortened chordae, and dissection of the
thickened papillary muscles is performed (see Fig. 6.10). Improved billowing of the retracted
leaflets can be obtained by secondary chordae resection and by anterior leafl et augmentation
with autologous pericardium (Fig. 6.60). Th e posterior leafl et can also be augmented in a similar
manner, e.g., if retracted due to left ventricular dysfunction. Th e enlarged area of the posterior
leafl et will enable its coaptation with the anterior leafl et.

Tricuspid Valve Surgery

Introduction
Similarly to aortic and mitral valve disease, both tricuspid stenosis and tricuspid regurgitation can
be treated surgically. In clinical practice, however, surgical procedures for tricuspid stenosis are
extremely rare. Numerous techniques for correction of tricuspid regurgitation have been
elaborated since the 1960s but for decades surgeons have remained rather conservative in
indications for tricuspid valve repair. Tricuspid regurgitation was traditionally believed to
ameliorate spontaneously after surgical correction of left-sided heart valve disease and, in
general, to be well tolerated by the patient. A shift in the paradigm towards a more aggressive
surgical approach to secondary tricuspid regurgitation has been advocated by many in recent
years in order to prevent further worsening of regurgitation and to avoid late reoperations with
unfavorable results. The number of surgical corrections of tricuspid regurgitation has been
increasing because modern indication criteria do rightly suggest surgical intervention, even in
less- signifi cant tricuspid regurgitation, as part of a combined cardiac operation.
Tricuspid Stenosis
Acquired organic stenosis of the tricuspid valve is very rare. It can be caused by rheumatic
disease as a part of mitro-tricuspid valve involvement or even more rarely as an isolated
rheumatic tricuspid stenosis. Similarly rare is the carcinoid that requires operation because of
causing tricuspid stenosis. Right atrial tumors may almost completely occlude the tricuspid orifi
ce and thereby imitate tricuspid stenosis. Operations of tricuspid stenosis as a part of mitro-
tricuspid rheumatic valve disease are currently extremely rare in developed countries. Indication
for surgical intervention is justifi ed in symptomatic patients with hemodynamically signifi cant
tricuspid stenosis (diastolic gradient >5 mmHg and orifi ce area <1.0—1.5 cm2). Treatment is
either a valvesparing procedure (dissection of the fused commissures, eventually followed by
valvular repair) or valve replacement in cases of rigid circular orifi ce with calcifi cations.

Tricuspid Regurgitation
Etiology of Tricuspid Regurgitation
Secondary (functional, non-organic) tricuspid regurgitation caused by dilation of the tricuspid
annulus is the most frequent reason for surgical intervention on the tricuspid valve. Secondary
tricuspid regurgitation evolves as a result of long-term elevated right ventricular pressure caused
most often by pulmonary hypertension. Pressure or volume right ventricular overload leads to
right ventricular hypertrophy and dilation together with the tricuspid annular dilation (Fig. 7.1).
Primary causes of development of secondary tricuspid regurgitation are left heart valve disease
(tricuspidalized disease), pulmonary stenosis, or regurgitation or congenital heart defects with
left- to-right shunt. Acquired organic tricuspid regurgitation is less frequent and may be caused
by myxomatous degeneration, infective endocarditis (Figs. 7.2, 7.3), trauma, and carcinoid.
Ebstein’s anomaly and various forms of atrioventricular

Dilation of the tricuspid annulus causing secondary tricuspid Regurgitation

Infective endocarditis of the tricuspid valve. Vegetation on the anterior leafl et septal defect are
the main instances of congenital tricuspid regurgitation. Echocardiography examination off ers
precise morphological analysis of tricuspid regurgitation and evaluation of its hemodynamic
signifi cance.
Indications for Surgery
Surgical procedure for tricuspid regurgitation is most often undertaken due to tricuspid annular
dilation or more rarely due to organic changes resulting from endocarditis or congenital cardiac
defects. Isolated tricuspid valve procedure is relatively rare, accounting for 5-10% of all tricuspid
valve procedures. It is indicated in symptomatic patients [fatigue, dyspnea, symptoms of low
cardiac output, hepatomegaly, edema of low extremities, New York Heart Association (NYHA)
stages III-IV] and also in those in whom clear progression of right-sided heart chambers can be
evidenced together with impairment of right ventricular systolic function. Uncontrolled sepsis
and development of right ventricular failure in tricuspid valve infective endocarditis is also an
indication for surgery. Surgery for tricuspid regurgitation as a part of multiple- valve procedure
(together with interventions on the left heart valves) is unequivocally indicated not only for
severe tricuspid regurgitation (vena contracta >6-7 mm, reversal of fl ow in the hepatic veins) but
also for moderate regurgitation with dilation of the tricuspid annulus (echocardiographically
documented dilation >40 mm or >21 mm/m2). The most recent recommendation for tricuspid
annuloplasty suggests a cut-off value of the annular dilation over 35 mm. The rationale for such
strategy is based on a his 316 Tricuspid Valve Surgery tory of unpredictable course of mild to
moderate tricuspid regurgitation that was left untreated at the time of mitral procedure. Th is is
also supported by poor results of reoperations of patients with advanced severe tricuspid
regurgitation many years after isolated mitral procedure. With regard to all these factors,
performance of tricuspid repair as part of a combined procedure must be justifi ed, even in cases
of mild tricuspid regurgitation if annular dilation or pulmonary hypertension are present. Dreyfus
et al. recommend tricuspid valve repair should the intraoperative anteroposterior tricuspid
diameter measurement exceed 7 cm (even in trivial regurgitation). Such advanced annular
dilation will not regress, even after left heart valve surgery, but will most likely advance progress.

Surgical Procedures on the Tricuspid Valve

There are three types of surgical interventions on the tricuspid valve: (1) repair; (2) replacement;
and (3) excision.

Tricuspid Valve Repair for Secondary Regurgitation Valve-sparing

procedures (repairs) are the most often performed operations on the tricuspid valve. The most
frequent reason for the repair is annular dilation causing secondary tricuspid regurgitation.
Tricuspid annulus typically dilates only in the area of the anterior and posterior leafl et, whereas
its septal-leafl et length remains unchanged (Fig. 7.4) . This fact is the key feature of all tricuspid
annuloplasty techniques: shortening of the tricuspid annulus in the area of the anterior and
posterior leafl ets. The shortening can be achieved by suture repairs or by annuloplasty ring
implantation A variety of suture techniques have been described and introduced into clinical
practice despite recent decline in their use in favor of annuloplasty ring implantation. The oldest
repair was described by Kay et al. in 1965. The principle is posterior tricuspid leafl et exclusion,
which transforms the incompetent tricuspid valve into a competent bicuspid valve; therefore, the
technique is called suture bicuspidalization of the tricuspid valve. Kay et al. Performed the repair
by suturing together the annulus in the area of the posterior leafl et with several over-and-over
stitches. In 1967 Reed and Cortes published a paper describing the bicuspidalization technique
with use of a mattress stitch with pledgets on both sides (Figs. 7.5, 7.6). Th ey also calculated that
the shortened annulus circumference has to be at least 8 cm. In 1984 Nakano et al. described an
analogous typ of a bicuspidalization repair. This technique is suitable for those valves where
regurgitation occurs predominantly through pathologically distended commissure between the
anterior and posterior leafl ets. Th e commissure is sutured and then Kay’s plasty is added to a
somewhat lesser extent (Figs. 7.7, 7.8). The most popular and widely used suture technique is
DeVega annuloplasty (described in 1972). The principle of this technique lies in shortening the
tricuspid annulus in the area corresponding to the anterior and posterior leaflets. Two pledgeted
parallel running stitches are placed in semicircular manner from the anterolateral to the
posteroseptal commissure and tied (Figs.
7.9, 7.10). Th e possibility of failure of this repair, however, has been also described. One of the
reasons for failure is cutting through of the stitches placed in a fragile tricuspid annulus (Fig.
7.11). To avoid this potential risk, Antunes and Girdwood in 1983 suggested modifi cation of
DeVega technique. The semicircular stitch is passed through a pledget between every bit of
annular tissue (Figs. 7.12, 7.13). Revuelta and Garcia-Rinaldi in 1989 published a diff erent
solution: for annular shortening they used separate pledgeted mattress stitches. Another
advantage of this technique is the possibility to aff ect selectively the degree of reduction in diff
erent portions of the annulus by the width of the mattress stitches (Figs. 7.14, 7.15). Modifi cation
of the classic DeVega technique, enabling selective regulation of the reduction of the anterior and
posterior portions of the tricuspid annulus, was used by Senning and published by Brugger et al.
in 1982. The stitch is fi rst tied in the area of anteroposterior commissure and then its arms are
passed through the tricuspid annulus in opposite directions analogous to the DeVega technique
(Fig. 7.16). It is interesting that even in the current era of annuloplasty rings Sarraj et al.
published in 2007 a very similar technique, which they named adjustable segmental tricuspid
annuloplasty (Fig. 7.17). In 1987 Kurlansky et al. described an interesting modifi cation of the
DeVega technique. Placement of two rows of stitches along the annulus from the anteroseptal
commissure to the posteroseptal commissure is the same, but then the stitches are led out through
the right atrial wall and snared through a tourniquet. After restoration of the heart rhythm and
weaning off the cardiopulmonary bypass, the surgeon evaluates regurgitation with a forefi nger
inserted through the right atrial appendage (Fig. 7.18). The stitches are tightened until the
moment of cessation of regurgitation. An identical principle can be applied with the aid of
peroperative echocardiography (published by Cook
 Placement of sutures in tricuspid repair. (According to Kay et al. [6] and Reed and Cortes [7])

Result of tricuspid repair (bicuspidalization of the tricuspid valve). (According to Kay et al. [6] and Reed and Cortes [7]) in
1994). Th e tightening proceeds until the echocardiography confi rms cessation of regurgitation
and simultaneously excludes creation of tricuspid stenosis. The overview of suture-repair
techniques should include also the less frequently used technique described by Minale et al. in
1987. With this technique the anterior and posterior leafl ets are partially detached from the
tricuspid annulus in the area of anteroposterior commissure to allow their central coaptation. The
isolated portion of the annulus is reduced by its plication and exclusion. Th e cut edges of the
leafl ets are then readapted to the shortened annulus (Figs. 7.19-7.21). Finally, there exists a
“triple-orifi ce” method termed also a trefoil or “ edge-to-edge” repair of the tricuspid valve. This
technique was first performed by Giedrius in 2000 and published by DeBonis in 2004. Tricuspid
regurgitation caused by myxomatous degeneration and leafl et prolapse can be treated in addition
to the annuloplasty ring implantation by suturing the midpoints of all three leafl ets together, thus
creating three orifi ces (Fig. 7.22). Competence of the tricuspid valve can also be restored by
implantation of the annuloplasty rings that have the ideal shape of tricuspid annulus (Fig. 7.23).
Th e implanted ring not only reduces the annular circumference within the extent of the anterior
and posterior leafl et, but also enforces its proper shape and guarantees annular shape and size
retainment in the long term. Implantation is performed with mattress sutures placed
proportionally in the non-dilated septal portion of the annulus, whereas in the dilated
anteroposterior circumference the sutures bite more of the annulus and are passed in narrower
intervals through the ring fabric (Fig. 7.24). This results in controlled plication

Tricuspid valve repair (“triple orifi ce,” “edge to edge,” and “trefoil method”). (According to
DeBonis [19])
Annuloplasty ring for tricuspid valve repair. a Standard Carpentier- Edwards. b Edwards MC3
mitral valve disease should be indicated for surgery before development of secondary tricuspid
regurgitation .
Repair for Ebstein’s Anomaly
Ebstein’s anomaly is characterized by downward displacement of the septal and posterior
tricuspid leafl et attachment toward the right ventricular apex. Th e trabeculized portion of the
right ventricle beneath the valve is small and dysfunctional. Th e atrialized portion of the right
ventricle above the valve is thin-walled and belongs to the dilated right atrium (Fig. 7.26).
Hemodynamically the situation is characterized by decreased pulmonary blood fl ow, tricuspid
regurgitation, and in the presence of atrial septal defect (in 50%), by a right-to-left shunt with
cyanosis. Clinical symptoms may be striking in infancy or childhood, but often problems present
only in adulthood (fatigue, cyanosis, signs of tricuspid regurgitation). Dysrhythmias occur
frequently (supraventricular tachycardia, Wolff -Parkinson- White syndrome). Indications for
surgery are worsening of exercise tolerance, progression of cyanosis, congestive right-sided heart
failure, and NYHA stages III-IV. Surgery is aimed at improvement of pulmonary blood fl ow,
correction of tricuspid regurgitation, and closure of the right-to-left shunt (if present). In case the
anterior leafl et of the tricuspid valve is suffi ciently developed, there exists a good chance for
correction by Danielson repair (fi rst performed in 1972) or by Carpentier repair (published in
1988). Th e principle of both techniques is based on reduction of the dilated right atrium by
plication of the atrialized right ventricular wall, reduction of the tricuspid annulus, and creation of
a competent monocuspid orifi ce from the anterior leafl et. Forms with severe malformation of
the anterior leafl et require valve replacement usually with a bioprosthesis. Bidirectional
cavopulmonary connection has to be performed sometimes in the most severe cases. With the
Danielson technique, plication of the atrialized right ventricular wall is achieved by a series of
interrupted pledgeted mattress sutures. After the sutures are tied, the atrialized right ventricular
wall is obliterated, which results in lowering the dilated right atrial capacity. Th e annulus in the
area of dysplastic posterior leafl et is moved toward the septum by another stitch. Th is results in
reduction of tricuspid annular circumference. Th e valve itself consists of the anterior tricuspid
leafl et only (Figs. 7.27, 7.28). The Carpentier technique is anterior leafl et rotating plasty. Th e
anterior leafl et is first detached from the tricuspid annulus, and then vertical (perpendicular to
the annular plane) plication of the atrialized right ventricular wall is performed in the area of
posterior leafl et. Th e anterior leafl et is reattached with simultaneous clockwise rotatory shift to
the area corresponding normally to the posteroseptal leafl et commissure (Figs. 7.29, 7.30).
Carpentier fi nally adds annuloplasty ring implantation. Th e atrial septal defect is closed with a
pericardial patch.

