CARDIOVASCULAR DISEASE IN THE ELDERLY
OO
David A. Hinchman, MD, and Catherine M. Otto, MD
The relative prevalence of calcific degenera-
tive valvular disease in patients undergoing
surgical intervention has increased dramati-
cally over the past several decades, in part
because of longer lifespans and prevention of
rheumatic fever.3oAlso, surgical intervention
is increasingly used in management of valvu-
lar disease in the elderly (Table l).z,114Recog-
nition of valvular disease in elderly patients is
hampered by the overlap in symptom profiles
between those with and without valvular dis-
ease and by the nonspecific physical examina-
tion findings in many elderly patients. Symp-
toms of chest pain, shortness of breath,
exercise intolerance, and dizziness are com-
mon and have many other potential causes
so that valve disease often is not considered
in the differential diagnosis. Similarly, since
systolic murmurs are so frequent in the el-
derly, the patient with severe aortic stenosis,
but a soft murmur, may be missed.
Although it is recognized that surgical in-
Table 1. CLINICAL FACTORS ASSOCIATED WITH
AORTIC SCLEROSIS
Demographic: Age
Male gender
Clinical History: Smoking
Physical Examination: Height
Hypertension
Laboratory Data: LDL cholesterol
LPk)
Diabetes
From the Department of Medicine, Division of Cardiology, University of Washington, Seattle, Washington
CARDIOLOGY CLINICS
-
VOLUME 17 * NUMBER 1 FEBRUARY 1999
0733-8651/99 $8.00 + .
VALVULAR DISEASE
IN THE ELDERLY
tervention can be performed with an accept-
able operative mortality and morbidity in se-
lected elderly patients, the importance of
considering comorbid conditions and func-
tional status in surgical decision making in
the elderly cannot be overemphasi~ed.~~. 'I4
Normal aging changes can substantially im-
pact the ability of the elderly to tolerate car-
diovascular surgery, so benefits of surgery
with regard to symptom relief and improved
survival must be balanced against the surgi-
cal risk, keeping in mind that surgical mor-
bidity (e.g., cerebrovascular events) may be
of even more concern than surgical mortality
rates (Fig. 1). Clearly, the elderly patient
should be fully informed and involved at ev-
ery stage of the decision-making process. Al-
though there is increasing data to make evi-
dence-based decisions on the elderly patient
with valvular disease, there are still many
areas of uncertainty. Thus, patient manage-
ment remains a complex task requiring a
highly individualized approach.
CALClFlC AORTIC VALVE DISEASE
Prevalence
Calcific or degenerative aortic valve disease
(Fig. 2) is the most common valvular lesion
encountered among elderly patient^,^^ with
up to 90% of all aortic valve replacements
137
138 HINCHMAN & OTTO

Figure 1. Annual number of octogenarians (bars) having cardiac operations and the annual hospital
mortality rate (circles) in a series of 600 consecutive patients over 80 years. (From Akins CW, Daggett
WM, Vlahakes GJ, et al: Cardiac operations in patients 80 years old and older. Ann Thorac Surg
64:606, 1997; with permission.)

in patients over age 75 being performed for Etiology and Pathology

calcific aortic s t e n o s i ~ . ~ ~Other
, causes of
aortic stenosis in the elderly include rheu-
matic aortic valve disease (always occurs in
conjunction with rnitral valve involvement)
and late degeneration of a congenitally bicus-
pid va1~e.I~.9H
Aortic sclerosis, defined as thickening and
calcification of the aortic valve without sig-
nificant obstruction to ventricular outflow, is
increasingly recognized because of the wide-
spread use of echocardiography. The preva-

Figure 2. Doppler aortic velocity in an elderly patient with aortic

stenosis showing a maximum velocity of 4.8 m/s (arrow) and a
mean gradient of 57 mm Hg. AS-Jet = aortic stenosis jet.

