Complications of Prosthetic Heart Valves
Jeanne M. Vesey, MD and Catherine M. Otto, MD*
Address
*Division of Cardiology, Box 356422, University of Washington, Seattle,
WA 98195, USA.
E-mail: cmotto@u.washington.edu
Current Cardiology Reports 2004, 6:106–111
Current Science Inc. ISSN 1523-3782
Copyright © 2004 by Current Science Inc.
Treatment of native valvular heart disease has resulted in an
increasing number of patients with prosthetic valves.
Although an improvement over the diseased native valve
removed at surgery, prosthetic valves have suboptimal
hemodynamics; mechanical valves require anticoagulation
and tissue valves wear out over time. Serious complications
of prosthetic valves occur at a rate of about 2% to 3% per
patient-year. Complications include thromboembolism,
prosthesis-patient mismatch, structural valve dysfunction,
endocarditis, and hemolysis. Prosthetic valve endocarditis is a
lethal disease with mortality rates of 50% to 80% even with
appropriate therapy. Echocardiography now provides
detailed information on valve function and hemodynamics,
allowing early detection of complications. Many of these
complications can be prevented by choosing the optimal
valve at the time of surgery, rigorous control of anticoag-
ulation and adherence to established anticoagulation
guidelines, dental hygiene and endocarditis prophylaxis, and
periodic echocardiographic monitoring by a cardiologist.
Introduction
More than 60,000 heart valve replacement procedures are
performed in the United States each year. Even in the setting
of advances in surgery and valve design, replacement of a
diseased native valve with a prosthetic valve is not a panacea
for patients. Instead, native disease is traded for prosthetic
valve disease, with clinical outcome affected by valve hemo-
dynamics and durability, complications related to the valve
prosthesis, and chronic anticoagulation [1•]. Many of these
complications can be prevented, or their impact minimized,
with careful medical management and periodic monitoring
of valve function.
Prevention of Valve Complications
Anticoagulation
Warfarin therapy is recommended for all patients with
mechanical valves per the American College of Cardiology/
American Heart Association guideline as shown in Table 1.
Patients are higher risk of thromboembolic complications if
they have atrial fibrillation, a history of a previous thrombo-
embolic event, a hypercoagulable state, or left ventricular
(LV) systolic dysfunction, so these patients should be moni-
tored more carefully and anticoagulation maintained at a
higher level. The use of the international normalized ratio
(INR) allows anticoagulation to be maintained more consis-
tently in the target range, compared with the prothrombin
time, and is associated with a lower risk of thromboembolic
and bleeding complications. In addition, pharmacist-based
anticoagulation clinics have been shown to be more effect-
ive than physician-based approaches to management of
anticoagulation, with lower rates of complications at a lower
overall cost [2].
In patients with mechanical valves, if interruption of
anticoagulation for surgical procedures is necessary, the
approach depends on the valve type and position and coex-
isting risk factors. For example, in a patient with a bileaflet
aortic prosthesis in normal sinus rhythm and normal ven-
tricular function, warfarin can be stopped 72 hours before
the procedure and then restarted after the procedure. In
contrast, in high-risk patients (eg, a patient in atrial fibrilla-
tion with a history of a prior embolic event and a mechani-
cal mitral valve) intravenous heparin should be started
when the INR falls below 2.0, briefly interrupted for the
surgical procedure, and then continued postoperatively
until the INR is therapeutic. The use of low molecular
weight heparin for prosthetic valves is controversial, and
these agents are not approved for this indication by the US
Food and Drug Administration.
There is no ideal approach to management of anticoagu-
lation in pregnant women with mechanical valves [3••]. The
basic goals are to maintain effective anticoagulation through-
out pregnancy and avoid the fetal embryopathy associated
with warfarin. Unfortunately, no clear method to achieve
these goals has been defined. Some centers advocate the use
of warfarin throughout pregnancy, as this poses the least risk
to the mother. However, the 5% to 10% risk of fetal defects is
considered unacceptable by most mothers. Subcutaneous
heparin is associated with an increased risk of thromboembo-
lic events, probably due to inadequate anticoagulation. Some
centers now use a continuous intravenous pump for heparin
administration. There is agreement that warfarin should be
replaced by heparin before delivery. Given the complex issues
in these patients, all women with mechanical valves contem-
plating pregnancy should be referred to a high-risk obstetrics
center that has a close working relationship with cardiologists
experienced in the management of these patients.