Tricuspid Valve Replacement

The decision for tricuspid valve replacement is the ultimate solution in case the valve cannot be
repaired. Th is situation occurs most often for advanced organic changes at rheumatic tricuspid
stenosis, in heavily damaged valves due to endocarditis, and in severe forms of Ebstein’s
anomaly. The problem of selecting the optimal valve for replacement has been extensively
debated. In general, there is a slight preference implantation of the bioprostheses. In the present
authors’ unit, we implant bioprostheses in tricuspid orifice. Th e reason for this strategy is the
very slow course of bioprosthesis degeneration thanks to lesser mechanical stress in low-pressure
right-heart circulation and good clinical tolerance of eventually developed mild tricuspid
regurgitation. Furthermore, mechanical valves in low-pressure right-heart circulation are
susceptible to thrombosis. Mechanical valves also disable introduction of the pacemaker leads
through the valve into the right ventricle. The advantage of bioprosthesis is, of course, avoidance
of thromboembolic and bleeding complications related to chronic anticoagulation. Tricuspid
valve replacement is a relatively simple procedure. The valve is sutured preferably with
pledgeted mattress sutures due to the very subtle and fragile tissue of the tricuspid annulus (Figs.
7.31, 7.32). It is advisable to leave the valve leafl
ets in place in case of non-infective lesion. Tricuspid valve replacement and repairs can both be
carried out in cardioplegic heart arrest as well as on a beating heart after release of aortic
crossclamping. Choice of the strategy is influenced by the surgeon’s customary practice,
accessibility of the tricuspid valve, and overall length of aortic cross-clamping. A compromise
procedure can also be chosen, i.e., placement of the principal and most diffi cult stitches during
asystole and then, after aortic declamping, accomplishment of the rest of the valve implantation
on an already beating heart.
Tricuspid Valve Excision
In certain circumstances the tricuspid valve can be excised and left unreplaced. Th is option has
been known since 1981, when Arbulu et al. reported on 55 intravenous heroin
Bioprosthesis St. Jude Medical Epic implanted into the tricuspid Orifice addicts operated for endocarditis in whom
the tricuspid valve was excised without replacement. Only 6 of them required prosthetic valve
insertion from 2 days to 13 years after excision of the valve. A prerequisite for this procedure is
low or normal pulmonary pressure, i.e., the absence of pulmonary hypertension. Postoperatively,
an intensive volumotherapy is mandatory to maintain elevated right atrial pressure (systole >25
mmHg). Th e rationale for this rather dubious strategy lies in the fear of prosthetic endocarditis,
which is very likely in patients who continue intravenous drug abuse. Th e authors have never
chosen this method of treatment. Perhaps it might be considered in those addicts whose personal
posture and history are unequivocally predictive of continuing the intravenous drug abuse.
Another cause might be excessive infective annular destruction, in which fear of sewing-ring
infection would justify choice of this procedure with the possibility to replace the valve later,
after curing the infection.
1. Aortic Dissection

I Definition/Classification and Pathology/Epidemiology

1. Definition

Aortic dissection is a condition in which the aortic wall is detached into two layers at the
medial level, causing two lumens having a certain length along the arterial course. This is a
dynamic condition characterized by the presence of blood flow or hematoma in the aortic wall.
Although the flap in aortic dissection usually has one to several tears, some cases have no clear
tear or no communication between the true lumen and the false lumen. The former type is called
communicating aortic dissection, and the latter noncommunicating aortic dissection (synonymous
with the conventional thrombosed type). Recent progress in diagnostic imaging has allowed us to
detect a condition in which the aortic media is detached due to hematoma, without an observable
tear. This condition is called IMH or intramural hemorrhage, representing the distinct
pathological concept termed “aortic dissection without tear. However, because IMH is based on a
pathological diagnosis, we have decided not to use this term in the clinical setting. Socalled IMH,
devoid of tears on diagnostic imaging, is clinically regarded as non-communicating aortic
dissection (synonymous with the conventional thrombosed type) and dealt with as a type of
dissection. Clinically, it is often difficult to clearly distinguish between IMH and aortic dissection
that has an intimal defect and tear (ULP on diagnostic imaging), without evidence of blood flow
in the false lumen (thrombosed false lumen with intimal defect, ULP-type). In addition, because
the ability to detect ULP varies among different diagnostic imaging techniques, and ULP-type
dissection includes some unstable cases regardless of the size of the ULP, this condition is
clinically important. To bring clinical attention to the importance of ULP, it is recommended that
ULP-type dissection be dealt with as communicating aortic dissection. In addition, cases with
partial thrombus in a false lumen and a thrombosed false lumen communicating with the true
lumen should definitely be classified into the category of communicating aortic dissection.
Although penetrating atherosclerotic ulcer (PAU) was proposed as a concept that represents an
ulcerated aortic atherosclerotic lesion that extends to the media, much remains unclear as to the
relationship between PAU and aortic dissection. Various issues about IMH and PAU remain to be
clarified, and due caution is therefore necessary when applying these terms.

2. Aortic Aneurysm
Aortic aneurysm is a circumferential or local enlargement (increased diameter) or
protrusion of a part of the aortic wall. When a part of the aortic wall is dilated and thereby forms
a bump, or when the diameter is increased to a degree at least 1.5-fold greater than normal
(exceeding 45 mm in the thoracic region and 30 mm in the abdominal region) in a fusiform
manner, the condition is called aneurysm. Aortic aneurysm is a localized dilatation (increased
diameter) or protrusion of the aortic wall, and is called a fusiform type aortic aneurysm (Figure
1) or a saccular type aortic aneurysm (Figure 2) according to whether the shape is fusiform or
saccular, respectively.

Figure 2. Saccular type aortic aneurysm. Figure 1. Fusiform type aortic aneurysm
 Classification of Aortic Dissection

1. Classification based on the extent of dissection

Stanford classification
Type A: Dissection involving the ascending aorta
Type B: Dissection not involving the ascending
aorta DeBakey classification
Type I: A tear located in the ascending aorta and dissection extending to the aorta distal
to the aortic arch
Type II: Dissection confined to the ascending aorta Type III: A tear located in the
descending aorta Type IIIa: Dissection not involving the abdominal aorta Type IIIb: Dissection
involving the abdominal aorta The following subcategories can be added to the DeBakey
classification Arch type: A tear located in the aortic arch Arch localized type: Dissection
confined to the aortic arch Arch extended type: Dissection extending to the ascending or
descending aorta Abdominal type: A tear located in the abdominal aorta Abdominal localized
type: Dissection confined to the abdominal aorta Abdominal extended type: Dissection extending
to the thoracic aorta (The term “retrograde type III dissection” is not used.)

2. Classification based on blood flow in the false lumen

Communicating type: Presence of blood flow in the false lumen. Also included in this
category are partially thrombosed false lumen or cases with blood flow in the long axis direction
in the false lumen from the ULP, despite a large portion of the false lumen being thrombosed.
ULP- type: No blood flow in a large portion of the false lumen, but blood flow localized near the
tear (ULP) Non-communicating type: Crescent-shaped false lumen without either tear (including
ULP) or blood flow in the false lumen

3. Classification based on the disease phase

Acute phase: Presentation within 2 weeks following the initial event. Very acute phase
refers to those presenting within the first 48 hours. Chronic phase: Presentation at 2 weeks or
longer following the initial event

2. Classifications and Pathological

Conditions
1. Aortic
Dissection
(1) Classifications
1) classification by the extent of dissection, 2) classification by status of blood flow in
the false lumen, and 3) classification by disease phase.
(2) Pathological Conditions
Aortic dissection essentially characterized by dissection of the aortic wall and blood flow
into the dissection is subject to changes over time beginning from immediately after onset, and
therefore presents as dynamic pathological conditions. These pathological conditions are also
variable because the lesion extends to a broad zone of the blood vessel. The wide spectrum of
pathological conditions is better understood if the status of the blood vessel is classified into 1)
dilatation, 2) rupture, and 3) stenosis or occlusion, and combined with the site of dissection.
1) Dilatation
(a) Aortic valve insufficiency
(b) Aneurysm formation
2) Rupture
(a) Cardiac tamponade
(b) Bleeding into the thoracic cavity or other areas
3) Peripheral Circulatory Disturbance Due to Stenosis or Occlusion of the Aortic
Branches
(a) Angina, myocardial infarction
(b) Cerebral ischemia
(c) Upper limb ischemia
(d) Paraplegia
(e) Intestinal tract ischemia
(f) Renal failure
(g) Lower limb ischemia
4) Other Pathological Conditions
(a) Disseminated intravascular coagulation syndrome
(DIC), pre-DIC
(b) Pleural effusion
(c) Systemic inflammatory response syndrome
(3) Definition of Non-Communicating Aortic Dissection
Because it is difficult to clinically distinguish between dissection without a tear and
dissection with a tear showing no blood flow in the false lumen, it is preferable to avoid the use
of the term aortic IMH, which pathologically denotes hematoma in the aortic wall due to rupture
of a blood vessel feeding the aorta.
Non-communicating aortic dissection is defined as follows:
1. It has a crescent-shaped false lumen.
2. There is no tear and blood flow entering from a tear. Namely, there is no
communication between the false lumen and the true lumen. If there is obvious blood flow in the
long axis direction in the false lumen, the lesion should not be dealt with as noncommunicating
aortic dissection. In these guidelines, ULPtype dissection and non-communicating dissection are
defined as different pathological conditions . On the other hand, cases with a thrombosed false
lumen resulting from retrograde dissection that arose from a tear in the descending thoracic aorta
or abdominal aorta should be classified as communicating dissection, although their imaging
findings closely resemble with those of non-communicating dissection.
 2. Aortic
Aneurysm (1)
Classification
1) Morphology of the Aneurysm Wall
(a) True aneurysm of the aorta
(b) Pseudoaneurysm of the aorta
(c) Dissecting aneurysm of the aorta
2) Location of the Aneurysm
(a) Thoracic region
(b) Thoracoabdominal region
(c) Abdominal region
3) Etiology
(a) Atherosclerotic
(b) Traumatic
(c) Inflammatory
(d) Infective
(e) Congenital
4) Shape of the Aneurysm
(a) Fusiform type
(b) Saccular type
(2) Pathological Conditions
Signs and symptoms of aortic aneurysm are shown in Table 2.

Table 2. Clinical Signs and Symptoms of Aortic Aneurysm

1. Pain
Dissection, rupture
2. Signs and symptoms caused by compression
In thorax: Hoarseness, dysphagia, facial
edema In abdomen: Abdominal distension
3. Sings and symptoms caused by ischemia of organs
Branches of the aortic arch (brain), spinal artery, branches of the abdominal aorta (e.g.,
intestinal tract), renal artery, arteries of the lower limb. Signs and symptoms vary according to
the organs perfused by the arteries

II Diagnosis
1. General Remarks
1. Acute Aortic Dissection
It is of utmost importance to maintain suspicion when diagnosing acute aortic dissection.
2. True Aortic Aneurysm
Although many TAA cases are asymptomatic, symptoms such as hoarseness, difficulty
swallowing, and vague back pain may occur. If TAA is detected, chest CT should first be
performed to determine the most appropriate therapeutic strategy. Abdominal aortic aneurysm
(AAA) may present symptoms such as a feeling of abdominal distension, constipation,
nonspecific low back pain. A pulsatile mass in the abdomen is an objective finding that leads to
suspicion of AAA in some cases. Abdominal ultrasonography is the simplest and non-invasive
evaluation technique for initial diagnosis. The patient should be followed up by ultrasonography
or CT to determine the most appropriate therapeutic strategy.

2. Radiological Diagnosis: Plain X-Ray

Examination, CT, Angiography
1. Plain X-Ray Examination
(1) Aortic Aneurysm
TAA is often detected by plain chest X-ray examination at regular health check-ups in
asymptomatic patients. Ascending aortic aneurysm usually presents a shadow protruding
rightward continuing from the contour of the ascending aorta in the frontal view, whereas aortic
arch aneurysm is often visualized as a tumorous shadow at the first left aortic arch in the frontal
view, and descending aortic aneurysm as a fusiform or round shadow continuing from the
contour of the aorta. In cases with AAA, calcification can sometimes be observed in the
aneurismal wall, indicating the presence of an aneurysm.
(2) Aortic Dissection
In cases with acute aortic dissection, mediastinal shadow enlargement can be seen on
plain chest X-rays, although this finding is nonspecific. Medial deviation of calcification of the
intima of the aortic wall is a finding suggestive of dissection.
2. CT
(1) Method
For CT of aortic aneurysm or aortic dissection, plain CT images and early contrast-enhanced
images are indispensable, and late contrast-enhanced images should be added depending on the
need in individual cases. Plain CT is useful for determining the degree of mural calcification,
presence/absence of medial deviation, identifying hematoma in the false lumen in cases with
noncommunicating dissection, and evaluating the high-density area in the mural thrombus
suggesting impending rupture of an aortic aneurysm.
(2) CT of Aortic Aneurysm
CT allows us to identify an aneurysm and provides data on the size and extent of the
aneurysm, calcification and the status of the aneurysmal wall (e.g., inflammatory aortic
aneurysm), the amount and status of the mural thrombus, the relationship between the aneurysm
and surrounding organs, and the positional relationship between the aneurysm and major aortic
branches. Although the diameter of the aneurysm is an important factor in determining whether
surgery is indicated, “the maximum minor-axis diameter” should be used in principle for CT
evaluation.
(3) CT of Ruptured Aortic Aneurysm and Impending
Rupture
When aortic aneurysm rupture is suspected, CT is useful if the patient’s condition allows
time for such examination. It is important to carefully interpret CT images to avoid overlooking
any minor bleeding.
(4) CT of Aortic Dissection
CT is a highly reliable, non-invasive examination for diagnosing dissection. This
examination is indispensable for diagnosing aortic dissection because it allows objective
evaluation of the whole aorta within a short period of time in response to an urgent need. On
plain CT, deviation of intimal calcification is a critical point in diagnosis.
1) Communicating Dissection
In some cases with communicating dissection, blood flow in the false lumen is so slow
that the false lumen cannot be visualized in the early-phase contrast, but inflow of the contrast
agent is observed in the late-phase contrast. Therefore, it is necessary to obtain late contrast-
enhanced images as well. The entry is recognized as a rupture of the flap.
2) Non-Communicating Dissection
CT images of non-communicating dissection are characterized by the presence of a false
lumen filled with clotted blood or hematoma in the acute phase. This false lumen is visualized as
a crescent-shaped or annular shadow resembling the mural thrombus that extends markedly in the
direction of the long axis of the aorta. When detected early, this shadow may show higher density
than the true lumen on plain CT. Contrast-enhanced CT does not allow visualization of the inside
of the closed false lumen.
3) Ulcer-Like Projection-Type Dissection
CT shows ULP as a localized luminal protrusion into the closed false lumen.
4) Diagnosis of Complications
Complications of aortic dissection often include serious conditions such as rupture,
cardiac tamponade, and ischemia in organs or limbs. On CT evaluation, it is important to pay
attention to the presence/absence of fluid accumulation around the heart, the relationship between
arterial branches and the dissecting lumen, and the presence/absence of extension of the
dissection into arterial branches.
3. Angiography
The role of angiography including digital subtraction angiography (DSA) in the diagnosis
of aortic aneurysm or aortic dissection is diminishing.
3. Ultrasonography
Body surface ultrasonography and transesophageal echocardiography that are minimally
invasive and provide large amounts of information are useful for visualizing the aorta. Body
surface ultrasonography allows observation of the aortic root, ascending aorta, aortic arch,
brachiocephalic artery, left common carotid artery, and left subclavian artery. In addition, arterial
branches from the abdominal aorta, i.e., the celiac artery, superior mesenteric artery, renal artery,
and common iliac artery, can also be observed. Transesophageal echocardiography can clearly
visualize the area from the aortic root to the ascending aorta, aortic arch, and descending aorta.
1. Aortic Aneurysm
First, in imaging an aortic aneurysm, it is necessary to obtain the long axis and short axis
views of the aorta on the body surface ultrasonography to observe the diameter of the aorta, shape
of the aneurysm, positional relationship with branching of blood vessels, and the nature of the
lumen and wall. Because there is a possibility that the aorta is flexed or deviated, the maximum
minor-axis diameter should be measured when the short axis view is used.
2. Aortic Dissection
Ultrasonography is very useful for rapid diagnosis of aortic dissection, and can be used
when it is difficult to use contrast agents because of issues such as renal dysfunction or allergy to
contrast agents. In particular, body surface ultrasonography allows evaluation of branch
dissection and complications of dissection, in addition to simple and non-invasive diagnosis of
dissection. It is very important to evaluate cardiac tamponade (a complication of Stanford type A
dissection), aortic valve regurgitation, progression of dissection into a branch, blood flow, and
cardiac function.