lence of aortic sclerosis increases with age
being present in approximately 25% of people
>aged 65 years and older and 48% of those
aged 75 years and It is clear on
pathologic studies that aortic sclerosis and
stenosis represent extremes of the same dis-
ease process, with hemodynamically signifi-
cant aortic stenosis present in 2% to 9% of
those over age 65.75,118
Although the factors that lead one elderly
patient to have severe stenosis requiring
valve replacement and another patient to
have only minimal sclerotic changes have not
been defined, there is increasing evidence that
several clinical factors are associated with the
presence of a calcific aortic valve disease. The
clinical factors associated with aortic sclero-
sis/ stenosis include age, male gender, height,
hypertension, smoking, serum LDL and Lp(a)
levels, and diabetes (see Table l).9, 34, 47, 53, 118
Histopathologic studies also support the
concept that calcific aortic valve disease rep-
resents an active disease process and is not
simply an inevitable consequence of aging. It
is likely that endothelial injury from mechani-
cal and shear stress on the aortic side of the
valve leaflets10s,lZ0 initiates an active, inflam-
matory process similar, but not identical, to
atherosclerosis. Histologic examination re-
veals subendothelial lesions with displace-
ment of the elastic lamina, lipid infiltration,
inflammatory cell accumulation and micro-
scopic mineralization (Fig. 3). Lipid deposi-
tion is present early in the development of
aortic sclerosis with demonstration of apoli-
poproteins B, (a), and E consistent with the
presence of oxidized LDL in early lesions.84
Additionally, foam cells are present with evi-
dence of macrophage activation including
production of proteins, such as osteopontin,
that modulate tissue cal~ification.~~, 91 All of
these changes are distinct from the normal
aging changes of the valve that include a
diffuse increase in leaflet thickness, an in-
creased number of adipose cells on the ven-
tricular side of the leaflet and increased prom-
inence of the nodules of Arantius.
Symptoms
Aortic stenosis in adults is characterized
clinically by a long asymptomatic period as
obstruction to left ventricular outflow devel-
ops gradually over many years.*13The aver-
age age at symptom onset for patients with
degenerative calcification of a trileaflet valve
VALVULAR DISEASE IN THE ELDERLY 139
is 70 to 80-years. In contrast, patients with
secondary calcification of a congenitally bi-
cuspid aortic valve typically present at age 50
to 60-~ears,'~* 98 whereas patients with rheu-
matic aortic stenosis become symptomatic
over a wider age range, with patients pres-
enting between 20 and 50-years of age. Al-
though the classic symptoms of aortic steno-
sis are angina, heart failure, and syncope, the
most common initial symptom in the elderly
is impaired exercise tolerance.90Other typical
early symptoms are exertional dyspnea or
dizziness.
Heart failure symptoms in patients with
aortic stenosis occasionally are due to systolic
ventricular dysfunction, especially if there is
associated coronary artery disease. More of-
ten, systolic function is normal. Heart failure
symptoms may be caused by an elevated left
ventricular end-diastolic pressure in associa-
tion with ventricular hypertrophy and dia-
stolic dysfunction. Alternatively, exercise in-
tolerance may be caused by the inability to
increase cardiac output across the stenotic
valve with exercise.
Exertional chest pain can result from an
increase in oxygen demand by the hypertro-
phied myocardium and abnormal patterns of
coronary blood flow in aortic stenosis, even
in the absence of significant coronary dis-
ease.48, lZ3 Coexisting coronary disease is
common with significant coronary narrowing
present in about 50% of adults with aortic
. ~ ~ as the absence of chest pain
s t e n o s i ~Just
does not exclude the presence of associated
coronary artery disease, the presence of an-
gina pectoris in patients with aortic stenosis
may be caused by subendocardial ischemia
associated with the hemodynamic effects of
aortic stenosis alone, without associated sig-
nificant coronary artery disease.
Several mechanisms have been postulated
to explain the third classic symptom of aortic
stenosis syncope or lightheadedness. Al-
though ventricular arrhythmias and left ven-
tricular systolic dysfunction have been pro-
posed, there is more evidence that an acute
drop in blood pressure is caused by an inap-
propriate LV baroreceptor response in the
presence of a fixed cardiac output.6',lo3 Sud-
den cardiac death has not been reported in
previously asymptomatic adults with aortic
s t e n o ~ i s .64,~yo~ ,
Aortic stenosis is frequently underdiag-
nosed in the elderly. The increase in hemody-
namic severity occurs slowly so many pa-
tients fail to recognize early symptoms or
140 HINCHMAN & OTTO

Figure 3. Potential roles of lipoproteins in the pathogenesis of aortic valvular lesions.

Endothelial injury allows insudation of circulating lipoproteins into the subendothelial
space. Sequestered in a microenvironment where actively metabolizing cells (i.e., resident
fibroblasts and endothelial cells) consume antioxidants, these lipoproteins become mini-
mally oxidized and possibly stimulate leukocyte adhesion. After more extensive oxidative
modification, lipoproteins could be recognized and endocytosed by macrophage scaven-
ger receptors, resulting in foam cell formation. Studies showing that HLA antigens and
interleukin-2 receptors are present in lesions suggest the possibility of induction of
cytokine and growth factor release by macrophages and fibroblasts. Lipid accumulation
in macrophages leads to expression of apoE. The cytokines released by macrophages
and fibroblasts stimulate fibroblast production of proteoglycans. LDL and apoE then may
be trapped by proteoglycans and Lp(a) by both proteoglycans and fibrinogen, leading to
lipoprotein accumulation and repetition of the cycle of events described above. Several
factors in this cascade of events, including lipoproteins, release of calcification-mediating
molecules such as osteopontin by inflammatory cells and possibly by fibroblasts, and
participation of proteoglycans in matrix vesicle formation could facilitate calcium deposi-
tion. Those features whose presence is inferred but not proved are indicated with question
marks. (From O'Brien KD, Reichenbach DD, Marcovina SM, et al: Apolipoproteins B, (a),
and E accumulate in the morphologically early lesion of degenerative valvular aortic
stenosis. Arterioscler Thromb Vasc Biol 16:523, 1996; with permission.)

simply attribute them to getting older. Pa-
tients presenting with more severe symptoms
of syncope, angina, or frank heart failure usu-
ally have had antecedent symptoms but may
have not sought medical attention. Less fre-
quently, a previously asymptomatic patient
may present with acute pulmonary edema
in the setting of an acute infectious process,
anemia, or other hemodynamic stress.
Physical Examination
The diagnosis of aortic stenosis is often
made by the auscultation of a murmur in an
asymptomatic patient. The typical murmur of
aortic stenosis is a harsh, crescendo-decre-
scendo systolic murmur that is loudest at the
base, over the right second intercostal space,
with radiation to the carotid arteries. In el-
derly patients, however, the murmur may ra-
diate to the apex instead of the carotids.
Whereas a loud murmur (grade 4) denotes
severe stenosis, most elderly patients with se-
vere valvular obstruction have only a grade 2
or grade 3 murmur and some have an even
softer murmur despite severe disease.78,y2
Clinical diagnosis is further complicated by
the high frequency of systolic murmurs in the
elderly with about one-third of all elderly
patients admitted to the hospital having a
basal systolic murmur, even though most do