 Complications of Prosthetic Heart Valves • Vesey and Otto 107

Table 1. Anticoagulation for prosthetic valves

Mechanical valves
AVR and no risk factor Long-term warfarin, INR 2.0–3.0
Bileaflet valves Long-term warfarin, INR 2.5–3.5
Tilting disc or ball-cage valves Long-term warfarin, INR 2.5–3.5
AVR + risk factor* Long-term warfarin, INR 2.5–3.5
MVR Long-term warfarin, INR 2.5–3.5
Biologic valves Warfarin for 3 months postoperatively, INR 2.0–3.0
Bioprosthesis with no risk factors Aspirin 80–100 mg/d
Aortic biologic valves with risk factor Long-term warfarin, INR 2.0–3.0
Mitral biologic valves with risk factor Long-term warfarin, INR 2.5–3.5
Embolic events while on anticoagulant therapy Increase INR to 2.5–3.5, if needed to 3.5–4.5; add aspirin 80–100 mg/d,
increase to 325 mg/d if needed
Therapy in patients requiring noncardiac surgery
Usual approach Stop warfarin 72 h before procedure; restart postprocedure after control
of active bleeding
High-risk patients† Stop warfarin 72 h before procedure; start heparin IV when INR falls below
2.0; stop heparin 6 h before procedure; restart heparin within 24 h of
procedure and continue until INR ≥ 2.0
*Risk factors: atrial fibrillation, left ventricular dysfunction, previous thromboembolism, hypercoagulable condition.
†High-risk patients are those with recent thromboembolism, Bjork-Shiley valve (Pfizer, New York, NY), AVR with three risk factors or MVR with one
risk factor (see above for risk factors).
AVR—aortic valve replacement; INR—international normalized ratio; IV—intravenous; MVR—mitral valve replacement.
(From Bonow et al. [14].)

Endocarditis prophylaxis
Patients with prosthetic valves are at high risk for endo-
carditis due to the foreign valve surface and sewing ring,
and the abnormal blood flow patterns across the valve. In
addition to using standard antibiotic prophylaxis for dental
and other procedures, patients should be instructed in the
importance of optimal dental hygiene and regular dental
care [4]. Patients also should be proactive in ensuring that
blood cultures are obtained for any febrile illness before
starting antibiotic therapy.
Echocardiographic monitoring
Echocardiographic evaluation of prosthetic valves requires
knowledge of the anticipated hemodynamics for the specific
valve size, type, and position [5,6•]. Expected velocities and
pressure gradients across a normally functioning prosthetic
valve are higher than across a normal native valve. Doppler
techniques for measurement of transvalvular pressure gradi-
ents and calculation of valve areas are similar to the methods
for native valves.
A small amount of valve regurgitation is typical with
mechanical valves. However, pathologic regurgitation can be
recognized and quantitated using standard echocardio-
graphic approaches, with the important caveat that shadow-
ing and reverberations limit the examination. Aortic valve
prosthesis often can be evaluated by transthoracic imaging.
However, when prosthetic mitral valve dysfunction is sus-
pected it is essential that both transthoracic and transesoph-
ageal examination be performed.
A small amount of spontaneous echocardiographic
contrast, due to microcavitation, often is seen with mechani-
cal valves and is not a marker for clinical events. These
microbubbles usually are seen downstream from the valve
(eg, in the LV for a mitral valve and in the aorta for an aortic
valve), and should not be confused with the left atrial spon-
taneous contrast associated with atrial fibrillation and
thrombus formation [7].
Patients with a prosthetic heart valve should be seen
annually by a cardiologist. A echocardiogram performed after
valve implantation provides a reference for future studies. The
optimal frequency of periodic echocardiography in an asymp-
tomatic patient is not well defined. Some clinicians request
annual echocardiograms, but examination every 3 to 5 years
is probably adequate, with an increase in the frequency of
examination for tissue valves starting 10 years after implanta-
tion. Any new cardiac symptoms or change in physical exami-
nation findings prompts repeat echocardiography.
Thromboembolic Complications
Prevalence and etiology
Thromboembolic complications are a major cause of mor-
bidity and mortality in patients with a prosthetic heart valve,
with an estimated clinical event rate between 0.6% and
2.3% per patient year (Table 2) [8–10]. The risk of systemic
embolism is similar for patients with mechanical valves on
warfarin therapy and bioprosthetic valves without warfarin
therapy. In addition, in patients on chronic anticoagulation
the annual risk of a hemorrhagic event is about 1% per
patient-year [8,9,11].