4. MRI
1. Imaging Procedures25-28
(1) MRI
Magnetic resonance imaging (MRI) allows evaluation of any section of the vascular wall
and lumen without the use of contrast agents. On the other hand, this procedure requires a long
imaging time and may have artifacts due to turbulent flow or delayed flow or respiration-related
artifacts.
(2) Cine MRI
This imaging technique allows evaluation of hemodynamics without the use of contrast
agents. However, a long imaging time is required, and information is basically limited to a single
section.
(3) MRA
Magnetic resonance angiography (MRA) techniques are broadly classified into the time-
of- flight (TOF) method, phase-contrast (PC) method, fresh blood imaging method in which a
contrast agent is not used, and contrast-enhanced MRA in which a contrast agent is used. Among
these techniques, the most common procedure for the aorta is contrast-enhanced MRA, which can
provide good views of the blood flow in the lumen when evaluating the flexed part and the
turbulent part. In comparison with the TOF or PC method, contrast-enhanced MRA is
advantageous in that a shorter imaging time is required, there is high spatial resolution, and an
arbitrary section can be set for imaging.
2. Clinical Application
MRI is more advantageous than CT in that it requires no X-ray exposure, allows
noncontrast imaging in patients with severe renal dysfunction, and enables the lumen to be
evaluated in cases with severely calcified lesions. On the other hand, its disadvantages include
lower spatial resolution, inability to visualize osseous structures due to the lack of information on
calcification, and difficulty with responding to emergency cases because of the long imaging
time. MRI is not recommended for diagnosis of acute aortic aneurysm in patients in a poor
general medical condition, because it is very time-consuming and has limitations in patient
monitoring.

III Choice of Treatment Methods

 1. Aortic Dissection (Recommendations for Choosing Treatment Methods for Acute
Aortic Dissection: Tables 3, and 4)
In the treatment of aortic dissection, choosing between medical and surgical treatment is
the most important decision affecting prognosis.
1. Treatment in the Acute Phase
(1) Stanford Type A Acute Aortic Dissection
Stanford type A aortic dissection in which dissection extends to the ascending aorta is a
condition that has an extremely poor prognosis. Mortality is reported to be 1 to 2% per hour after
the onset of symptoms. The main causes of death include rupture, cardiac tamponade, circulatory
failure, cerebral infarction and intestinal tract ischemia. In general, surgical treatment, i.e.,
emergency surgery, is indicated for this condition, bebecause the prognosis with medical
treatment alone is extremely poor.
(2) Stanford Type B Acute Aortic Dissection
Because Stanford type B acute aortic dissection follows a better natural course than type
A acute aortic dissection, medical treatment is generally chosen as the initial management
strategy. On the other hand, surgical treatment is necessary for patients with complications such
as rupture, refractory pain, or organ ischemia because the prognosis is extremely poor.However,
because inhospital mortality after surgical treatment in the acute phase is not low, a good
alternative to the currently available surgical treatments is awaited. In recent years, endovascular
treatment has been achieving favorable results as a therapeutic option for acute type B aortic
dissection, and is now becoming a first-line therapy for patients with acute type B aortic
dissection who have fatal complications.

Table 3. Recommendations for Acute-Phase Treatment for Stanford Type A Aortic

Dissection
Class I
1. Surgical treatment (emergency surgery) for type A communicating aortic dissection
(type I , II, and retrograde type III) (Level of Evidence: C)
2. Surgical treatment for aortic dissection in patients with severe complications*
directly related to aortic dissection where surgery is expected to achieve improvement or stop
progression (Level of Evidence: C) *e.g., rupture of the false lumen, re-dissection, cardiac
tamponade, disturbed cerebral circulation accompanied by disturbance of consciousness or
paralysis, aortic valve insufficiency accompanied by heart failure, myocardial infarction, renal
failure, intestinal circulatory disorder, thromboembolism of the limbs
Class IIa
1. Surgical treatment for aortic dissection where drug therapy has failed to control blood
pressure and pain and for type A non-communicatin aortic dissection (Level of Evidence: C)
2. Medical treatment to be started under certain conditions (see Section 1.1.3 of Chapter
III) for type A dissection without complications or persistent pain where the false lumen of the
ascending aorta is thrombosed (Level of Evidence: C)
3. Revascularization with surgical or endovascular procedures for impaired intestinal
perfusion accompanied by acute aortic dissection where emergency aortic surgery is not indicated
(Level of Evidence: C)
Class IIb
1. Aortic surgery for patients with serious brain damage (Level of Evidence: C)
Class III
1. Revascularization for impaired organ perfusion where emergency aortic surgery is indicated
(Level of Evidence: C)

Table 4. Recommendations for Acute-Phase Treatment for Stanford Type B Aortic

Dissection
Class I
1. Medical treatment for uncomplicated type B communicating/ULP-type/non-
communicating aortic dissection (Level of Evidence: C)
2. Surgical treatment for aortic dissection in patients with severe complications*
directly related to aortic dissection where surgery is expected to achieve improvement or stop
progression (Level of Evidence: C)*e.g., rupture of the false lumen, re-dissection, cardiac
tamponade, disturbed cerebral circulation accompanied by loss of consciousness or paralysis,
aortic valve insufficiency accompanied by heart failure, myocardial infarction, renal failure,
intestinal circulation disorder, thromboembolism of the limbs
3. Revascularization with surgical or endovascular procedures for impaired lower limb
perfusion accompanying type B communicating aortic dissection where emergency aortic surgery
is not indicated (Level of Evidence: C)
Class IIa
1. Surgical treatment for aortic dissection where drug therapy has failed to control blood
pressure and pain (Level of Evidence: C)
2. Medical treatment for aortic dissection where drug therapy has failed to control blood
pressure (Level of Evidence: C)
3. Revascularization with surgical or endovascular procedures for impaired intestinal
perfusion accompanied by acute aortic dissection where emergency surgery is not indicated
(Level of Evidence: C)
Class IIb
1. Aortic surgery for patients with serious brain damage (Level of Evidence: C)
Class III
1. Surgical treatment for uncomplicated type B aortic dissection (Level of Evidence: C)
2. Revascularization for impaired organ perfusion where emergency aortic surgery is
indicated (Level of Evidence: C)

(3) Treatment for Special Dissection 1) Stanford Type A Non-Communicating Acute

Aortic Dissection
There is a discrepancy in the view as to the treatment policy for Stanford type A
noncommunicating aortic dissection between Western countries and Japan or South Korea. It is
also common within the country for surgeons and internists to have different opinions on this
issue. Table 5 shows the therapeutic results described in previous reports. At present, the
treatment strategy for Stanford type A noncommunicating acute aortic dissection is as follows.
First, emergency surgery should be considered for patients with complicated aortic valve
insufficiency or cardiac tamponade. When there is ULP in the ascending aorta, surgery at an early
stage should be considered because it is presumed that the already existing tear has developed
into a ULP-type lesion. Patients with an aortic diameter of 50 mm or greater or a hematoma
thickness of 11 mm or greater are regarded as being at high risk, and surgery may be considered
according to circumstances. In other cases, initial medical treatment seems to be possible.
However, diagnostic imaging should be performed frequently during medical treatment, and it is
advised that cases showing an increase in the thrombosed false lumen or a change to ULP or
communicating type promptly undergo surgery.
2) Stanford Type A Retrograde Dissection With a Tear in the Descending Thoracic
Aorta
In some cases, there is no tear in the ascending aorta, and retrograde dissection extends
from a tear located in the descending thoracic aorta (or abdominal aorta in rare cases) to the
ascending aorta. Such retrograde dissection can be managed with medical treatment by
performing diagnostic imaging frequently during follow-up, while observing for possible
increases in the thrombosed false lumen or new blood flow into the false lumen.
3) Stanford Type B Non-Communicating Acute Aortic Dissection
Stanford type B non-communicating acute aortic dissection shows a better prognosis than
type A non-communicating ortype B communicating acute aortic dissection. Caution is necessary
for ULP occurring in the acute phase (i.e., transition to a ULP-type lesion), an aortic diameter of
40 mm or greater, and a false lumen thickness of 10 mm or greater, because these are reported to
be risk factors for disease progression such as increasing aortic diameter in the chronic phase.
2. Treatment in the Chronic Phase (Recommendations for Treatment of Chronic
Aortic Dissection: Table 5)
The prognosis of aortic dissection in the chronic phase (i.e., at least 2 weeks after onset)
is favorable. If the patient is stable, medical treatment is recommended, regardless of whether the
dissection is of Stanford type A or type B. Invasive treatment should be considered if the patient
has conditions such as rupture, impending rupture, an increased aortic diameter, aortic valve
insufficiency, branch occlusion, extended dissection, recurrence.
(1) Results of Surgery in the Chronic Phase
According to the Japanese Association for Thoracic Surgery, the in-hospital mortality rate
in 2008 was 6.5% for chronictype A, 8.7% for chronic type B (descending arch replacement:
15.0%, descending aortic replacement: 7.9%, thoracoabdominal aortic replacement: 13.9%).
(2) Results of Stent-Graft Insertion in the Chronic Phase
According to the Japanese Association for Thoracic Surgery, the in-hospital mortality rate
was 22.2% for chronic type A and 4.2% for chronic type B in 2008.
(3) Results of Medical Treatment in the Chronic Phase
Acute-phase factors associated with a poor prognosis in chronic phase are listed below.
1) Stanford Type A Communicating Dissection
2) Stanford Type A Non-Communicating Dissection
Thickness of hematoma, ULP in the ascending aorta,maximum aortic diameter.
3) Stanford Type B Communicating Dissection
Acute-phase maximum aortic diameter, acute-phase maximum aortic diameter located in
the distal arch, presence of chronic obstructive pulmonary disease (COPD).
4) Stanford Type B Non-Communicating Dissection
New appearance of ULP, age 70 years or older, acute-phase maximum aortic diameter,
thickness of hematoma, ULP located in the distal arch or surrounding the diaphragm.

Table 5. Recommendations for Chronic-Phase Treatment for Aortic Dissection

Class I
1. Surgical treatment for ruptured aorta or rapidly enlarging aortic diameter (>5 mm
per 6 months) (Level of Evidence: C)
2. Surgical treatment for aortic dissection with increased diameter (>60 mm) (Level of
Evidence: C)
3. Medical treatment for aortic dissection with a maximum aortic diameter of less than
50 mm without complications or rapid enlargement (Level of Evidence: C)
Class Ila
1. Surgical treatment for communicating aortic dissection with hypertension
uncontrollable with drug therapy (Level of Evidence: C)
2. Surgical treatment for aortic dissection with a maximum aortic diameter of 55 to 60
mm (Level of Evidence: C)
3. Surgical treatment for aortic dissection accompanied by Marfan syndrome with a
maximum aortic diameter of 50 mm or greater (Level of Evidence: C)
Class Ilb
1. Surgical treatment for aortic dissection with a maximum aortic diameter of 50 to 55 mm
(Level of Evidence: C

(5) Increased Surgical Risk With Age

Although it is apparent that the risk of surgery generally increases with advanced age,
activity of daily living (ADL) is also important. The in-hospital mortality rate in patients 70 years
of age or older with a TAA is reported to be 1.25-fold higher than in younger patients.

Table 6. Indications of Treatment for Thoracic or Thoracoabdominal Aortic

Aneurysms (Excluding Marfan Syndrome and Saccular Type Aneurysm)
Class I
1. Surgical treatment for aneurysms with a maximum minor-axis diameter of 60 mm
or greater (Level of Evidence: C)
Class IIa
1. Surgical treatment for thoracic or thoracoabdominal aortic aneurysms accompanied
by pain where the maximum minor-axis diameter is 50 to 60 mm (Level of Evidence: C)
2. Medical treatment for thoracic or thoracoabdominal aortic aneurysms with a maximum
minor-axis diameter of less than 50 mm without symptoms or chronic obstructive pulmonary
disease (excluding Marfan syndrome) (Level of Evidence: C)
Class IIb
1. Surgical treatment for thoracic or thoracoabdominal aortic aneurysms not
accompanied by pain with a maximum minor-axis diameter of 50 to 60 mm (Level of Evidence:
C)
2. Surgical treatment for thoracic or thoracoabdominal aortic aneurysms accompanied
by pain with a maximum minor-axis diameter of less than 50 mm (Level of Evidence: C)
Class III
1. Surgical treatment for thoracic or thoracoabdominal aortic aneurysms not
accompanied by pain with a maximum minor-axis diameter of less than 50 mm (Level of
Evidence: C)
2. Thoracic Aortic Aneurysm (Recommendations for Choosing Treatment Methods for
Thoracic
Aortic Aneurysm: Table 6)
Because TAA are often asymptomatic, the actual status of this disease remains unclear. In
addition, there have been no double- blind comparative studies of medical versus surgical
treatment in patients with TAA or TAAA and therefore no comparative data on the available
treatments.
1. Medical Treatment of Thoracic or Thoracoabdominal Aortic Aneurysm
Age, pain, COPD, and aortic diameter are cited as factors involved in rupture.76 A strong
positive correlation between aortic diameter and rupture or aortic dissection has been reported.
2. Surgical Treatment of Thoracic or Thoracoabdominal Aortic Aneurysm
The early mortality rate of more than 5% for surgical cases of TAA or TAAA overall,
even today with improved therapeutic efficacy, remains a major issue.75 If the risk of death after
surgery for TAA is assumed to be 5%, a reasonable criterion for

IV Medical Treatment
1. Aortic Dissection
1. Management in the Acute Phase
The most important aspects of treatment in the hyperacute phase are control of
hypertension (goal, 100 to 120 mmHg), pulse rate control, pain relief, and rest. ^-blockers should
be used simultaneously with antihypertensive therapy to achieve aggressive pulse rate control,
and analgesic or sedative therapy should be used to manage persistent pain.
2. Management in the Chronic Phase
The major goals of patient management in the chronic phase are to prevent re-dissection
and rupture and to determine the timing and technique of (any subsequent) surgery.
(1) Blood Pressure Control
The most important aspect of medical management is to control blood pressure. ^-
blockers are reported to reduce dissection- related events such as hospitalization, and inhibit
aneurysm enlargement.
(2) Bed Rest Level and Exercise
Although there may be few or minimal restrictions on routine ADL, evidence on exercise
is limited.
(3) Follow-up by Imaging Tests
It is necessary to follow patients at regular intervals performing imaging modalities such
as CT and MRI until 2 years after onset, the period associated with frequent dissection-related
events. If the aortic diameter approaches that of the surgical indication, CT should be performed
at shorter intervals. Considering the radiological exposure and contrast-induced nephropathy,
prolongation of the interval between CT tests may be warranted in patients who have a small
aortic diameter and a thrombosed false lumen in the absence of ULP.
(4) Cautions in Chronic-Phase Management of Surgical Cases
Remaining dissection and postoperative long-term complications are important issues,
regardless of whether the dissection is Stanford type A or type B.
1) Long-Term Postoperative Complications
Major problems are aortic valve insufficiency, anastomotic pseudoaneurysm, re-
dissection, and enlargement of the remaining false lumen.
2) Aneurysm Formation via the Remaining Dissection
It is not rare to find enlargement of the remaining distal false lumen in patients after
surgery for aortic dissection.
3) Frequency of Reoperation (The Initial Surgery May Be in Either the Chronic
Phase or the Acute Phase)
The reoperation rate after surgery for aortic dissection is reported to be 8 to 10%. It has
also been reported that reoperation- free rate was 95%, 64%, and 35% of patients at 5, 10, and 15
years, respectively, after the initial surgery.