not have severe aortic s t e n o s i ~ .Thus,
~ ~ the
clinical sensitivity and specificity of a systolic
murmur for detection of severe aortic stenosis
in the elderly is low.
Other key features in the physical examina-
tion of patients with suspected aortic stenosis
are the carotid pulse contour and amplitude,
timing of the murmur, splitting of the second
heart sound, and signs of heart failure. As the
severity of valvular obstruction progresses,
the murmur peaks later in systole. Most pa-
tients with aortic stenosis have some compo-
nent of coexisting aortic regurgitation, how-
ever, that also affects the timing of the
murmur peak intensity, limiting the sensitiv-
ity of a late peaking murmur for detection
of severe aortic stenosis. A clearly split S2
indicates that severe obstruction is unlikely
because as leaflet motion becomes impaired
by calcification, the leaflets no longer snap
shut, resulting in a single S2 caused by an
inaudible aortic c o m p ~ n e n t . ~ ~
As aortic stenosis becomes severe, the ca-
rotid pulse amplitude is decreased (pulsus
parvus) and occurs later in systole (pulsus
tardus). It is important to realize, however,
that pulse amplitude and timing may appear
to be normal even when severe stenosis is
present if there is coexisting atherosclerosis.
This occurs because the stiff vessels lead to a
rapid and excessive rise in aortic pressure. A
slow rising, low amplitude carotid pulse has
a relatively high specificity, but low sensitiv-
ity, for severe aortic stenosis in the elderlyy*
When the diagnosis of aortic stenosis is
suspected, further evaluation is warranted if
symptoms are present or if the diagnosis
would change clinical management, for ex-
ample in the preoperative evaluation of a pa-
tient undergoing noncardiac surgery. Aortic
stenosis cannot be reliably excluded by physi-
cal examination unless there is no systolic
murmur, the second heart sound is normally
split, and the carotid upstroke is normal.
Diagnostic Approach
Although electrocardiography and chest ra-
diography have traditionally been used to
evaluate patients with aortic stenosis, the di-
agnostic accuracy of these approaches is low.
Electrocardiographic evidence of left ventric-
ular hypertrophy is seen in only 50% of adults
with severe aortic stenosis.yoEvidence for
ventricular hypertrophy, conversely, may be
present in the absence of significant stenosis
VALVULAR DISEASE IN THE ELDERLY 141
owing to coexisting hypertension. On chest
radiography, valve calcification seen on the
lateral projection is specific, but not sensitive
for the diagnosis of valvular aortic stenosis.
Valve calcification, however, is seen on fluo-
roscopy in a high percentage of elderly adults
with valvular aortic stenosis.
Echocardiography
Doppler echocardiography is a cost-effec-
tive and accurate strategy for diagnosing aor-
tic stenosis in the elderly.x9Imaging reveals
cusp thickening and calcification, and Doppler
evaluation allows accurate determination of
the severity of valvular obstruction (Table 2).
Table 2. USE OF ECHOCARDIOGRAPHY IN
ASSESSMENT OF VALVULAR DISEASE
(TTE AND TEE)
Valve anatomy and etiology of disease
Evaluation of stenosis severity
Aortic stenosis
Jet velocity
Maximum and mean transaortic gradient
Continuity equation valve area
Mitral stenosis
Mean transmitral gradient
Two-dimensional valve area
Pressure half-time valve area
Prosthetic valves
Jet velocity
Mean gradient
Valve area
Evaluation of regurgitant severity
Color Doppler flow imaging (0 to 4 + scale)
Continuous wave Doppler velocity curve
Flow reversals (pulmonary veins for MR, descending
aorta for AR)
Quantitation of regurgitant volume, fraction and
orifice area in selected cases
Prosthetic valve regurgitation*
Left ventricle and atrium
Left atrial enlargement
Left atrial thrombus*
Left ventricular end-diastolic and end-systolic
dimensions and volumes
Left ventricular ejection fraction
Left ventricular dP/dt (from MR jet)
Right heart
Pulmonary artery systolic pressure estimate
Right ventricular size and systolic function
Tricuspid regurgitation
Right atrial size
Endocarditis
Detection of valvular vegetations‘
Evaluation of the extent of valve dysfunction
Evaluation of complications (abscess, fistula)*
“Transesophageal imaging usually necessary for accurate diag-
nosis
MR = mitral regurgitation; AR = aortic regurgitation; dP/dt
= rate of rise in pressure over time.
142 HINCHMAN & OTTO
The most clinically useful measures of aortic
stenosis by echocardiography are maximum
aortic jet velocity and continuity equation
valve area. The advantages of aortic valve jet
velocity are that a direct Doppler measure-
ment involves no calculations, has a low in-
terobserver variability and is predictive of
clinical outcome.y0
Jet velocity, however, has two major limita-
tions as a descriptor of disease severity. First,
the search for the highest aortic valve velocity
at multiple acoustic windows must be per-
formed meticulously by a trained and experi-
enced sonographer because stenosis severity
can be seriously underestimated if Doppler
signals are recorded from a nonparallel inter-
cept angle.'3 Second, jet velocities (and pres-
sure gradients) are flow dependent so that a
low velocity may be seen with severe stenosis
if cardiac output is depressed because of co-
existing mitral regurgitation or left ventricu-
lar systolic dysfunction. This limitation can
be avoided by calculation of valve area using
the Doppler continuity equation.86, 95, 130
Echocardiographic examination also allows
evaluation of left ventricular size, global and
regional systolic function, the presence and
extent of coexisting aortic regurgitation, eval-
uation of associated mitral valve disease, and
estimation of pulmonary artery pressures.
Exercise Testing
Although exercise stress testing has been
performed in asymptomatic patients with sig-
nificant aortic stenosis in an effort to further
define the relationship between hemody-
namic severity and clinical symptoms, exer-
cise testing is not routinely needed in the
clinical setting.23,y7 Certainly, in the patient
with clear symptoms, exercise testing is un-
necessary and may be risky. In most patients,
exercise testing adds little if any prognostic
value to a clinical evaluation and resting
echocardiographic examination.'" On the
other hand, in the patient with equivocal
symptoms or when symptoms are denied but
suspected, exercise testing may provide both
the patient and physician convincing evi-
dence of symptom onset.2hWhen needed, ex-
ercise testing should be performed with cau-
tion, with close supervision and prompt
termination of the test for any decline in
blood pressure, excessive ST-segment depres-
sion, or the onset of an arrhythmia.
Cardiac Catheterization
Cardiac catheterization rarely is needed for
evaluation of stenosis severity given the accu-
racy of echocardiographic data. When echo-
cardiographic data are nondiagnostic or when
there are discrepancies between the clinical
evaluation and echocardiographic data, how-
ever, measurement of transaortic pressure
gradient and calculation of valve area at cath-
eterization can be very helpf~l.'~,46 The value
of fluoroscopic examination for valve calcifi-
cation also should not be overlooked.
All elderly patients with symptomatic se-
vere aortic stenosis undergoing surgical inter-
vention require coronary angiography preop-
eratively because surgical outcome is
improved if concurrent coronary artery by-
pass grafting is performed. Many elderly pa-
tients also require coronary angiography ear-
lier in the disease course because anginal
symptoms with only mild or moderate aortic
stenosis are likely because of coexisting coro-
nary disease.
Disease Progression
Asymptomatic Patients
Adults with asymptomatic aortic stenosis
have an excellent clinical outcome, indistin-
guishable from age-matched controls without
aortic valve disease. There have been few re-
ports of sudden death in the absence of prior
symptoms in adults with asymptomatic aortic
stenosis, none in more recent series.55,64, ' O , 12*
Recent data on the likelihood of symptom
onset based on baseline jet velocity is quite
useful in patient education and in planning
the frequency of clinical follow up. In the
patient with a jet velocity greater than 4.0 m/
s, symptoms occur at a rate of 40% per year
compared to 17% per year for a jet between
3.0 and 4.0 m/s and only 8% per year if jet
velocity is less than 3.0 m/s (Fig. 4).90
In addition to baseline jet velocity, the only
other multivariate predictors of clinical out-
come, defined as death or aortic valve re-
placement, were the annual rate of change
in aortic jet velocity and baseline functional
status. This last observation deserves particu-
lar emphasis because even though these sub-
jects had no overt cardiac symptoms, func-
tional status (an easily determined parameter)
was such a strong predictor of outcomeyo
In patients with asymptomatic aortic steno-
sis, there is considerable individual variability
 VALVULAR DISEASE IN THE ELDERLY 143