The risk of thromboembolic events in patients with pros-
thetic valves is related to the thrombogenicity of the valve
108 Valvular Heart Disease
Table 2. Complications of prosthetic valves
Thromboembolic complications
Systemic emboli
Valve thrombosis
Anticoagulation-related hemorrhage
Primary structural failure
Mechanical valves
Paravalvular regurgitation
Valve stenosis
Pannus ingrowth
Thrombosis
Tissue valves
Regurgitation
Tissue degeneration
Paravalvular
Calcific stenosis
Endocarditis
Vegetations
Paravalvular abscess and fistula formation
Embolic events
Hemolytic anemia
Pseudoaneurysm formation
Aortic root
Left ventricular
Mitral-aortic intervalvular fibrosa
materials, flow separation and stagnation, and shear stress
damage of blood elements and endothelium with platelet
activation and release of thrombogenic factors [12,13]. The
risk of thromboembolism is higher in patients with other risk
factors, such as atrial fibrillation and LV systolic dysfunction.
Clinical management
In patients with a prosthetic valve, ischemic neurologic events
must be presumed to be due to the valve unless another defi-
nite source is identified. Although valve thrombosis is rarely
identified on echocardiography, thrombus may not longer be
present on the valve (because it just embolized), the size of
the thrombus may be too small to be detected by ultrasound,
or it may be obscured by valve shadowing or reverberations.
The first step in management of a patients with a pros-
thetic valve and an embolic event is to carefully review the
adequacy of anticoagulation. If suboptimal, therapy is
adjusted or reinstituted to achieve and maintain a therapeutic
effect. If review indicates that anticoagulation has been ade-
quate, aspirin should be started, in addition to warfarin with a
higher target INR. Repeat valve replacement for thrombo-
embolic events is considered only if definite thrombosis on
the valve is documented and a less thrombogenic valve can be
used instead. In this circumstance, the risks of repeat valve
surgery should be carefully weighted in the clinical decision.
Valve thrombosis
In addition to embolic events, thrombosis of mechanical
valves can occur, resulting in functional stenosis or regurgi-
tation. Valve thrombosis may present as a chronic slowly
progressive event (eg, with a slowing enlarging pannus forma-
tion), or may have an acute onset (eg, with thrombosis of the
valve hinges leading to limitation of disk motion). Thrombo-
sis of left-sided heart valves is nearly always due to inadequate
anticoagulation therapy. Prompt echocardiography is essen-
tial when a diagnosis of valve thrombosis is suspected, with
transesophageal imaging needed for valves in the mitral posi-
tion, as thrombus most often involves the left atrial side of the
valve sewing ring.
The treatment of valve thrombosis remains controversial.
In a patient with stable hemodynamics, most clinicians rec-
ommend a conservative approach with intravenous anticoag-
ulation as the first step. When hemodynamic compromise is
present, the choice between thrombolytic therapy and surgi-
cal re-replacement of the valve remains problematic. The risk
of surgical intervention is high, with an operative mortality
of 17% to 40% [14]. Operative risk is highest in those with
coexisting LV systolic dysfunction, coronary artery disease,
emergency surgery, or a poor overall functional status. In a
series of 127 cases of prosthetic valve thrombosis treated
with thrombolytic therapy, hemodynamic improvement was
seen in 71%, with about one third requiring more than one
course of therapy [15,16]. However, the complication rate
was high, as seen in other series, with embolic events in 15%,
hemorrhagic complications in 5%, and a mortality rate of
12%. Despite the high complication rate, thrombolytic ther-
apy may be the preferred approach in patients at high risk of
surgery [17–20].
Patient-Prosthesis Mismatch
In some patients, the functional area of the prosthetic valve
is too small for the cardiac demands in that patient, a phe-
nomenon called patient-prosthesis mismatch [21,22]. The
current definition of severe patient-prosthesis mismatch is
an indexed valve area less than or equal to 0.65 cm2/m2
with an indexed valve area between 0.65 and 0.85 cm2/m2,
indicating moderate mismatch. In patients with severe aor-
tic patient-prosthesis mismatch, the risk of early postoper-
ative mortality is more than 10 times higher than in those
with an adequate functional valve area [23••].
Patient-prosthesis mismatch can be avoided by compar-
ing published data on the expected effective orifice area with
the patient’s body size and choosing a valve type that will pro-
vide an adequate valve area. If a small aortic root allows
implantation of only a small-sized mechanical or biopros-
thetic valve, aortic root enlarging procedures should be con-
sidered. Clinically, patients with an inadequate prosthetic
valve area have persistent symptoms postoperatively and have
persistent LV hypertrophy [22].