Table 7. Patients Indicated for a Course of Standard Rehabilitation

Selection criteria: Stanford type A non-communicating and Stanford type B aortic

dissection
- Maximum aortic diameter of less than 50 mm
- No organ ischemia
- Not complicated with DIC (FDP >40)
Exclusion criteria (where this approach should not be used)
1. Type of dissection for which this approach is not indicated
2. Type of dissection for which this approach is indicated but where there is a serious
complication
3. Restlessness
4. Re-dissection
5. Mediastinal hematoma
6. Cardiac tamponade, predominantly right-sided pleural effusion Setting the goal
(discharge criteria)
1. Blood pressure controlled throughout the day with systolic blood pressure less
than
130 mmHg
2. Stable general status with no development of complications
3. Rehabilitation in bath completed or ADL recovered to the prehospital level
4. Understanding of what care needs to be taken in daily life (e.g., medication, diet,
exercise, visiting doctors)
ADL, activity of daily living; DIC, disseminated intravascular coagulation syndrome;
FDP, fibrin degradation products.
Table 8. Patients Indicated for a Course of Short-Term Rehabilitation

Selection criteria: Stanford type B aortic dissection

- Maximum minor-axis diameter <40 mm
- No ULP in non-communicating dissection
- True lumen occupying one quarter or greater in communicating dissection
- Not complicated with DIC (FDP >40)
Exclusion criteria (where this approach should not be used)
1. Type of dissection for which this approach is not indicated
2. Type of dissection for which this approach is indicated but where there is a serious
complication
3. Re-dissection
Setting the goal (discharge criteria)
1. Blood pressure controlled throughout the day with systolic blood pressure less than
130
mmHg
2. Stable general status with no development of complications
3. Rehabilitation in bath completed or ADL recovered to the prehospital level
4. Understanding of what care needs to be taken in daily life (e.g., medication, diet,
exercise, visiting the doctor)
3. Rehabilitation
The rehabilitation program for cardiovascular diseases is designed separately for Phase I
(acute phase and during hospitalization), Phase II (early after discharge and 1 to 2 months after
onset), and Phase III (more than 2 months after onset)
(Tables 7 to 9).

2. Thoracic Aortic Aneurysm

1. Basic Considerations for Medical Treatment

(1) Management of Atherosclerotic Risk Factors
It is important to provide treatment and management of atherosclerotic risk factors such
as hypertension, dyslipidemia, diabetes mellitus, hyperuricemia, obesity, and smoking.
(2) Management of Atherosclerotic Complications
It is common for patients to have atherosclerotic diseases such as cerebrovascular disease,
carotid artery disease, coronary artery disease, nephrosclerosis (renal arteriosclerosis), lower limb
artery disease, and aortic aneurysms involving other sites. In particular, the frequency of
concomitant coronary artery disease is high, indicating the importance of searching for the
presence of major arterial lesions throughout the body.
2. Medical Treatment in Non-Surgical Cases
(1) Signs and Symptoms
Although most TAA cases are basically asymptomatic, an increase in the aneurysmal
diameter may lead to the manifesta tion of (1) aortic valve insufficiency due to enlargement of
the aortic root or ascending aorta; (2) coughing, shortness of breath, wheezing, recurrent
pneumonia originating from compression of the trachea or the main bronchus; (3) dysphagia due
to compression of the esophagus; (4) hoarseness due to compression on the recurrent laryngeal
nerve; and (5) chest pain or back pain due to compression on surrounding organs or erosion into
the ribs.
Because a progressive enlargement in aneurysmal diameter is suggested at the onset of
symptoms, CT or MRI (MRA) examinations should be performed promptly.
(2) Blood Pressure Control During Follow-up Observation
The antihypertensive goal in non-surgical TAA cases should be 105 to 120 mmHg for
systolic blood pressure, a level lower than in most hypertensive patients. ^-blockers are
considered to be the first-line treatment. If ^-blockers at a maximum dose cannot achieve a
sufficient hypotensive response, it is necessary to add other antihypertensive drugs, as needed, to
reach the antihypertensive goal.
(3) Restriction of Physical Activity During Follow-up Observation
Patients should be instructed to avoid smoking, excessive drinking and eating, overwork,
poor sleep, and mental stress. Patients should also be instructed to be careful when lifting or
dragging heavy materials/objects that may result in a rapid blood pressure increase, straining
during bowel movements, and persistent coughing.
(4) Imaging Evaluation During Follow-up Observation
Although it is difficult to predict the timing of rupture or the enlargement rate of
aneurysmal diameter in TAA cases, the annual incidence of cardiovascular accidents is reported
to be 6.5% when the TAA diameter is 50 to 60 mm and 15.6% when the diameter exceeds 60
mm. It is necessary to evaluate changes in the diameter and morphology by CT or MRI on a
regular basis, depending on the aneurysmal diameter and the tendency for enlargement.

Table 9. Evidence of Acute-Phase Rehabilitation Therapy in Aortic Dissection

Class IIa
1. Standard rehabilitation course for Stanford type B acute aortic dissection (maximum
minor-axis diameter <50 mm without organ ischemia and FDP <40) (Level of Evidence: B)
Class IIb
1. Standard rehabilitation course for Stanford type A non-communicating acute aortic
dissection (maximum minor-axis diameter <50 mm without evidence of ULP in the ascending
aorta, without organ ischemia and FDP <40) (Level of Evidence: C)
2. Short-term rehabilitation course for Stanford type B acute aortic dissection
(maximum minor-axis diameter <40 mm without organ ischemia). The minimum true lumen
exceeds one quarter of the whole lumen in the case of communicating dissection, and no ULP
with FDP <40 in the case of non-communicating dissection. (Level of Evidence: C)

3. Medical Treatment in Surgical Cases

(1) Clinical Signs and Symptoms
Because enlargement of the aorta at the non-replacement site or pseudoaneurysm or
rupture of an anastomosed artificial graft is suspected when clinical symptoms are observed in
patients after surgery, these manifestations should be treated in the same manner as in non-
surgical patients.
(2) Blood Pressure Control
The antihypertensive goal should also be under 130 mmHg for systolic blood pressure
even in surgical patients.
(3) Restriction of Physical Activity
Although artificial grafts are considered to have sufficient strength at the site of
replacement, mild restriction of physical activity seems to be necessary, essentially as in non-
surgical patients, for the purpose of avoiding aneurysm formation in the area without aortic
replacement or in the anastomosed part.
(4) Imaging Evaluation
It is preferable that patients be evaluated for postoperative conditions by CT or MRI
examinations at 3 to 6 months after surgery, and then annually thereafter.

V Surgical
Treatment
1. Thoracic
Aorta
1. Overview of Surgical Treatment of Thoracic Aortic Aneurysms
Surgical resection and replacement of the thoracic aorta is the gold standard for treatment
of TAA and Stanford type A aortic dissection.
2. Fundamental Surgical Techniques and Surgical Adjuvant Treatments for
Thoracic Aortic Surgery
(1) Aortic Root or Ascending Aorta Replacement 1) Standard Surgical Techniques
Surgical techniques for the aortic root are broadly classified into those based on
replacement of the valve, such as valved graft (Bentall operation), homologous aorta (homograft),
heterologous aorta, autologous pulmonary valve (Ross operation), and those preserving the
autologous valve (aortic valve sparing surgery).
2) Reconstruction of Coronary Artery
The button-Bentall operation has become common in recent years. When mobilization of
the coronary artery involves risks or is not possible because of reoperation, inflammation, among
others, Piehler operation by interposing an artificial graft is effective.
3) Aortic Valve Sparing Surgery
This technique is broadly classified into the remodeling method1 and the reimplantation
method. Aortic valve sparing surgery is more advantageous than the Bentall operation in that
there is no need for anticoagulant therapy, leading to a decrease in prosthesis-related
complications. Issues of concern include increased surgical risk due to prolonged aortic
crossclamping, and unclear long-term durability of the autologous aortic valve. To date, evidence
strongly supporting recommendation of either Bentall operation or aortic valve sparing surgery is
lacking. The Bentall operation is currently the standard procedure (Class Ilb, level of evidence
by Agency for Health Care Policy and Research [AHCPR], the same as below).
(2) Aortic Arch Replacement
1) Standard Surgical Techniques
Access to aortic aneurysms in the arch or distal arch is generally achieved by a median
sternotomy. On the other hand, left thoracotomy is used for distal aortic arch aneurysms mainly
extending to the peripheral side. In cases with an extensive aortic aneurysm, an elephant trunk
should be inserted prior to the second-stage treatment (surgery or stent-grafting).
2) Brain Protection
Although hypothermic circulatory arrest (HCA) is the basic adjuvant procedure during
arch reconstruction, antegrade selective cerebral perfusion (SCP)or retrograde cerebral perfusion
(RCP) has been added for the purpose of achieving longer and safer brain protection, resulting in
better outcomes (Class Ilb). For left thoracotomy, HCA or HCA + RCP/SCP should be used, and
the arch should be reconstructed by the open proximal technique.
(3) Descending Thoracic or Thoracoabdominal Aortic Replacement
1) Standard Surgical Techniques
In cases of descending aortic replacement, the descending aortic aneurysm is usually
reached via a left thoracotomy through the 5th to 6th intercostal space. The thoracotomy through
the 4th to 5th intercostal space may be used in cases with a proximal descending aortic aneurysm,
and the thoracotomy through the 7th to 8th intercostal space may be used in cases with a distal
descending aortic aneurysm near the diaphragm. In addition, TAAA should be reached via a
thoracotomy through the 5th to 6th intercostal space and a spiral incision extending to the
abdominal region. The intercostal artery and abdominal branch should be reconstructed
individually, using small-caliber artificial grafts measuring 8 or 10 mm in diameter, or
reconstructed in an island shape by an en bloc technique. Individual reconstruction is performed
for Marfan syndrome.
2) Adjuvant Procedures
In general, the distal perfusion method by partial cardiopulmonary bypass (femoro-
femoral [F-F] bypass) or left heart Bypass is used for protection of the spinal cord and abdominal
organs, although reconstruction can be performed under simple cross-clamping.For patients in
whom proximal cross-clamping near the arch is difficult or in whom lysis of adhesion for prior
surgery is difficult, the HCA method under total cardiopulmonary bypass is used.
3) Spinal Cord Protection
The Adamkiewicz artery should be identified by MRI or CT prior to surgery, as the
findings can facilitate determining reconstruction or preservation of the intercostal artery during
surgery (Class IIb). In addition, the usefulness of cerebrospinal fluid (CSF) drainage to be
performed either during surgery or up to 3 days after surgery has been demonstrated (Class Ia).
Patients should be monitored for spinal cord ischemia during surgery by means of motor evoked
potential (MEP) or somatosensory evoked potential (SEP) (Class IIb) recordings. Referring to
these data, the culprit intercostal (lumbar) arteries between the 8th thoracic vertebra and the 1st
lumbar vertebra should be reconstructed. The staged segmental aortic clamping is used for
reconstruction of the aorta, in order to shorten the duration of spinal cord ischemia. On the other
hand, favorable surgical results under deep HCA have been reported despite the increased risk of
bleeding or pulmonary disorder. Although clear evidence is as yet lacking, the spinal cord-
protecting effects of some agents, such as naloxone, barbiturates, mannitol, adrenocortical
hormone, papaverine, tetracaine, calcium channel blockers, and adenosine, have been reported.
4) Abdominal Organ Protection
Selective continuous perfusion of abdominal branches should be performed using a
balloon- tipped cannula via partial cardiopulmonary bypass or collateral of the left heart bypass
circuit.
3. Aortic Dissection
(1) Surgical Strategies for Acute Aortic Dissection
In the acute phase, emergency surgery is basically indicated for Stanford type A
dissection, whereas medical antihypertensive therapy is indicated for Stanford type B dissection.
Prompt treatment is essential for complications of dissection. Cases complicated by extensive
brain damage including coma are often excluded from surgical indications because irreversible
brain damage is commonly present. However, whether the brain damage is reversible or
irreversible should be determined with due caution.
(2) Practical Aspects of Surgery for Acute Aortic Dissection
1) Principles of Surgery
Artificial graft replacement of the aorta including entry should be performed. Techniques
are described below. (1) Ascending aortic replacement: Extracorporeal circulation by blood
perfusion from the femoral artery, the true lumen of the ascending aorta or the axillary artery is
used as an adjuvant procedure. Multiple routes of blood perfusion may be used when there is
concomitant organ malperfusion. The current standard adjuvant procedure is deep HCA, by
which the core temperature is reduced to 20 degrees C or lower. RCP may also be used
concomitantly. For peripheral anastomosis, an open distal anastomosis is used under deep HCA
without aortic crossclamping. (2) Total arch replacement: When the tear is present in the aortic
arch, ascending and total arch replacement is preferable in principle, from the viewpoint of tear
resection. In Marfan syndrome cases with Stanford type A aortic dissection, total arch
replacement is indicated because hemiarch replacement may result in enlargement of the
remaining aortic arch. The elephant trunk method is used, with the aim of adding strength from
the intimal side, preventing anastomosis leakage, and closing the peripheral therafalse lumen. In
addition, in recent years, hybrid surgery combining total arch replacement with insertion of the
frozen elephant trunk into the descending aorta has been increasing. (3) Stanford type B
dissection: Most acute type B dissections indicated for surgery are accompanied by rupture or
seriously impaired organ perfusion. In such cases, surgical results are inevitably poor. The
mainstay of treatment for complicated lesions of acute type B dissection is shifting to an
endovascular approach.
 2) Aortic Valve Regurgitation
(1) Aortic valve resuspension: Except in cases with annuloaortic ectasia (AAE) or organic
aortic valve disease, resuspension of the aortic commissure is effective (2) Aortic root
replacement: When the tear extends deep into the Valsalva sinus or when there is already AAE,
the Bentall operation has conventionally been indicated. Although this operation is still the
standard procedure, aortic valve sparing surgery has also recently been attempted.
3) Branch Malperfusion
Branch malperfusion is the main cause of increased complexity and severity of the
disease state in cases with acute aortic dissection; this condition manifests with various symptoms
in 20 to 40% of patients. As a rule, if aortic dissection shows an unstable course, aortic repair is
the first priority, and intervention for peripheral vascular disease should be secondary. The results
of aortic dissection repair in patients who have a concomitant branch malperfusion are poor, and
the early mortality rate is reported to be 30 to 50%.
(3) Chronic Aortic Dissection
There are certain points to keep in mind when dealing with chronic dissection cases, and
strategies tailored to individual patients are necessary.
1) Stanford Type A Dissection
The site of blood perfusion should be chosen chiefly from among the axillary
artery,femoral artery and the cardiac apex, and the choice should be appropriate to each case.
(1) Repair of Aortic Valve Regurgitation i) Aortic Valve Replacement
In cases with chronic aneurysms accompanied by aortic valve regurgitation, aortic valve
sparing surgery involving aortic valvuloplasty should be performed. If this procedure is difficult,
aortic valve replacement should be performed instead.
ii) Aortic Root Replacement With a Valved Artificial Graft
When aortic valve sparing surgery is difficult in patients with AAE complicated by
dissection, aortic root replacement with a valved artificial graft should be performed.
iii) Aortic Valve Sparing Surgery
Among patients with AAE or dissection extending to the aortic root and requiring aortic
root replacement, aortic valve sparing surgery is performed in patients with normal aortic valve
leaflets or indicated for valvuloplasty.
(2) Aortic Reconstruction With an Artificial Graft
For ascending aortic replacement, “open distal anastomosis”, by which peripheral
anastomosis is performed under circulatory arrest, is a common procedure. Although SCP is
gener ally a safe method of brain protection, the most appropriate protective method is chosen
according to each case. Although anastomosis to the true lumen is preferable for avoiding
reoperation of the distal aorta in the remote phase, the possibility of organ ischemia should also
be taken into consideration. Total arch replacement is indicated for retrograde dissection with a
tear in the descending aorta, rupture or enlargement of the aortic arch, occlusion of an arch
branch, Marfan syndrome, among others. In general, open distal anastomosis assisted by SCP is
performed. It is common to insert an elephant trunk into the descending aorta after resecting the
flap and to perform the double-barreled anastomosis. When staged surgery is not possible in
extensive aneurysm cases, ascending, arch and descending aortic replacement should be
performed via bilateral anterior thoracotomy or median sternotomy (+ left thoracotomy) as a
single-stage procedure.
2) Stanford Type B Dissection i) Descending Aortic Replacement
The enlarged descending aorta should be replaced with an artificial graft via left
thoracotomy and distal aortic perfusion (e.g., F-F bypass, left heart bypass). To avoid retrograde
dissection associated with proximal cross-clamping, not a few surgeons choose the technique of
open proximal anastomosis for descending replacement. The technique of true lumen
anastomosis or double-barreled anastomosis should be chosen as the distal anastomosis
technique, depending on the individual case, taking into account peripheral blood flow.If the
Adamkiewicz artery is fed by the false lumen, double-barreled anastomosis or reconstruction of
the same artery is preferable.
ii) Partial Arch or Descending Aortic Replacement by Open Proximal Anastomosis
This procedure is indicated for patients in whom the intimal tear is located in the aortic
arch
and those in whom extension has reached the arch, as well as those in whom proximal
crossclamping is not possible. Although this surgery can be implemented with retrograde
perfusion from the femoral artery alone, the route of blood perfusion to the proximal aorta is also
often secured. After circulatory arrest is induced at 18 degrees C or lower, the proximal aorta is
transected while the aortic arch is opened, and anastomosed to the artificial graft.
iii) Thoracoabdominal Aortic Replacement
To prevent spinal cord ischemia, following procedures are usually undertaken: (1) distal
aortic perfusion and maintenance of blood pressure at a relatively high level; (2) implementation
of CSF drainage; (3) prevention of steal phenomenon from the intercostal artery and lumbar
artery while the aorta is opened; (4) identification of the preoperative spinal cord feeding artery
and its reconstruction; (5) staged segmental aortic clamping; (6) pharmacologic spinal cord
protection; (7) moderate hypothermia. Surgery must be planned with special attention to items (3)
and (5). For reconstruction of the abdominal major arterial branches, selective perfusion of the
celiac artery, the superior mesenteric artery, and the renal arteries should be performed, and cold
Ringer’s lactate solution can be applied for renal arteries reconstruction only
4. Results of Surgical Treatment for Aortic Dissection and True Aortic Aneurysm
(1) Current Status and Efficacy of Surgical Treatment for Aortic Dissection
Advances in diagnostic imaging have allowed early diagnosis of aortic dissection
immediately after onset, and better therafalse peutic results have been obtained owing to arch
replacement using improved adjuvant measures and the recent introduction of fibrin glue and
stentgrafts. The in-hospital mortality rate of acute type A dissection surgery has recently
improved to about 10% in Japan. Listed risk factors for surgical death in patients with acute type
A aortic dissection include advanced age (80 years or older), preoperative shock, malperfusion of
the vital organs, preoperative brain damage, and massive bleeding during surgery.
(2) Results of Surgical Treatment for True Thoracic or Thoracoabdominal
Aneurysm
Results of elective surgery for ascending and aortic root aneurysms are generally
favorable.
In cases with an aortic arch aneurysm, death and cerebral complications are clinically important
outcomes. Paraplegia is a clinically important outcome in cases with a dissecting aneurysm of
thoracic aorta or TAAA. The risk of paraplegia varies greatly according to the extent of the
aneurysm, being particularly high in cases with Crawford type II. The incidence of paraplegia
among series of clinical TAAA is reported to be 2 to 27%, with an average of about 10%. The
preoperative risk factors for early death that have consistently been identified in various reports
include emergency surgery, age, renal failure, and cerebrovascular disease.