:........ L-- 1 Vmax <3.0 m/s

...#

.-.-.L--------------------------
-m .. .. .-.
. ..,
.-> ...-.
.,.
2 -,
3.0-4.0 m/s
a 6,
b-.,
v)
Q,
b,
& ...
......
b
?2
L
.4 .
b...
.-.
>
&
C
Q,
..-.
.-,
w
.2

1
>4.0 m/s

1
00 I*
12 24 36 48 60

Time from Enrollment (months)

Figure 4. Cox regression analysis showing event-free survival in groups defined by aortic jet
velocity at entry (P<O.OOOl by log-rank test) in a prospective series of 123 adults (mean age
6 3 f 1 6 years with asymptomatic valvular aortic stenosis. (From Otto CM, Burwash IG, Legget
ME, et al: Prospective study of asymptomatic valvular aortic stenosis: Clinical, echocardiographic
and exercise predictors of outcome. Circulation 95:2262, 1997; with permission.)

in the rate of hemodynamic progression of
aortic valve obstruction (Table 3). The average
rate of increase in jet velocity is about 0.2 to
0.4 m/s per year, the average increase in the
mean aortic valvular gradient is 6 to 8 mm
Hg per year and the average decrease in
valve area is 0.1 cm2 per year.21,3y, yo, 94, loo, *05
Predictors of the rate of hemodynamic pro-
gression in individual patients have not been
defined.
Symptomatic Patients
Once symptoms occur, mortality in adults
with valvular aortic stenosis is extremely high
in the absence of valve replacement with sur-
vival rates less than 50% at 2 years.", h4, 85, 122
Interestingly, despite the marked difference in
clinical outcome between symptomatic and
asymptomatic patients, there is broad overlap
in the jet velocities, mean gradients, and valve
areas.55,yo, y6, 122 This observation suggests that
instead of a set numerical value that applies
to all patients, severe aortic stenosis is best
defined as the point at which the metabolic
demands of the patient cannot be met in the
face of a narrowed aortic valve. Although to
some extent the degree of valve narrowing
that causes symptoms is related to body size,