Structural Failure
Mechanical prosthetic valves are very durable, and primary
structural failure is rare with current valves. Instead, structural
failure of mechanical valves usually is related to the interface
between the valve ring and the native cardiac tissue, or to
 Complications of Prosthetic Heart Valves • Vesey and Otto
thrombus formation interfering with normal valve motion.
Paravalvular regurgitation typically is due to infection, dehis-
cence of some of the sutures attaching the sewing ring to the
annulus, or to fibrosis and calcification of the native annulus
leading to inadequate contact between the sewing ring and
annulus. Less commonly, mechanical valve dysfunction is
related to thrombus or tissue overgrowth (eg, pannus) at the
annulus blocking normal opening or closing of the valve disk
resulting either in stenosis or regurgitation.
Structural failure of tissue valves is predictable with calcifi-
cation and spontaneous tissue degeneration of the valve leaf-
lets occurring 10 to 20 years after implantation, depending on
the specific type of valve implanted. With conventional
stented tissue valve, the overall incidence of bioprosthesis
failure is 20% to 30% at 10 years [24] and over 50% at 15
years. The use of stentless aortic valve prosthesis, bovine peri-
cardial valves, and anticalcification treatments integral to
newer tissue valves are expected to be more durable than
older conventional stented tissue valves [25–28]. In addition,
the likelihood of primary tissue failure decreases with age, so
that tissue valves are now the valve of choice patients over 70
years of age and are often appropriate in younger patients as
well [29••,30].
Prosthetic valve stenosis
Stenosis of bioprosthetic valves is due to progressive valve
calcification, with a variable time from valve implantation to
calcification depending of the specific valve type and on
patient characteristics. An increased rate of tissue valve calci-
fication is seen with younger age, pregnancy, mitral valve
position, chronic renal failure, and hypercalcemia. Mech-
anical valve stenosis is less common but can occur due to
thrombus or pannus ingrowth restricting disk motion.
Patients with prosthetic valve stenosis have symptoms,
physical examination, and echocardiographic findings
similar to native valve stenosis, with the exception that
prosthetic valve clicks are present with mechanical valves
[31•]. If echocardiography is nondiagnostic, fluoroscopy
may be helpful for defining the extent of disk motion.
Reoperation for prosthetic stenosis is indicated in patients
with symptoms or hemodynamic compromise due to the
prosthetic valve stenosis.
Prosthetic valve regurgitation
A small degree of prosthetic valve regurgitation is normal with
characteristic patterns of regurgitation for each valve type
[32,33]. Pathologic mechanical prosthetic valve regurgitation
most often is paravalvular. Regurgitation of tissue valves may
either be paravalvular or may be related to leaflet calcification
and degeneration. Specifically, tissue valves are prone to rup-
ture of thin areas adjacent to a calcific nodule and in the set-
ting of endocarditis.
The clinical presentation and diagnosis of prosthetic valve
regurgitation is similar to native valve regurgitation. With
slow hemodynamic progression, patients may be asymptom-
atic with regurgitation first noted on physical examination or
109
echocardiography. With acute valve rupture or endocarditis,
the presentation is that of acute aortic or mitral regurgitation.
With small paravalvular leaks, hemolytic anemia may be the
presenting symptom. Evaluation of the presence and severity
of prosthetic regurgitation is possible with transthoracic and
transesophageal echocardiography in nearly all patients.
Occasionally, angiography is needed when echocardiography
is nondiagnostic or when there is a discrepancy between clini-
cal and echocardiographic findings.
Indications for surgery for prosthetic regurgitation are
similar to the indications for native valve regurgitation.
Clearly, surgery is appropriate for symptomatic severe pros-
thetic regurgitation. With asymptomatic prosthetic regurgi-
tation, measurements of LV size and systolic function, and
evidence of pulmonary hypertension are important con-
siderations, as per American College of Cardiology/Ameri-
can Heart Association guidelines for native valve disease
[14]. Patients with asymptomatic moderate or severe pros-
thetic regurgitation should be followed carefully with
echocardiography at no less than annual intervals.
Infective Endocarditis
Prosthetic valve endocarditis accounts for about 15% of all
endocarditis cases, with a risk of prosthetic valve endocarditis
of 0.5% per year, even with appropriate antibiotic prophy-
laxis [11,24,34,35]. Early prosthetic valve endocarditis, occur-
ring within 2 months of valve implantation, most often is
due to Staphylococcus epidermidis, gram-negative bacteria, or
fungi. Late prosthetic valve endocarditis has a bacteriologic
spectrum similar to that seen in native valve endocarditis.