VI Endovascular Treatment
1. Aortic Dissection (Recommendations for Endovascular Treatment of
Aortic Dissection: Table 10)
Endovascular treatment of aortic dissection includes transcatheter fenestration, stent
placement, and stent-graft insertion. Although closure of the entry site with stent-grafting is
currently the mainstay of treatment, its indications, the device to be used, and the placement
technique still vary among institutions.
1. Transcatheter Fenestration, Stent Placement for Stenotic or Occluded True
Lumen or Branch Vessels
(1) Indications
These procedures are performed mainly for the treatment of malperfusion syndrome
associated with acute dissection.
(2) Methods
1) Transcatheter Fenestration
A guide wire should be passed from the true lumen into the false lumen, and the flap is
then split by inflating the balloon to create a reentry site.
2) Stent Placement
A stent should be inserted into the lumen of the ischemic branch artery, and placed
therein.
2. Entry Closure by Stent-Graft Insertion
(1) Indications
Although basically this technique is indicated for patients with chronic type B dissection
in whom conventional open thoracotomy is considered to be a high-risk procedure or those with
acute type B dissection accompanied by rupture, organ ischemia, among others.Because surgical
results are poorin type A aortic dissection with the primary entry site in the descending aorta,
ever more specialists are taking the view that this condition is treatable, depending on the
patient’s condition, even in the acute phase.
(2) Methods
See the section on treatment of true aortic aneurysm (Section 2.3 of Chapter VI).
(3) Results
It has been reported that the initial success rate was 70.8 to 94.4%, the incidence of
endoleak was 2.8 to 19%, and the early mortality rate was 2.7 to 13%. Reports of longterm results
are as yet limited, however.

2. Thoracic Aortic Aneurysm (Recommendations for Stent-Graft Treatment of Thoracic

Aortic Aneurysm: Table 11)
1. Introduction
Thoracic stent-grafts provided by manufacturers were approved in Japan in March 2008,
and their use is now spreading rapidly. Evidence of the efficacy of this treatment in TAA is still
limited in Japan, and therefore this revision of the guidelines reflects mainly evidence obtained in
Western countries.
2. Indications
Indications in various diseases are described below. Due caution is necessary when using
stent-grafts provided by manufacturers, because each device has its own anatomical criteria for
the procedure.

Table 10. Endovascular Treatment for Aortic Dissection

Class I
1. Chronic follow-up after endovascular treatment (including imaging diagnosis)
(Level of Evidence: C)
2. Support from a surgical team (Level of Evidence: C)
3. Entry closure with stent-grafting for complicated acute type B aortic dissection
(Level of Evidence: C)
Class IIa
1. Stent placement for ischemic branch vessels resulting from compression of the true
lumen due to aortic dissection (Level of Evidence: B) *Early treatment after the onset of
dissection is important in acute cases.
2. Transcatheter fenestration early after the onset of acute type B aortic dissection with
blocked true lumen (Level of Evidence: B)
3. Entry closure with stent-grafting for chronic type B aortic dissection where surgery
is indicated (Level of Evidence: B)
4. Entry closure with stent-grafting for acute type A aortic dissection caused by
retrograde dissection (Level of Evidence: B)
Class IIb
1. Entry closure with stent-grafting for patients with chronic type B aortic dissection
having high surgical risk (Level of Evidence: B)
2. Stenting for a narrowed segment of the true lumen in acute aortic dissection (Level
of Evidence: C)
3. Entry closure with stent-grafting for acute type B aortic dissection to prevent
formation of future aneurysms (Level of Evidence: C)
Class III
1. Use in patients who do not meet anatomical criteria (Level of Evidence: B)
2. Entry closure with stent-grafting for acute type B aortic dissection where branch
vessels are obviously ischemic due to static compression (Level of Evidence: C)
3. Entry closure with stent-grafting for chronic type B aortic dissection where main
branch vessels are perfused from the false lumen (Level of Evidence: C)
*When transcatheter fenestration is performed simultaneously with or prior to
stentgrafting, Class II b and Level of Evidence:

Table 11. Stent-Graft Treatment for Thoracic Aortic Aneurysms and Aortic
Dissection
Class I
1. Support from a surgical team (Level of Evidence: C)
2. Traumatic aortic injury* (Level of Evidence: B)
3. Complicated acute type B aortic dissection* (Level of Evidence: B)
Class IIa
1. Descending aortic aneurysm with high surgical risk* (Level of Evidence: B)
2. Ruptured descending aortic aneurysm* (Level of Evidence: C)
Class IIb
1. Descending aortic aneurysm with low surgical risk* (Level of Evidence: C)
2. Hybrid procedures for arch and thoracoabdominal aortic aneurysm with high surgical
risk (Level of Evidence: C)
3. Chronic dissection where the false lumen tends to enlarge* (Level of Evidence: B)
Class III
1. Intervention for asymptomatic thoracic aortic aneurysm 55 mm or less in diameter
(Level of Evidence: C)
2. Arch and thoracoabdominal aortic aneurysms with low surgical risk (Level of
Evidence: B)

(1) Ascending Aortic Aneurysm

At present, endovascular treatment is not indicated for ascending aortic aneurysm.
(2) Aortic Arch Aneurysm
Endovascular treatment for aortic arch aneurysm should be performed only in patients of
advanced age or with high surgical risk. Currently, the use of stent-grafts in this lesion is centered
on hybrid approaches combining extra-anatomical bypass surgery for arch branches. The
mortality rate and incidence of complications after open stent-graft placement (frozen elephant
trunk technique, stented elephant trunk technique) are equivalent or superior to those after routine
surgery. Therefore, this procedure should be accepted as a treatment option in this lesion. In
particular, this procedure is useful for treating extensive aortic arch aneurysm or type A aortic
dissection.
(3) Descending Aortic Aneurysm
Stent-graft treatment for descending aortic aneurysm is associated with reduced acute-
phase mortality and a lower incidence of adverse events than surgical treatment, and shows
favorably maintained conditions in the intermediate phase, so long as anatomical situations agree
with the indications for the device. Therefore, this treatment should be considered as the firstline
therapy in high-risk surgical patients (Class Ila, Level of Evidence: B). In addition, because the
spinal cord injury incidence is also lower, and QOL is thus more likely to be maintained than
with surgical treatment in low-risk surgical patients, many are of the opinion that this treatment
should be regarded as the first-line therapy (Class IIb, Level of Evidence: C).
(4) Thoracoabdominal Aortic Aneurysm
Endovascular treatment for TAAA requiring reconstruction of abdominal major branches
is indicated for high-risk patients or those in whom surgery is difficult. However, stent-graft
treatment for TAAA that secures enough landing zone by placing it just above the branch of the
celiac artery or placing it to cover the celiac artery with good collateral circulation should be
regarded as equivalent to surgery, as same as in cases with a descending aortic aneurysm.
(5) Traumatic Aortic Injury
Stent-graft treatment is the first-line therapy for traumatic aortic injuries, particularly
those involving the arterial ligament or the descending aorta (Class I, Level of Evidence: B).
(6) Ruptured Thoracic Aortic Aneurysm
The results of thoracic endovascular aneurysm repair (TEVAR) for ruptured descending
TAA are more favorable than those of surgical treatment. Therefore, TEVAR is recommended
for ruptured descending TAA if the lesion is located at a site appropriate for this treatment (Class
IIa, Level of Evidence: C).
3. Methods of Stent-Graft Treatment
(1) TEVAR
TEVAR is focused on two main issues: “how to safely deliver the stent-graft to the target
site and place it there” and “how to set a favorable landing zone”.
1) Access
Because the catheter sheath used for TEVAR is thick (20 to 27 Fr), it is more likely for
iliac injury to occur during the approach from the femoral artery. A number of patients reportedly
require surgical repair because of arterial dissection, iliac artery interruption, among others.
Therefore, it is necessary to implement TEVAR in an environment in which a back-up system for
such situations is in place (Class I, Level of Evidence: C).
2) Landing Zone for Stent-Graft Placement
The most important aspect of stent-graft treatment is to obtain the landing zone for the
stent on the proximal and distal sides of the aneurysm.
i) Left Subclavian Artery Coverage, Celiac Artery Coverage
When covering the left subclavian artery, ischemic symptoms of the left upper limb and
the brain do not appear in most cases, but it has been pointed out that cerebral infarction and
spinal cord injury are frequent complications. In cases requiring left subclavian artery coverage,
the patency of the right subclavian artery and right vertebral artery and communication between
the right and left vertebral arteries at the basilar artery level should be confirmed. When the
patency and communication of these vessels cannot be confirmed, bypass to the left subclavian
artery is considered to beindispensable. When covering the celiac artery, it is rare to have
complications or problems involving the blood flow to the abdominal organs or intestinal tract
because there is perfusion from the collateral circulation via the superior mesenteric artery in
most cases. However, an increased incidence of spinal cord injury has frequently been reported,
similar to cases of left subclavian artery coverage.
ii) Extensive Coverage of the Intercostal Artery
 This is closely related to spinal cord injury and will be described in the section on
complications.
3) Touch-up of the Stent-Graft
Although it is common for touch-up with a balloon to be performed after stent-graft
deployment, the balloon may cause graft migration when it drifts out of its original location due
to blood flow. Therefore, balloon dilatation for touch-up of the stent-graft is often performed
under some form of blood flow control. These blood flow control measures include (1)
pharmacological hypotension, (2) pharmacological cardiac arrest using adenosine triphosphate
(ATP), among others,
(3) rapid pacing, (4) inferior (or superior) vena cava occlusion. Measures (2) to (4) are
theoretically justified because the lower the blood flow through the balloon-dilated portion, the
lower the resistance to the balloon itself.