Table 3. HEMODYNAMIC PROGRESSION OF AORTIC STENOSIS AS ASSESSED BY ECHOCARDIOGRAPHY

(SELECTED SERIES)
Mean Increase
Follow-up in Mean Increase in Decrease
Type of Interval AP VlSlaX in AVA
Series Study n MeanAge(y) (YO (mmHg/yr) (m/s per yr) (cm*/yr)

Otto 1989y4 Prospective 42 66 2 66 1.7 7 . 9 t 7.1 0.36 2 0.31 0.1 (0-0.5)

Roger 1990Iu5 Retrospective 112 69 f 11 2.1 0.23 2 0.37
Faggiano 199Py Prospective 45 72 5 10 1.5 0.4 i.0.3 - 0.1 2 0.13
(-0.7-0.1)
Peter 19931"0 Retrospective 49 Range 16-81 2.7 7.2
Brener 19952L Retrospective 394 65 t 12 3.1 6.3 0.14
Otto 199790 Prospective 123 63 5 16 2.5 757 0.32 t0.34 0.12t 0.19

AP = pressure gradient; V,, = maximum aortic jet velocity; AVA = aortic valve replacement
144 HINCHMAN & OTTO
other factors, such as activity levels, also play
a role. Thus, a small 85-year-old woman with
aortic stenosis may not be symptomatic until
the valve area is less than 0.5 cm2.In contrast,
an active 65-year-old man may recognize
symptoms with a valve area in the 1.0 to 1.2
cm2 range. Jet velocity avoids some of the
limitation of valve area in that transaortic
velocity is, in effect, already indexed to heart
size. In addition, differences in clinical out-
come often are related to coexisting coronary
artery disease, the presence and severity of
mitral regurgitation, and comorbid noncar-
diac diseases.
Treatment
Because symptom onset is insidious and
often not appreciated by the patient, patient
education is key in the management of el-
derly patients with aortic stenosis. The health
care provider should carefully and routinely
question the patient at each visit to elicit
symptoms, specifically asking the patient to
compare current activity levels to those at a
set time in the past. In addition, the patient
should be educated about the expected dis-
ease course, the probable need for valve sur-
gery at some point in the future, and the
importance of seeking medical attention im-
mediately at symptom onset.
Medical Therapy
Symptomatic patients with aortic stenosis
should undergo surgical intervention. In the
asymptomatic patient, medical therapy
should focus on patient education, periodic
echocardiographic follow-up, endocarditis
prophylaxis, and careful management of pre-
load and afterload when noncardiac surgical
procedures are needed. In the symptomatic
patient who refuses or is not a candidate for
surgical intervention, medical management of
heart failure symptoms is difficult. Diuretics
should be used with caution because a low
preload may exacerbate symptoms due to low
cardiac output. Although afterload reduction
theoretically is desirable, if the stenotic valve
serves as a fixed resistance, peripheral vasodi-
lation may lead to systemic hypotension
without a compensatory increase in cardiac
output. Despite these concerns, standard ap-
proaches to heart failure management may
be attempted in these patients with careful
clinical monitoring. Although medical ther-
apy is unlikely to prolong survival, it may
provide limited symptomatic relief. Although
infective endocarditis is rare, mortality is
high, so antibiotic prophylaxis is indicated for
dental and other procedures per the AHA
recommendation^.^^
Patients with asymptomatic aortic stenosis
undergoing noncardiac surgery are at higher
risk; however, many of these patients can be
managed without aortic valve replacement if
there is a careful preoperative evaluation plus
invasive hemodynamic monitoring with opti-
mization of loading conditions in the periop-
erative period.lZ1
At this time, there is no known therapy to
prevent or slow disease progression in adults
with aortic sclerosis or stenosis. The recent
demonstration of associated clinical factors
and an increased understanding of the histo-
pathology of this disease suggest, however,
that intervention may be possible in the fu-
ture.
Alternatives to Valve Replacement
When mechanical relief of aortic stenosis is
needed, there are no acceptable alternatives
to valve replacement in the elderly. Percuta-
neous balloon valvuloplasty seemed promis-
ing when initially introduced, however, sev-
eral large series have demonstrated that
mortality for elderly adults undergoing bal-
loon aortic valvuloplasty is no different from
untreated aortic stenosis, with 1-year actuar-
ial mortality rates of 35% to 50'/0.'~,76, 91
Valve-sparing treatments, such as ultra-
sonic debridement of the valve have been
abandoned because of the development of
moderate or severe aortic regurgitation in
most Since little normal tissue re-
mains after ultrasonic debridement of a de-
generative aortic valve, no valve-sparing
technique holds significant promise.
Surgical Intervention
Indications. Symptom onset remains a
clear indicator for surgical intervention in el-
derly adults with aortic stenosis, regardless
of patient age. The benefit of surgery is so
great, that only an extremely high surgical
mortality caused by comorbid medical condi-
tions is a contraindication to surgical inter-
vention.
In addition, aortic valve replacement in the
asymptomatic patient with a jet velocity over
4.0 m/s who is undergoing coronary artery
bypass surgery should be strongly consid-
ered, given the high likelihood of progression
 VALVULAR DISEASE IN THE ELDERLY 145