Prosthetic valve endocarditis often involves the sewing ring
with paravalvular abscesses formation, paravalvular regurgi-
tation, and intracardiac fistula formation. Prosthetic valve
endocarditis is a lethal disease, even with aggressive therapy,
with mortality rates as high as 80% for early and 30% to 50%
for late prosthetic valve endocarditis [36].
Accurate diagnosis of prosthetic valve endocarditis
depends on transesophageal as well as transthoracic echo-
cardiographic imaging. With mechanical valve prostheses it
is rare to visualize vegetations on the disks themselves. A
paravalvular abscess is recognized as an echo-lucent or
echo-dense, irregularly shaped area adjacent to the valve
sewing ring.
Although prompt and prolonged antibiotic treatment is
appropriate, most patients with prosthetic valve endocarditis
require surgical intervention. Surgery as early as possible in
the disease course is recommended, because delay is associ-
ated with more tissue destruction, hemodynamic decompen-
sation, and systemic embolic events.
Hemolytic Anemia
In 50% to 95% of patients with mechanical valves, there is
some evidence of intravascular hemolysis. However, anemia
due to hemolysis is rare unless there is prosthetic regurgita-
110 Valvular Heart Disease
tion [37,38]. Hemolysis may occur with either central or
paravalvular regurgitation due to rapid acceleration and
deceleration or high-peak shear rates [39], and has even been
reported after mitral valve repair [40].
Most patients with mild anemia can be treated conserva-
tively with iron and folate replacement therapy. However,
repeat valve surgery or surgical repair of a paravalvular leak
may be needed when prosthetic valve hemolysis is associated
with severe refractory anemia, significant paravalvular regurgi-
tation, or high-output failure.
Other Complications
When a homograft or valved conduit is used in the aortic
position, complications include stenosis at the distal anasto-
mosis or distorted anatomy and the site of coronary reim-
plantation, resulting in myocardial ischemia [41]. With older
surgical techniques that retained the native aorta, dehiscence
at the proximal or distal suture line or at a coronary reimplan-
tation site can lead aortic pseudoaneurysm formation. An
aortic pseudoaneurysm may be diagnosed on transthoracic or
transesophageal echocardiography, but often is better evalu-
ated by wide-angle magnetic resonance or computed tomog-
raphy imaging, with three-dimensional reconstruction of the
pseudoaneurysm. This complication is less common with
current surgical approaches.
Mitral valve replacement is complicated by LV pseudoa-
neurysm formation in up to 0.5% to 2.0% of cases. Typi-
cally, the pseudoaneurysm arises at the site of the posterior
annular suture line, and consists of a disruption in the
integrity of the basal LV wall with escape of blood outside
the heart contained by pericardial adhesions. The wall of a
pseudoaneurysm contains no myocardial cells, unlike a
true aneurysm. A LV pseudoaneurysm can be diagnosed by
echocardiography, with definitive features including a
thin-walled chamber that communicates with the LV via a
narrow neck, with a ratio of the diameter of the neck to the
maximum aneurysm diameter less than 0.5, and an abrupt
transition from a normal myocardial wall to the opening
into the aneurysm [5]. LV pseudoaneurysms require surgi-
cal repair, as these structures are prone to further rupture,
which often is catastrophic in nature.
Another rare complication after mitral valve replace-
ment is a pseudoaneurysm of the mitral aortic intervalvu-
lar fibrosa. The small area of normal fibrous tissue between
the posterior aortic root and base of the anterior mitral
leaflet becomes dilated, creating a blind pouch that lies
between the aorta and left atrium, which communicates
with the LV. Most pseudoaneurysms of the mitral-aortic
intervalvular fibrosa are secondary to infection and they
are most common with prosthetic valves [42]. Rupture of
the pseudoaneurysm can lead to aortic or mitral regurgita-
tion, or rupture into the pericardial space.
Conclusions
Although life-saving, replacement of a diseased native valve
with a prosthetic valve often leaves the patient with persistent
symptoms and a risk of serious complications due to the valve
or associated anticoagulation. Serious complications in
patients with prosthetic valves include thromboembolism,
prosthesis-patient mismatch, structural valve dysfunction,
endocarditis, and hemolysis, with an average annual compli-
cation rate of approximately 2% to 4%. The key elements in
prevention of valve dysfunction are effective anticoagulation,
prevention of endocarditis, and periodic echocardiography,
along with patient education. When serious complications
occur, echocardiographic evaluation allows accurate and pre-
cise evaluation of prosthetic valve dysfunction and hemody-
namics. Prompt recognition of complications allows early
treatment, often with repeat surgical intervention.
References and Recommended Reading
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major importance
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