Figure 3. Hybrid procedures with thoracic stent-grafting. (A) Left common carotid artery-to- left
subclavian artery bypass grafting + TEVAR (debranching of one vessel + TEVAR). (B) Right
axillary artery-to-left common carotid/left axillary artery bypass grafting + TEVAR (debranching
of two vessels + TEVAR). (C) Right common carotid artery-to-left common carotid/left
subclavian artery bypass grafting + TEVAR (debranching of two vessels + TEVAR). (D)
Ascending aorta-to- left common carotid/left axillary artery bypass grafting + TEVAR
(debranching of two vessels + TEVAR). (E) Ascending aorta-to-brachiocephalic/left common
carotid/left axillary artery bypass grafting + TEVAR (debranching of three vessels + TEVAR).
(F) Iliac artery-to-celiac/superior mesenteric/left and right renal artery bypass grafting + TEVAR.
(G) Open stent-grafting (with surgery on ascending aorta and aortic arch). The ascending aorta
and branches of the aortic arch are reconstructed using four-branch artificial graft. A stent-graft is
inserted intothe descending aorta with only the distal end fixed in the vessel, and the artificial
graft of the aortic arch and the stentgraft inserted in the descending aorta are sutured at the aortic
arch. TEVAR, thoracic endovascular aneurysm repair.

4) Devices
As of December 2010 in Japan, two types of devices for the treatment of TAA were
approved and in use. There were three more devices to treat TAA that were under clinical trial or
were in the application approval process. The latter three include a device that has fenestrations
for coping with arch branches and another designed for the open stent-graft procedure.
(2) Hybrid Procedure
Concerning the major branches of the aortic arch and abdominal aorta that must be
covered to obtain the landing zone, there are reports describing methods for stent-graft insertion
after bypass revascularization through an extra-anatomical
route (Figure 3). Stent-graft treatment combined with bypass is not associated with
marked differences in the mortality rate or the incidence of cerebral complications in cases with
lesions involving the arch, in comparison with routine surgery. On the other hand, in the
thoracoabdominal lesion, it has often been reported that the incidence of paraplegia, the foremost
concern, is low.
Acute Infective Endocarditis

Introduction

Despite advances in medical and surgical therapy, infective endocarditis (IE) remains a highly
morbid and deadly infection. Endocarditis is an inflammation of the endocardium, the inner
lining of the heart and heart valves. While such inflammation can be caused by a variety of
disease states, the majority of endocarditis is caused by infectious agents. In his Gulstonian
lectures of 1885, Sir William Osler drew a distinction between “simple” and “malignant” forms
of endocarditis . The “simple” form described by Osler correlates to what has become known as
subacute bacterial endocarditis. Subacute IE typically presents with subtle constitutional
symptoms, and is frequently not diagnosed until it has been present for months. The “malignant”
form described by Osler, characterized by an acute onset and fulminant course, correlates to what
is now known as acute IE. The focus of this review will be acute IE, though many studies of
diagnosis and treatment do not differentiate between acute and subacute disease, and indeed
many of principles of diagnosis and management of IE are identical between acute and subacute
disease.

Pathogenesis

Vegetation formation is a multistep process. The first step is endocardial injury, which may occur
by many mechanisms. The most common mechanism is injury by turbulent blood flow from an
acquired or congenital intracardiac abnormality. The most common site of such injury, and thus
the most common site of vegetation formation, is on the line of closure of a valve surface,
typically on the atrial surface of atrioventricular valves, or the ventricular surface of semilunar
valves. Alternatively, an intravascular catheter or other device may directly abrade the
endocardium. In injection drug users, direct injection of contaminating debris may damage the
tricuspid valve surface.The endothelial damage triggers sterile thrombus formation, which occurs
by deposition of fibrin and platelets. Though mechanical endocardial damage usually precedes
sterile thrombus formation, a sterile thrombus can be induced without direct trauma. Physiologic
 stresses such as hypersensitivity states, hormonal changes, and high altitude can also induce
sterile endocardial thrombosis. Clinical states associated with sterile thrombus formation in
humans include malignancy, rheumatic diseases, and uremia. Once a sterile thrombus is present,
transient bacteremia can seed the thrombus. Bacteria are introduced into the bloodstream when a
body surface that is heavily colonized by bacteria (oral cavity, gut lumen, genitourinary mucosa)
is traumatized. Routine daily activities such as chewing food and tooth brushing lead to frequent
low- level, transient bacteremias in healthy adults . Bloodborne bacteria may adhere to the
damaged endocardial surface. Bacteria have different adhesive capacity, based on bacterial
surface characteristics and virulence factors called adhesins. For example, the adhesive properties
of viridans streptococci are related the amount of dextran present in the streptococcal cell wall, as
well as specific surface proteins such as FimA. Once bacteria have attached to the endocardium,
the vegetation “matures” through additional deposition of fibrin and bacterial proliferation.
Histologically, the vegetation consists primarily of fibrin, platelets, and bacteria; the absence of
vasculature makes penetration by phagocytic cells rare. The majority of bacteria in a mature
vegetation are found below the surface of the vegetation, protected from phagocytes and high
concentrations of antibiotics.
Epidemiology

Demographics and Risk Factors

The incidence of IE is between 2 and 10 episodes per 100,000 person-years in most population-
based studies, and as high as 20 episodes per 100,000 person-years in the elderly. There are
approximately 15,000 new cases of IE diagnosed each year in the United States, and it accounts
for about 1 in 1000 admissions to the hospital. Most studies demonstrate that the rate of IE has
been stable over time, though changes in diagnostic tools and criteria make temporal comparisons
difficult. Despite a relatively stable rate, the nature of IE has changed dramatically over the past
several decades. IE is more commonly associated with invasive medical procedures and old age,
and less associated with rheumatic heart disease and poor dentition. These epidemiologic trends
support the observation that acute IE is increasing in frequency relative to subacute and chronic
IE: in the preantibiotic era, approximately 20% of IE was acute, while more recent studies show
that about 33% of IE is acut. IE is more common in men than women, and is more common with
increasing age. The mean age of IE patients has increased over time, from under 30 years in the
preantibiotic era to nearly 60 years in 1990s. In the elderly, IE is more often associated with
intracardiac prosthetic devices and bacteria from the gastrointestinal tract. In a large
observational cohort study, IE most commonly involved the mitral valve only (approximately
40% of patients), followed by the aortic valve only (36% of patients), followed by multivalvular
disease. Right-sided valves are rarely affected except among injection drug users. The pulmonic
valve is least likely to be involved in IE. Structural heart disease is a risk factor for IE because it
results in turbulent blood flow. About 75% of patients who develop IE have underlying structural
heart disease. In the past, rheumatic heart disease with mitral stenosis was the most common
valvular defect in patients with IE. Recently, the most common predisposing lesions are mitral
regurgitation, aortic valve disease (stenosis and regurgitation), and congenital heart disease.
Mitral valve prolapse is a risk factor for IE, primarily when regurgitation is present. The presence
of a prosthetic cardiac valve is a strong risk factor for IE. The risk is highest in the first year after
valve implantation. Mechanical valves are associated with higher risk than bioprosthetic valves in
the first years after surgery, but that relationship reverses in later years after surgery. Implanted
valve rings are associated with lower risk of IE than prosthetic valves. In addition to structural
heart disease and prosthetic valves, established risk factors for IE include prior episodes of IE,
invasive medical procedures, and injection drug use. Some studies have demonstrated that
diabetes mellitus and kidney disease may be risk factors as well. Nosocomial IE is increasing in
frequency and importance. Between 14% and 31% of all IE is nosocomial in recent case series. In
a longitudinal single-center study in Spain, the proportion of IE that was acquired in the hospital
increased almost ten-fold in a 15-year period. Compared to community-acquired IE, nosocomial
IE was associated with three-fold higher mortality, and was most commonly caused by S. aureus,
coagulase-negative staphylococci, and enterococci.
IE in Critical
Care

Because IE often occurs in patients with multiple co-morbid illnesses and those who have
undergone recent invasive procedures, it is commonly diagnosed and treated in the intensive care
unit (ICU). From 1993-2000, IE was diagnosed in 3% of ICU patients in 2 medical ICUs in
France. Among 228 cases of IE in this study, 64% of cases were native valve endocarditis (NVE),
of which
21% were nosocomial. S. aureus was the causative agent in half of all IE cases. Complications
were frequent: Neurological events complicated 40% of cases, CHF 29%, and septic shock 26%.
Inhospital mortality was 45%. Septic shock, neurological complications, and immunocomprimise
predicted in-hospital mortality. In another study taking place between 1994 and 1999, IE was
identified in 0.8% of all ICU patients in 4 medical ICUs in Vienna, Austria. Just over half of the
33 patients came to the ICU with the diagnosis of IE, while 45% of them were first diagnosed in
the ICU. The majority (79%) had NVE, and S. aureuswas the most common pathogen, causing
36% of IE. Severity of illness was high, with 79% of patients receiving mechanical ventilation,
73% receiving vasopressors, and 54% dying during their hospital stay. Acute renal failure
occurred in 39% of patients, and was the only independent predictor of mortality. Nosocomial IE
in the ICU can usually be attributed to a hospital acquired infection at another primary site. Of 31
nosocomial cases of IE described by Mourvillier et al, 21 were related to intravenous catheter
infection and 3 to surgical site infection. In another study, among 22 nosocomial IE cases in an
ICU, 11 were related to an intravascular device and 8 to a surgical site infection. Fifteen of these
22 patients had no predisposing cardiac lesion. S. aureus was the causative pathogen in 68% of
patients, and 68% of the patients died. Wolff et al described 122 cases of prosthetic valve
endocarditis (PVE) in a French ICU from 1978 to 1992. S. aureus accounted for 61% of disease
occurring in the first 2 months after valve implantation, and streptococci and S. aureus were the
most common causes of late disease. Heart failure was seen in half of cases, and mortality was
34% at 4 months. Predictors of mortality among S. aureus cases were septic shock, heart failure,
mediastinitis, and elevated prothrombin time.
 Approach to the Patien|

Diagnosis

Diagnostic Criteria
The Duke Criteria incorporate information from echocardiography, history and physical exam,
microbiology, and pathology to diagnose IE (Table 1). They were originally proposed in 1994,
and were subsequently shown to be superior to previous diagnostic criteria. The criteria were
modified in 2000 to revise the definition of “possible IE,” add criteria for microbiologie diagnosis
of Q fever IE, eliminate echocardiographic minor criteria, and include recommendations for
choosing between transthoracic echocardiography (TTE) and transesophageal echocardiography
(TEE).

Table 1
Modified Duke Criteria for Diagnosis of Infective Endocarditis

Definite endocarditis requires 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria.

Possible endocarditis requires 1 major and 1 minor criterion, or 3 minor criteria.

Major Criteria:
Major Criteria:

1. Microbiologic evidence
of IE:

Typical organisms cultured from 2 separate blood cultures:

• *Viridans streptococci, Staphylococcus aureus, HACEK organism, or

Streptococcus bovis, OR

• * Community-acquired enterococcus in the absence of an alternative

primary site of infection
Persistently positive blood cultures with other organism:

• *At least 2 positives drawn >12 hours apart, OR

• * All of 3 or majority of 4, with first and last drawn >1 hour apart

One culture (or phase 1 IgG >1:800) for Coxiella burnetii

2. Evidence of
Echocardiogram showing:
enclocarclial involvement
• * Oscillating intracardiac mass without alternative explanation, OR

• *Abscess, OR

• * New partial dehiscence of a prosthetic valve, OR

• * New valvular regurgitation

 Minor Criteria:

1. Predisposition to Previous IE, injection drug use, prosthetic heart valve, or cardiac lesion
infective endocarditis: causing turbulent blood flow
2. Fever >38 C
3. Vascular phenomenon:
Arterial embolism, pulmonary infarct, mycotic aneurysm, intracranial or
conjunctival hemorrhage, or Janeway’s lesions
4. Immunologic Glomerulonephritis, Osier’s nodes, Roth’s spots, or positive rheumatoid
phenomenon: factor

5. Microbiologic finding not

meeting major criteria

History and Physical Exam

The clinical presentation of subacute IE is variable, but the presentation of acute IE is more
straightforward. Unlike patients with subacute IE who typically report longstanding constitutional
symptoms, patients with acute IE typically describe the abrupt onset of fever and rigors, and may
present with symptoms of embolism. The history should include specific inquiry about known
risk factors for IE, including invasive procedures, injection drug use, structural heart disease, and
prior endocarditis. Symptoms referable to other organ systems may indicate a primary source of
bacteremia. Complications of IE may be apparent from the history, including heart failure,
conduction disturbances, or embolism. The physical exam must be comprehensive, with special
attention to examination of the heart, dentition, all sites of invasive devices and recent
procedures, and potential destinations of embolism. Heart murmur is present in 85% of patients
with IE, but a changing murmur is only apparent in 5 to 10% of cases. About half of patients with
IE have evidence of embolic phenomena on physical exam. When clinical suspicion is present, a
lack of clinical findings does not rule out the diagnosis of IE.

Laboratory tests

At least three blood cultures should be drawn when IE is suspected, with the first and last drawn
at least one hour apart. The microbiology lab should be informed that IE is on the differential
diagnosis, if fastidious organisms are suspected. Electrocardiogram, chest radiograph, urinalysis,
and rheumatoid factor may assist in making the diagnosis or identifying complications of IE.

Echocardiography

Diagnosis of IE is made in part by echocardiographic findings. The presence of an oscillating

intracardiac mass, either on a valve, in the path of a regurgitant jet, or on implanted material, is
the classic finding, though abscess or new partial dehiscence of a prosthetic valve also meets
diagnostic criteria. Other findings associated with IE include aneurysm, fistula, and leaflet
perforation. The use of echocardiography to rule out IE should be based on the clinician’s pretest
probability of disease. Pretest probability, in turn, is based on the presence of clinical and
microbiologic features unique to each patient, including the likelihood of alternative diagnoses.
Studies have proposed algorithms for use of echocardiography to diagnose IE. While these
studies can not substitute for the judgment of an experienced clinician, they highlight some of the
features which impact on pretest probability of IE: presence of bacteremia, type of organism,
presence of known IE risk factors, and clinical exam.TTE and TEE both have a role in the
diagnosis and evaluation of IE. TTE has low sensitivity compared to TEE (46% vs. 93%), though
both are highly specific (95% vs. 96%). TTE is a reasonable first test in patients with low pretest
probability of IE despite its sensitivity of less than 50%. In some patients who undergo TTE and
are found to have IE, subsequent TEE may be advisable to evaluate perivalvular extension of
disease, vegetation size, and other factors which may inform surgical decision-making. In
patients with higher pretest probability for disease, or in whom TTE is rendered less sensitive by
obesity, lung hyperinflation, or valve prosthesis, TEE is the initial echocardiographic modality of
choice in IE. Several studies have demonstrated that TTE alone will miss a significant number of
cases of IE in patients with medium to high pretest probability of disease, including those
meeting Duke criteria for “possible” IE, and patients with S. aureus bacteremia.

The vegetation is indicated by arrows

Vegetation on the aortic valve

Vegetation on the mitral valve

 Alternative imaging modalities

Cardiac CT and MRI have been reported to diagnose complications of IE, including aortic root
abscesses and arteriovenous fistulae. Current limitations to these modalities include difficulties in
evaluating valve motion, spatial resolution, and time required to acquire images. A recent study
of cardiac multislice CT showed that its test characteristics were similar to TEE for the diagnosis
of IE in 37 patients, 29 of whom underwent cardiac surgery, though all 4 leaflet perforations were
missed with CT. While CT and MRI may be useful as an adjunct to echocardiography in selected
cases at centers with expertise in these techniques, they are not part of the current standard of
care in the routine diagnosis of IE. The technology involved in cardiac CT and MRI is evolving
rapidly, and at some point in the future they may be useful in IE diagnosis.