Table 4. OPERATIVE RISK OF AORTIC VALVE REPLACEMENT IN THE ELDERLY (SELECTED STUDIES)
30 daylOp Neurologic
Series Age Procedure n Mort MI Events
Craver 19WX Age 270 yrs AVR 188 10.1% 1.6% 5.3%
AVR + CABG 130 12.3% 7.7% 10.8%
Fremes 198943 Age 270 yrs AVR 110 2.7%
AVR + CABG 150 8.0%
Age (70 yrs AVR 566 4.9%
AVR + CABG 212 3.3%
Azariades 1991'3 Age 280 yrs AVR i- / - CABG 88 16%
Olsson 199288 Age 280 yrs AVR + / - CABG 44 14% 7% 9%
Age 65-75 yrs AVR i- / - CABG 83 4% 5% 3%
Elayda 199338 Age 280 yrs AVR 77 5.2% 11.1%
AVR + CABG 75 24%
Logeais 1994" Age 275 yrs AVR + / - CABG 154 9%
Gehlot 1996@ Age 280 yrs AVR + / - CABG 322 13.7%
Asima kopoulos 1997" Age 280 yrs AVR i- / - CABG 1100 6.6%
Shapira 1997'14 Age >75yrs AVR + / - CABG 105 4.8% 0.7% 4.8%

MI = myocardial infarction; AVR = aortic valve replacement; CABG = coronary artery bypass grafting

to symptoms in the next 2 years. Management
of patients with intermediate degrees (jet ve-
locity 3.0 to 4.0 m/s) of aortic stenosis under-
going coronary surgery is less clear.90
Although surgical intervention in the
asymptomatic patient with severe aortic ste-
nosis has been proposed to prevent progres-
sive left ventricular hypertrophy with conse-
quent diastolic dysfunction, there is little data
to support the potential benefit of this ap-
proach. Most clinicians continue to follow
asymptomatic patients closely, regardless of
stenosis severity, delaying surgical interven-
tion until symptoms supervene. It is im-
portant, however, that even mild symptoms,
such as decreased exercise tolerance, lead to
prompt valve replacement.
Surgical Mortality and Morbidity in the
Elderly. Current surgical mortality rates in
elderly patients undergoing aortic valve re-
placement range from 4% to 24% (Table 4).3,
11. 13. 28, 38. 43. 44. 77. 88, 114 Recent improvements in
mortality rates likely reflect advances in anes-
thetic management, surgical and periopera-
tive care techniques, and in patient selection.
Risk factors for operative mortality include
functional class, lack of sinus rhythm, preop-
erative left ventricular systolic dysfunction,
aortic regurgitation, concomitant surgical pro-
cedures, previous bypass surgery, emergency
surgery, coronary artery disease, female gen-
der, concurrent mitral valve surgery, hyper-
tension, and LV systolic dy~function.~, 28, 38, 77
Although operative mortality is acceptable
in comparison to the high mortality without
surgical intervention, both the physician and
patient need to be aware of high postopera-
tive complication rates in the elderly.38Car-
diac arrhythmias, prolonged ventilatory sup-
port requirements and congestive heart
failure are common, perioperative myocardial
infarction is seen in 3 to 8%, and cerebrovas-
cular events are reported in as many as 11%
of patients.3, 13, 28,38. 77
Concomitant Bypass Surgery. Aortic valve
stenosis and coronary atherosclerosis fre-
quently coexist and about 50% of patients
undergoing valve replacement also undergo
coronary revascularization. The higher opera-
tive mortality of combined valve replacement
and bypass surgery (8% to 25% versus 4% to
5%) most likely reflects the increased risk of
the disease combination since weaning from
cardiopulmonary bypass is problematic if sig-
nificant coronary ischemia is pre~ent.~, 38, 43,
77, 114 Remarkably, female gender is an inde-
pendent risk factor for mortality after com-
bined coronary artery bypass-aortic valve re-
placement? 43, 79 possibly because of smaller
coronary arteries or a late referral pattern in
women.
The addition of mitral valve surgery to aor-
tic valve replacement increases operative
mortality rates to the 15% to 25% range in
patients over 80 years.3s Although it may
seem prudent to avoid combination valve
procedures, these poor outcomes likely reflect
a high-risk subgroup at baseline.
Surgical outcomes are optimized when at-
tention is given to patient preparation, such
as respiratory training, early mobilization,
early removal of indwelling tubes and cathe-
ters, management of arrhythmias, avoidance
of nephrotoxic drugs, and maintaining good
nutritional status.38
Long-Term Outcome After Valve Replace-
146 HINCHMAN & OTTO

o AVR + Concomitant procedures P <0.01

0 '
30 Days 1 2 3 4 5

Year

Figure 5. Plot of actuarial survival by operative procedure in 171 consecutive patients aged 80-91
years undergoing aortic valve surgery. AVR indicates aortic valve replacement. Solid circle =
Isolated AVR; open circle = AVR plus concomitant procedures. (From Elayda MA, Hall RJ, Reul
RM, et al: Aortic valve replacement in patients 80 years and older: Operative risks and long-term
results. Circulation 88(2):11, 1993; with permission.)