Antibiotic Therapy: General Principles

All patients with IE should receive antibiotic therapy, and more than half of cases are managed
with antibiotic therapy alone. Some organism-specific recommendations for treatment are
discussed below in the “Specific organisms” section. A recent scientific statement by the
American Heart Association provides an excellent summary of evidence and antibiotic
recommendations, and should be consulted for IE cases that are beyond the scope of this review.
Though treatment must be individualized, some general principles of antibiotic therapy apply to
all patients. Because the vegetation structure sequesters bacteria from the bloodstream, long
durations of therapy are necessary. Parenteral antibiotics are preferred over oral regimens because
of the need for sustained and reliable blood levels of antibiotic. Blood cultures should be drawn
every 24 to 48 hours after initiation of antibiotics, until they are negative. Duration of treatment
should be counted from the time of the first negative blood cultures. If vancomycin or an
aminoglycoside is used, drug levels should be monitored to ensure adequate dosing and to
prevent toxicity. Aminoglycosides are often used in combination with a cell wall-active agent (P-
lactam or vancomycin) for synergy in the treatment of IE caused by staphylococci, streptococci,
and enterococci. Cell wall-active agents increase aminoglycoside entry into bacteria, and
therefore synergy requires dosing in close temporal proximity to one another. The use of
combination therapy is supported by in vitro and animal studies, but clinical data in humans are
scarce. A recent meta-analysis of clinical trials of combination therapy included 261 patients with
IE due to S. aureus or viridans streptococci in 5 separate studies. There was no benefit of
combination therapy in terms of mortality or treatment success. However, in a single study,
combination therapy for S. aureus IE did reduce the duration of bacteremia, though it did not
improve clinical outcomes. Because of the small size of these studies, it is possible that a
meaningful clinical benefit does exist, but studies have not been adequately powered to detect it.

Surgical Therapy
Decisions regarding surgical therapy for patients with IE are multifactorial and complex, and the
need for surgery should be individualized to each patient. For these reasons, early input from an
experienced cardiothoracic surgeon can be invaluable in managing a patient with IE. Among all
patients with IE, 40-45% eventually undergo surgery, and rates of surgery are similar for NVE
and PVE. Predictors of surgery include younger age, CHF, abscess, and coagulase-negative
staphylococcal IE. The majority of surgery for IE is performed for hemodynamic indications such
as congestive heart failure. Because there have been no randomized controlled trials of surgical
plus medical therapy versus medical therapy alone in the treatment of IE, current guidelines for
surgical treatment of IE are based primarily on observational data, which are prone to biases such
as confounding by indication, and survival treatment selection bias. Because of these biases,
careful adjustment for factors associated with risk of death and likelihood of receiving surgery
are necessary. Several recent studies have attempted to account for these factors, and results have
been conflicting regarding the benefit of surgery. In a study reporting a ten-year experience at
seven US hospitals, 230 of 513 adults with NVE underwent cardiac surgery. After propensity
analyses to account for differences in treatment assignment and prognostic factors, surgery was
associated with reduced mortality (15% vs. 28%, p=.01), especially in patients with moderate to
severe heart failure (14% vs. 51%, p=.001). In contrast, a study that matched 27 surgical and 27
non-surgical ICU patients with IE by propensity score found no benefit of surgery (OR 0.96). A
study of NVE from the International Collaboration on Endocarditis Merged Database, which
included patients from 7 centers in 5 countries, showed a survival benefit from surgery only in
patients in the highest quintile of surgical likelihood (11.2% in the surgery group vs. 38.0% in the
no surgery group, p<.001). A study of PVE from the same study group found a statistically non-
significant benefit of surgery (22.1% in the surgery group vs. 32.4% in the no surgery group,
p=0.18) in patients with PVE matched on propensity score. Finally, in an analysis of an 18-year
experience with left-sided IE at a single center in the USA, after matching by propensity score,
decade of diagnosis, and follow-up time, surgery was not significantly associated with mortality
(adjusted HR 1.3, 95% confidence interval 0.5—3.1). Thus, the benefit of surgery is unclear, and
is likely restricted to specific subgroups of patients. There are several subgroups of patients in
which early surgery should be strongly considered. Patients with CHF or severe valvular
dysfunction likely to precipitate acute CHF should be considered for surgery, particularly when
the aortic valve is involved. Patients with intracardiac abscess should be strongly considered for
surgery, in light of decreased penetration of antibiotics to the site of infection, and the possibility
of the abscess causing heart block acute valvular dysfunction. Patients with IE caused by
organisms known to be refractory to medical management, including Pseudomonas, Candida,
and multi-drug resistant organisms, may benefit from surgical management, as well as those at
highest risk for embolism. Patients with PVE should be carefully considered for surgery, though
low-risk patients with PVE may be adequately managed with medical therapy alone.
Characteristics which suggest lower risk include absence of heart failure, abscess, or valve
dehiscence, and those whose IE is caused by less virulent organisms such as viridans
streptococci.

Right-sided IE
Right-sided IE, which accounts for about 10% of cases of IE, occurs most commonly in injection
drug users, and has different clinical characteristics and outcomes compared to left-sided IE.
Patients with right-sided IE are typically younger, with fewer comorbid medical conditions and
less underlying valve disease than patients with left-sided IE. S. aureus is responsible for about
70% of right-sided IE. Patients with right-sided IE often present with signs and symptoms of
septic pulmonary emboli, including pleuritic chest pain, dyspnea and hemoptysis. More than half
present with chest radiograph consistent with septic pulmonary emboli. The mortality rate among
patients with right-sided IE is typically less than 10%. In a study of 1529 episodes of IE in
injection drug users in Spain, 79% had right-sided IE, 16% had left-sided IE, and 5% had both.
Only 1% of the right-sided IE was of the pulmonic valve. It has not been definitively established
why the tricuspid valve is so frequently involved in IE in injection drug users. While it may be
related to valve damage caused by bombardment of the tricuspid valve by impurities in injected
material, this damage has not always been apparent in autopsy studies of injection drug users.
Other theories include drug-induced microthrombi on the valve, drug-induced pulmonary
hypertension, and increased right-sided expression of molecules which bind bacteria. Carefully
selected cases of tricuspid valve IE may be managed with short courses of parenteral antibiotics,
or with oral regimens. Patients with factors associated with poor prognosis, including concurrent
left-sided IE, metastatic infection, heart failure, large vegetation, or immune compromise should
not be considered for shorter course therapy or oral regimens.
Prosthetic Valve Endocarditis (PVE)

The risk of PVE is 1 to 5% in the first year after implantation, and decreases to about 1% per
year thereafter. The risk of PVE is similar overall among mechanical and bioprosthetic valves,
though early IE risk may be higher and late IE risk lower among mechanical valves compared to
bioprosthetic valves. PVE risk is comparable among valves in the aortic and mitral positions.
PVE occurring in the first 12 months after surgery is most often caused by coagulase-negative
staphylococci or S. aureus, while late-onset PVE has similar microbiology to NVE. Mortality in
PVE is predicted by heart failure, S. aureus, and the presence of intracardiac abscess or fistula .
 Surgical therapy for PVE is frequently indicated, as discussed above, and is performed in about
half of all cases of PVE. Recommendations for medical therapy in the treatment of PVE are
generally similar to those for treatment of NVE, though they differ substantially for
staphylococcal PVE. For PVE caused by oxacillin-susceptible strains of staphylococci, duration
of nafcillin or oxacillin should be at least 6 weeks, rifampin should be added for the same
duration, and low-dose gentamicin should be given for 2 weeks.
Cardiovascular Device-Related
IE

Use of intracardiac pacemakers and implantable cardioverter-defibrillators (ICDs) has been

steadily increasing, but infection of these devices has been increasing even more rapidly. Most
infections of pacemakers and ICDs occur only at the pocket, but 10% of pacemaker-associated
infections include IE. Pacemaker/ICD IE is best diagnosed with TEE, as TTE has sensitivity of
less than 30% for lead vegetations. However, it may be impossible to definitively distinguish a
sterile thrombus from an infected thrombus on a lead. An intracardiac oscillating mass on a
pacemaker/ICD lead qualifies as a major criterion in the Duke criteria for IE diagnosis. There
have been no randomized studies of device removal plus antibiotics versus antibiotics alone in
the treatment of pacemaker/ICD IE, but optimal management includes removal of the device, at
a minimum until bacteremia clears, but longer if possible. One retrospective study of any
pacemeaker/ICD infection showed a relapse rate of less than 1% among 117 patients who
underwent device removal, and 50% among 6 patients in whom the device was retained. If a
pacemaker/ICD must be replaced before completion of therapy, it may be advisable to treat as
PVE.

Specific organisms

For IE caused by organisms not addressed below or in Tables 2 and , the American Heart
Association’s Scientific Statement on Infective Endocarditis should be consulted for treatment
recomm endati ons.

Selected Native Valve Endocarditis Treatment Regimens All doses based on normal renal
function
Table 2

Organism Drug Duration Notes

Oxacillin- oxacillin/nafcinin 2g IV 6 weeks For non-anaphylactoid penicillin allergy,

Organism Drug Duration Notes

 sensitive Staphylococcus q4h 3 to 5 substitute cefazolin 2g IV q8h for
WITH OR WITHOUT days oxacillin/nafcillin. For anaphylactoid
gentamicin 1 mg/kg IV/IM penicillin allergy, substitute vancomycin 15
mg/kg IV q12hb for oxacillin/nafcillin, and do
not use gentamicin

00

Oxacillin- vancomycin 15 mg/kg IV 6 weeks

resistant Staphylococcus q12hb

Viridans streptococci/S. penicillin G 12-18 million 4 weeks For penicillin/ceftriaxone allergy,

bovis with penicillin MIC < U IV per 24hc 4 weeks vancomycin 15 mg/kg IV q12hb
0.12 pg/mL OR
ceftriaxone 2g IV/IM q24h

Viridans streptococci/S. bovis penicillin G 24 million U 4 weeks For penicillin/ceftriaxone allergy,

with penicillin MIC > 0.12 to < IV per 24hc 2 weeks vancomycin 15 mg/kg IV q12hb
0.5 pg/mL PLUS 4 weeks
gentamicin 3 mg/kg IV/IM 2 weeks
q24h
OR
ceftriaxone 2g IV/IM q24h
PLUS
gentamicin 3 mg/kg IV/IM
q24h

Viridans streptococci/S. See treatment regimen for

bovis or Nutritionally-variant penicillin/ampicillin-
Streptococci with PCN MIC > resistant enterococcal
0.5 pg/mL endocarditis

Enterococcus spp. Susceptible ampicillin 2g IV q4h 4-6 For penicillin/ampicillin allergy,

to penicillin, ampicillin, PLUS weeks vancomycin 15 mg/kg IV q12hb for 6
gentamicin, and vancomycin gentamicin 1 mg/kg 4-6 weeks PLUS gentamicin 1 mg/kg IV/IM
IV/IMq8ha weeks q8ha for 6 weeks
OR 4-6
penicillin G 18-30 million weeks
U IV per 24hc 4-6
PLUS weeks
gentamicin 1 mg/kg
IV/IMq8ha
Organism Drug Duration Notes

6 weeks If p-lactamase production, ampicillin-

6 weeks sulbactam 3g IV q6h PLUS gentamicin 1
vancomycin 15 mg/kg IV mg/kg IV/IM q8hc for 6 weeks
Enterococcus spp resistant to q12hb
penicillin/ampicillin, susceptible PLUS
to vancomycin and gentamicin gentamicin 1 mg/kg IV/IM
q8ha

Organism Drug Duration Alternative/Comments

Oxacillinsensitive > 6 weeks For non-anaphylactoid penicillin allergy, substitute

Staphylococcus >6 weeks cefazolin 2g IV q8h for oxacillin/nafcillin. For
oxacillin/nafcillin 2g 2 weeks anaphylactoid penicillin allergy, substitute
IV q4h vancomycin 15 mg/kg IV q12hb for
PLUS oxacillin/nafcillin
rifampin 300 mg
IV/PO q8h
PLUS
“target gentamicin peak 3-4 micrograms/mL;
gentamicin 1 target
b
mg/kgtrough <1 microgram/mL target
vancomycin peak 30-45 micrograms/mL;
IV/IM q8ha target trough 10-15 micrograms/mL
c
penicillin dosing can be by continuous infusion, or dosed q4-6h in equal divided doses adapted with permission from
Baddour LM et al [40]
Oxacillin- >6 weeks
resistant Staphylococcus >6 weeks
Table 3 vancomycin 15 2 weeks
mg/kg IV q12hb
PLUS
Selected Prosthetic Valve rifampin Endocarditis
300 mg Treatment Regimens All doses based on
IV/PO q8h
normal renal functionPLUS
gentamicin 1 mg/kg
IV/IM q8ha

Viridans streptococci/S. 6 weeks For penicillin/ceftriaxone allergy, vancomycin 15

bovis with penicillin MIC < 0.12 2 weeks mg/kg q12hb for 6 weeks without gentamicin
pg/mL 6 weeks
penicillin G 24 million 2 weeks
U IV per 24hc
WITH OR
WITHOUT
gentamicin 3 mg/kg
IV/IM q24h
OR
ceftriaxone 2g
IV/IM q24h
WITH OR
 Organism Drug Duration Alternative/Comments

WITHOUT
gentamicin 3 mg/kg
IV/IM q24h

Viridans streptococci/^. 6 weeks For penicillin/ceftriaxone allergy, vancomycin 15

bovis with penicillin MIC > 0.12 6 weeks mg/kg q12hb for 6 weeks without gentamicin
penicillin G 24 6 weeks
c 6 weeks
million U IV per 24h
PLUS
gentamicin 3 mg/kg
IV/IM q24h
OR
ceftriaxone 2g
IV/IM q24h
PLUS
gentamicin 3 mg/kg
IV/IM q24h

Enterococcus spp. - -

PVE treatment
regimens identical to
NVE treatment
regimens. See Table 2.

“target gentamicin peak 3-4 micrograms/mL; target trough <1 microgram/mL •target vancomycin peak 30-45
micrograms/mL; target trough 10-15 micrograms/mL
penicillin dosing can be by continuous infusion, or dosed q4-6h in equal divided doses adapted with
permission from Baddour LM et al

Staphylococcus aureus
S. aureus is the leading cause of acute IE. The incidence of S. aureus IE has been steadily
increasing in recent decades, becoming the predominant organism in IE in most reports.
Increasing use of intravenous catheters and implanted prosthetic devices have led to higher rates
of healthcare- associated staphylococcal bacteremia, placing more patients at risk for IE. S.
aureus IE tends to involve the mitral valve more often than the aortic, and is the most common
cause of IE among injection drug users. IE caused by community-associated strains of
methicillin-resistant S. aureus (CA-MRSA), compared to strains of hospital-acquired MRSA,
occurs in a younger population with a higher prevalence of injection drug use. S. aureus IE is
associated with higher rates of embolism and mortality compared to IE caused by other
organisms. In a large cohort study of S. aureus IE, embolism occurred in 60% of cases of S.
aureus IE versus 31% of cases caused by other organisms. NVE caused by methicillin-
susceptible strains of S. aureus (MSSA) should be treated with 6 weeks of intravenous (IV)
nafcillin or oxacillin (Table 2). Gentamicin can be added for 3 to 5 days at 3mg/kg/day in 2 or 3
divided doses, though its use is considered optional based on existing studies and potential
toxicities. MRSA IE should be treated with vancomycin alone for 6 weeks, with goal vancomycin
troughs of 10-15 micrograms/dl. Antibiotic therapy for PVE caused by S. aureus is shown in
Table 3.
Coagulase-negative staphylococci
While coagulase-negative staphylococci cause about 6% of NVE, they cause very little acute IE.
Coagulase-negative staphylococcal IE caused is more indolent than IE caused by other
organisms. One significant exception is the species S. lugdunensis, a coagulase-negative
staphylococcus that behaves clinically like S. aureus, and has been described to cause acute IE
with an aggressive clinical course. In the first year after prosthetic valve implantation, coagulase-
negative staphylococci are the second most common cause of PVE, after S. aureus. IE caused by
coagulase- negative staphylococci should be treated with antibiotic regimens similar to those
used to treat S. aureus (Tables 2).