ment. Long-term survival after valve replace-
ment for aortic stenosis is excellent with 1-,
3- and 5-year survival rates of 91%, 84% and
76%, in patients over age 80 (Fig. 5).,, The
use of age-adjusted life tables to compare the
survival of age-matched patients without aortic
stenosis can be useful in predicting survival
after successful aortic valve replacement.
Postoperatively, left ventricular systolic
performance improves (even if in the normal
range preoperatively), and hypertrophy re-
gresses owing to the favorable effects on
afterload. Clinical and histologic evidence for
diastolic dysfunction, however, persists for
up to 8 years postoperatively.hyIn the absence
of coexisting left ventricular dysfunction or
uncorrected coronary artery disease, nearly
all patients have resolution of symptoms and
an improvement in functional class with most
elderly patients being able to live at home
and function inde~endently.~~. 88, 114
Choice of Valve Prosthesis
There are several choices of valve substi-
and risks of bleeding versus thromboembo-
lism.
A recent c o m p a ~ i s o nof~ bioprosthetic
~ and
mechanical valves in a series of elderly pa-
tients found that the rates of early and late
mortality, thromboembolic events, endocardi-
tis, and hemorrhage were no different for the
two valve types. Reoperation, however, was
required in four (2%) patients, all of whom
had bioprosthetic valves, and there were no
structural failures with the mechanical valves.
The risk of hemorrhage with anticoagulation
for the mechanical valves was also low (98.4%
t 0.02% free from hemorrhage at 5 years),
leading the investigators to conclude that me-
chanical prostheses are reasonable and un-
derused in the elderly.
Bioprosthesis. Although the major disad-
vantage of a bioprosthetic valve is limited
durability, several studies suggest there is an
inverse relationship between age and biopros-
thetic valve failure and that outcomes with
bioprosthetic valves are excellent, making
these valves an appropriate choice in many
elderly patients.27, *14 It should be noted,
5y7

tutes in the elderly with the major decision
being whether to implant a mechanical or
bioprosthetic valve.
Mechanical. Mechanical aortic valve re-
placements offer acceptable hemodynamics
and excellent long-term durability, factors
that should not be underestimated given the
increasing longevity of our patients. On the
other hand, chronic warfarin anticoagulation
is needed, with the attendant inconvenience
however, that the hemodynamics of small
stented bioprosthetic valves are suboptimal
so that some patients (particularly women)
will have functional stenosis due to a small
prosthesis after surgical intervention. Because
root enlarging procedures significantly in-
crease operative mortality, alternate valve
types should be considered in patients with a
small aortic root. Newer stentless biopros-
thetic valves offer better hemodynamics and

improved durability compared to conven-
tional valves.126The use of this type of valve
prosthesis may increase as we gain further
experience with optimal surgical implanta-
tion and long-term outcome.
Homograft valves offer few advantages in
the elderly and are rarely used. A pulmonic
autograft (Ross procedure) is not feasible be-
cause of the discrepancy in size between the
aorta and pulmonary artery, aging changes of
the tissues, and the increased operative time
for this approach.
MITRAL ANNULAR CALCIFICATION
Pathology
Mitral annular calcification (Fig. 6) is a de-
generative calcific process, possibly similar to
that of aortic sclerosis and s t e n o ~ i s .Calcific,
'~~
crescent-shaped deposits in the posterior por-
tion of the mitral valve annulus can be seen
in about half of elderly patients by echocardi-
ography4 and with significantly less sensitiv-
ity by chest radiography or fluoro~copy.~ In
echocardiographic series, the prevalence has
been reported to be roughly 20% at age 62 to
70 years, 33% at 71 to 80,62% at 81 to 90, and
approaches 100% by age 101 to 103.6
Figure 6. Apical 4-chamber echocardiographic image showing typi-
cal mild mitral annular calcification (arrow). LA = left atrium; LV =
left ventricle; RV = right ventricle; RA = right atrium.
VALVULAR DISEASE IN THE ELDERLY 147
Associated Cardiac Events
Some degree of mitral regurgitation is seen
in about half of elderly patients with mitral
annular calcification and is moderate or se-
vere in about 20% to 339'0.~' The calcification
process occasionally encroaches on the annu-
lar orifice or affects the base of the valve
leaflets, resulting in some degree of mitral
stenosis in 6% to 8% of patients. The process
has been associated with left atrial enlarge-
ment and atrial fibrillation, conduction de-
fects, and the need for permanent pacemaker
implantation.80, Mitral annular calcification
has been found to be associated with a higher
incidence of thromboembolic strokes and car-
diovascular events including myocardial in-
farction and sudden cardiac death, although
whether the process is causal or merely asso-
ciated with other precursors of these events
is less clear.5,6. 16. 81, 106
MITRAL REGURGITATION
Prevalence and Etiology
Some degree of mitral regurgitation is pres-
ent in many elderly patients but typically is
mild in severity. In most elderly patients, mi-
tral regurgitation is an incidental finding that
is unlikely to ever require surgical interven-
148 HINCHMAN & OTTO

Figure 7. Predominant pathologic findings in 50 consecutive patients

270-years-old undergoing surgery for mitral regurgitation. (From Azar H,
Szentpetery S: Mitral valve repair in patients over the age of 70 years.
Eur J Cardiothorac Surg 8:29,1994; with permission.)