Streptococci
Streptococcal IE comprises about 30% of all IE, though it is less prevalent among acute IE. Most
streptococcal IE is caused by viridans streptococci, which are oral flora and include S. mitis, S.
mutans, S. salivarius, S. sanguis, and the S. intermedius group (S. intermedius, S. anginosus, and
S. constettatus). S. bovis, a group D streptococcal species, is the most common non-viridans
streptococcal species to cause IE. S. bovis bacteremia is strongly associated with colon polyps
and cancer. S. bovis accounts for 5 to 15% of cases of IE in the United States. Other streptococci
account for less than 5% of cases of definite IE. Treatment of IE caused by viridans streptococci
or by S. bovis depends on the degree of penicillin resistance of the infecting organism.
Aminoglycosides are recommended in some settings for synergistic effects, though clinical data
in humans is incomplete. See Tables 2 for treatment recommendations.

Enterococci
After staphylococci and streptococci, enterococci are the third leading cause of IE, causing about
10% of cases. Enterococcal IE tends to occur in older men with many comorbid medical
conditions. It occurs disproportionally on the aortic valve, and is less commonly associated with
embolic events compared to IE caused by other organisms. Enterococci were formerly designated
as a member of genus streptococcus, but now are a genus unto themselves. Unlike streptococci,
enterococci are relatively resistant to penicillin, ampicillin, and vancomycin, and killing of
susceptible strains often requires the addition of gentamicin or streptomycin for synergy. For this
reason, all enterococcal isolates in IE cases should be tested for high-level resistance to
gentamicin and streptomycin. Current guidelines suggest 4 to 6 weeks of aminoglycoside in
combination with a cell-wall active agent for IE caused by appropriately susceptible isolates, but
observational data suggest that outcomes may be similar when the aminoglycoside is given for a
shorter duration. In cases where aminoglycoside is contraindicated because of toxicities, or when
high-level resistance is present, there is in vitro data but limited clinical data suggesting that the
combination of ampicillin and ceftriaxone achieve synergistic killing of susceptible enterococci,
and may be a reasonable therapeutic alternative when aminoglycosides can not be used. See
Tables 2 for treatment recomm endati ons.

Gram Negative Bacilli

Gram negative bacilli account for approximately 5% of IE diagnoses. These can be divided into
HACEK and non-HACEK IE. The acronym HACEK stands for Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, and Kingella. IE due to HACEK organisms is rarely acute. Older
literature suggest that these fastidious organisms require prolonged incubation periods to grow in
the microbiology lab, but with modern culture techniques, most HACEK organisms grow within
5 days. In a recent international cohort including 2761cases of IE from 2000 to 2005, only 1.8%
of cases were caused by non-HACEK gram-negative organisms, most commonly Escherichia
coli and Pseudomonas aeruginosa. Unlike older case series in which injection drug use was
strongly implicated in the majority of cases, most cases in this cohort (57%) were healthcare-
acquired, and mortality was high (24%).

Complications

Congestive Heart Failure

CHF is the most common complication of both NVE and PVE, occurring in over half of all cases
of IE. It is usually caused by valvular dysfunction, not myocardial failure, and is most commonly
associated with aortic valve dysfunction. In retrospective studies of IE patients with CHF,
medical management alone is associated with higher mortality than surgical and medical
management combined, even after adjustment for propensity to receive surgical therapy .
Intracardiac
Abscess

Intracardiac abscesses occur in approximately 10 to 40% of cases of IE, and are particularly
common in PVE and aortic valve disease. Abscess related to the aortic valve can extend into the
conduction system, causing heart block. S. aureus is the organism most commonly associated
with intracardiac abscess. Diagnosis usually requires TEE, though even TEE has a sensitivity of
only about 50% compared to intraoperative examination. Surgical intervention is usually
necessary to achieve cure of abscess.

Embolism

Embolic events occur in 20 to 50% of patients with IE. The central nervous system is the most
common destination of embolism, followed by the spleen, kidneys, lungs, and liver. Risk of
embolism is highest in the time immediately following after diagnosis, and risk decreases once
antibiotic therapy has been initiated. Vegetations measuring greater than 10 millimeters, and
vegetations on the anterior mitral valve leaflet are most likely to embolize. Central nervous
system embolism accounts for 40 to 65% of all embolic events in IE, and the middle cerebral
artery is the most common site. In a study of 60 patients with left-sided IE who underwent brain
MRI, cerebrospinal fluid analyses, and structured neurological exams, 35% of patients had a
symptomatic cerebrovascular event, and another 30% had an asymptomatic event, for a total
incidence of 65%. The risk of CNS embolism declines after initiation of antimicrobial therapy. In
a prospective study of 1437 patients with left-sided IE at 61 medical centers, the risk of CNS
embolism declined by 65% between the first and second week of antibiotics.

Mortality

Mortality among IE patients has been estimated at 15 to 20% during the index hospitalization,
and 20 to 30% at one year. Mortality is similar between NVE and PVE, and between mitral and
aortic IE. Right-sided IE has lower mortality than left-sided disease. In NVE, viridans
streptococci and enterococci are associated with lower mortality compared to S. aureus. IE
caused by gram-negative bacilli and fungi has greater than 50% mortality. Nosocomial
acquisition of IE , older age, immunocompromise, diabetes mellitus, APACHE II score,
hemodynamic instability, altered mental status and renal failure are significant predictors of
mortality. IE complications which are predictive of mortality include CHF, intracardiac abscess,
embolism, and large mobile vegetation.

Prevention

Though there have been no randomized controlled trials that prove the effectiveness of IE
prophylaxis around the time of dental, GI, or GU procedures, it has been common practice since
the 1950’s. Recent literature, however, has shown that only a small percentage of IE cases are
attributable to dental procedures, and that a huge amount of prophylaxis would be needed to
prevent only a small number of cases. The most recent practice guideline from the American
Heart Association for the Prevention of Infective Endocarditis, published in 2007, calls into
question many of the long-held assumptions about IE prevention, and contains many new and
revised recommendations. Prophylaxis solely for IE prevention is recommended only in patients
undergoing a high-risk procedure, and with a high-risk cardiac lesion. A high-risk procedure is
defined as: 1) any dental procedure that involves manipulation of gum tissue, or the periapical
region of teeth, or perforation of oral mucosa; 2) invasive respiratory tract procedure involving
breaks in the respiratory mucosa; or 3) invasive procedure involving infected skin or soft tissue.
A high-risk cardiac lesion is defined as one of the following: 1) prosthetic heart valve or
prosthetic material used in a valve repair; 2) previous IE; 3) unrepaired cyanotic heart disease; 4)
completely repaired congenital heart defect in the first 6 months after repair only; 5) repaired
congenital heart defect with residual defect adjacent to prosthetic material; or 6) cardiac
transplant recipient with cardiac valvulopathy. Prophylaxis is no longer recommended for those
undergoing GI or GU procedures.
 Summary

Acute IE is a complex disease with changing epidemiology and a rapidly-evolving knowledge

base. In order to consistently achieve optimal outcomes in the management of IE, the clinical
team must have an understanding of the epidemiology, microbiology, and natural history of IE, as
well as guiding principles of diagnosis and medical and surgical management.

Footnotes

Conflict of Interest Statement: The author has no conflicts of interest to disclose.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for
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Kaplan Medical

USMLE® STEP 2 CK SURGERY - 2018.

p. 72-73, 203-205

ACQUIRED HEART DISEASE

Aortic stenosis produces angina, syncope, and dyspnea. There is a harsh midsystolic heart
murmur best heard at the right second intercostal space and along the left sternal border. Start the
workup with an echocardiogram. Surgical valvular replacement is indicated if there is a gradient
>50 mm Hg, or at the first indication of CHF, angina, or syncope.

Chronic aortic insufficiency produces wide pulse pressure and a blowing, high-pitched, diastolic
heart murmur best heard at the second intercostal space and along the left lower sternal border,
with the patient in full expiration. Patients are often followed with medical therapy for many
years, but should undergo valvular replacement at the first evidence on echocardiogram of the
beginning left ventricular dilatation.

Acute aortic insufficiency because of endocarditis is seen in young drug addicts who suddenly
develop CHF and a new, loud diastolic murmur at the right second intercostal space. Emergency
valve replacement and long-term antibiotics are needed.

Mitral stenosis is caused by a history of rheumatic fever many years before presentation. It
produces dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, cough, and hemoptysis.
There is a low-pitched, rumbling diastolic apical heart murmur. As it progresses, patients become
thin and cachectic and develop atrial fibrillation. Workup starts with echocardiogram. As
symptoms become more disabling, mitral valve repair becomes necessary with a surgical
commissurotomy or mitral valve replacement.

Mitral regurgitation is most commonly caused by valvular prolapse. Patients develop exertional
dyspnea, orthopnea, and atrial fibrillation. There is an apical, high-pitched, holosystolic heart
murmur that radiates to the axilla and back. Workup and surgical indications are as above, with
repair of the valve (annuloplasty) preferred over prosthetic replacement.

Coronary disease can happen to anybody (including women), but the typical patient is as follows:
• Middle-age sedentary man • Has family history, smoking history, type II diabetes and/or
hypercholesterolemia

Progressive, unstable, disabling angina is the main reason to do cardiac catheterization and
evaluate as a potential candidate for revascularization. Intervention is indicated if ≥1 vessels have
≥70% stenosis and there is a good distal vessel. Preferably, the patient should still have good
ventricular function (you cannot resuscitate dead myocardium).

The general rule is that the simpler the problem, the more it is amenable to angioplasty and stent;
whereas more complex situations do better with surgery. • Single vessel disease (that is not the
left main or the anterior descending) is perfect for angioplasty and stent. • Triple vessel disease
makes multiple coronary bypass (using the internal mammary for the most important vessel) the
best choice.

Post-operative care of heart surgery patients often requires that cardiac output be optimized. If
cardiac output is considerably under normal (5 liters/min, or cardiac index 3), the pulmonary
wedge pressure (or left atrial pressure, or left end-diastolic pressure) should be measured. Low
numbers (0–3) suggest the need for more IV fluids. High numbers (≥20) suggest ventricular
failure.

Chronic constrictive pericarditis produces dyspnea on exertion, hepatomegaly, and ascites, and
shows a classic “square root sign” and equalization of pressures (right atrial, right ventricular
diastolic, pulmonary artery diastolic, pulmonary capillary wedge, and left ventricular diastolic)
on cardiac catheterization. Surgical therapy relieves it.

ACQUIRED HEART DISEASE

1. A 72-year-old man has a history of angina and exertional syncopal episodes. He has a harsh
midsystolic heart murmur best heard at the right second intercostal space and along the left
sternal border.

What is it? Aortic stenosis with the triad of angina, dyspnea, and syncope.

Management. Diagnose with echocardiogram. Surgical valvular replacement is indicated if there

is a gradient of >50 mm Hg, or at the first indication of CHF, angina, or syncope.

2. A 72-year-old man has been known for years to have a wide pulse pressure and a blowing,
high-pitched, diastolic heart murmur best heard at the right second intercostal space and along the
left lower sternal border with the patient in full expiration. He has had periodic echocardiograms,
and in the most recent one there is evidence of beginning left ventricular dilatation.

What is it? Chronic aortic insufficiency.

Management. Aortic valve replacement.

3. A 26-year-old drug-addicted man develops CHF over a short period of a few days. He has a
loud, diastolic murmur at the right, second intercostal space. A physical examination done a few
weeks ago, when he had attempted to enroll in a detoxification program, was completely normal.

What is it? Acute aortic insufficiency caused by endocarditis.

Management. Emergency valve replacement, and antibiotics for a long time.

4. A 35-year-old woman has dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea,

cough, and hemoptysis. She has had these progressive symptoms for about 5 years. She looks
thin and cachectic and has atrial fibrillation and a low-pitched, rumbling diastolic apical heart
murmur. At age 15 she had rheumatic fever.

What is it? Mitral stenosis.

Management. Start with echocardiogram. Eventually, consider surgical mitral valve repair.

5. A 55-year-old woman has been known for years to have mitral valve prolapse. She now has
developed exertional dyspnea, orthopnea, and atrial fibrillation. She has an apical, high-pitched,
holosystolic heart murmur which radiates to the axilla and back.

What is it? Mitral regurgitation.

Management. Start with the echocardiogram. Eventually, consider surgical repair of the valve
(annuloplasty) or valve replacement.

6. A 55-year-old man has progressive, unstable, disabling angina that does not respond to
medical management. His father and 2 older brothers died of heart attacks age <50. The patient
stopped smoking 20 years ago, but still has a sedentary lifestyle, is a bit overweight, has type 2
diabetes mellitus, and has high cholesterol.

What is it? It’s a heart attack waiting to happen: this man needs a cardiac catheterization to see
whether he is a suitable candidate for coronary revascularization.

7. A 55-year-old man has progressive, unstable, disabling angina that does not respond to
medical management. His father and 2 older brothers died of heart attacks age <50. The patient
stopped smoking 20 years ago, but still has a sedentary life style, is a bit overweight, has type 2
diabetes mellitus, and has high cholesterol. Cardiac catheterization demonstrates 70% occlusion
of 3 coronary arteries, with good distal vessels. His left ventricular ejection fraction is 55%.

Management. The patient is lucky. He has good distal vessels (smokers and diabetics often do
not) and enough cardiac function left. He clearly needs coronary bypass, and with triplevessel
disease he is not a good candidate for angioplasty.

8. A postoperative patient who underwent open heart surgery is determined to have a cardiac
index 1.7 L/min/m2 and left ventricular end-diastolic pressure 3 mm Hg.
The postoperative management of open heart surgery is too esoteric for the exam, but a bit of
applied physiology is not. You should be able to recognize a dangerously low cardiac index,
without a high end-diastolic pressure—a clear indication for increased fluid intake.

9. A 72-kg patient who had a triple coronary bypass is determined on postoperative day 2 to have
a cardiac output of 2.3 L/min. Pulmonary wedge pressure is 27 mm Hg. Cardiac output is low,
but the ventricle is failing.

Management. Cardiac output of 2.3L/min in a 72-kg patient is an indicator of heart failure. Given
the elevated pulmonary wedge pressure, hypovolemia is not the issue. In the post-CABG period,
myocardial dysfunction is common and inotropic support is indicated. Common pharmacological
agents for this scenario include epinephrine, norepinephrine, and dobutamine.