tion. The exceptions are those elderly patients
with severe myxomatous mitral valve disease
in whom valve repair or replacement is likely
and patients with ischemic mitral regurgita-
tion for which surgery might include an
annuloplasty ring and coronary bypass graft-
ing (Fig. 7).
Mitral regurgitation in the elderly can re-
sult from several pathologic processes and
often is the result of a complex interaction of
several factors in a given patient. Competency
of the mitral valve requires normal anatomic
relationships and function of the entire mitral
valve apparatus including the annulus,
leaflets, chordal apparatus, papillary muscles,
and left ventricular wall. Abnormalities of
any one or a combination of these compo-
nents can result in mitral regurgitation. For
example, mitral annular calcification is a com-
mon cause of mild to moderate mitral regur-
gitation caused by loss of the normal systolic
contraction of the annulus. Another example
is dilated cardiomyopathy for which associ-
ated mitral regurgitation is common owing to
distortion of the normal relationship between
the papillary muscles and mitral annulus.
Ischemic heart disease causes mitral regur-
gitation in the elderly by several different
mechanisms, including papillary muscle rup-
ture with acute myocardial infarction, left
ventricular dilation and systolic dysfunction
with chronic ischemic disease, and intermit-
tent mitral regurgitation during ischemic epi-
sodes due to regional myocardial dysfunc-
tion.68, 102
Although primary abnormalities of the mi-
tral leaflets and chordae due to rheumatic
disease or endocarditis are uncommon in the
elderly, chordal rupture may be seen either
as an isolated finding or in association with
myxomatous mitral valve disease (Fig. 8).
Myxomatous mitral valve disease, or mitral
valve prolapse, is the most common cause
of significant mitral regurgitation requiring
valve replacement or repair in the elderly.
Typically, the elderly male patient has the
characteristic findings of mitral leaflet thick-
ening and redundancy with prolapse of one
or both leaflets into the left atrium in systole
in association with significant mitral regurgi-
With
t a t i ~ n .Io1~ ~ , increasing age, the incidence
of ruptured chordae increases.3s,127
Diagnosis
On physical examination, mitral regurgita-
tion is appreciated as a holosystolic murmur
that is loudest at the apex and radiates to the
axilla. A loud murmur (grade 4 or greater)
denotes severe regurgitation; however, regur-
gitant severity varies widely in those with
a softer (grade 2 or 3 ) murmur. When left
ventricular dilation is present, the apical im-
pulse is enlarged and laterally displaced but

Figure 8. Transesophageal echocardiographic image showing se-
vere prolapse of the posterior leaflet (PL) with a small ruptured
chord (arrow). LA = left atrium; LV = left ventricle.
typically is normal earlier in the disease
course.
The murmur of mitral regurgitation can be
distinguished from aortic stenosis by changes
in the loudness of the murmur with changes
in preload or afterload. Both a decrease in
preload (squat to stand maneuver) or an in-
crease in afterload (handgrip) typically aug-
ment the murmur of mitral regurgitation. In
contrast, an aortic stenosis murmur dimin-
ishes with an increase in afterload.
The optimal approach to evaluation of the
patient with suspected mitral regurgitation is
echocardiography. Two-dimensional Doppler
and color flow imaging allow delineation of
the etiology of and severity of regurgitation
and assessment of left ventricular systolic
function, left atrial dilation, and pulmonary
pressures.
Medical Therapy
Medical management of mitral regurgita-
tion in the elderly focuses on endocarditis
prophylaxis, periodic echocardiographic eval-
uation, patient education, and symptomatic
relief of pulmonary congestion with diuretics.
Afterload reduction may be beneficial in pa-
VALVULAR DISEASE IN THE ELDERLY 149
tients with coexisting left ventricular systolic
dysfunction, but there is no convincing evi-
dence that afterload reduction affects the nat-
ural history of the disease.25,73
Acute mitral regurgitation due to papillary
muscle rupture, chordal rupture, or endocar-
ditis often requires stabilization with intrave-
nous afterload reduction therapy (nitroprus-
side) or with an intra-aortic balloon pump
before consideration of surgical intervention.
Surgical Intervention
lndications
Symptoms due to severe mitral regurgita-
tion clearly are an indication for surgical in-
tervention. In patients with asymptomatic mi-
tral regurgitation, surgical intervention also
may be considered to prevent occult deterio-
ration of left ventricular systolic function. In
younger adults criteria for surgical interven-
tion based on measures of left ventricular
size, ejection performance, and parameters of
end-systolic wall stress have been well de-
fined.37
Indications for surgical intervention in the
elderly patient with mitral regurgitation are
150 HINCHMAN & OTTO

Table 5. OPERATIVE RISK OF MITRAL VALVE SURGERY IN THE ELDERLY

Etiology of Mean Age
AuthorlYear MR n (years) Hospital Mortality Long-term Survival

Fremes 1989” Mixed 81 270 yrs MVR only 8.6%

56 270 yrs MVR + CABG 19.6%
Jebara 1 9 9 P Myxomatous 79 >70 3.8% 81% at 5 yrs
David 1993” Myxomatous 184 57 4% 94% at 8yrs
Kay 1986”’ Ischemic 101 62?8 -10% EF >40% 5 8 k 12Y0 at 10 yrs
EF 2140% 33 +- 10% at 10 yrs
EF <20% 16 2 14% at 10 yrs
Hendren 19915’ Ischemic 65 66210 9.1% Restrictive motion 48% at 3 yrs
Prolapse 96% at 3 yrs
Azar 199412 Mixed 50 Age 270 yrs 6%
Lee 1996’’ Mixed 190 Age 270 yrs 3.7%
424 Age <70 yrs 3.5%
Asimakopoulos 1997” Mixed 86 Age 280 yrs 10.4% 80% at 1 year
64% at 3 years
41% at 5 years
Shapira 1997ll4 1 / 3 Ischemic 30 Age >75 yrs 16.6%

less clear. First, surgical mortality rates are
relatively high overall ranging from 3% to
17% in recent series.31. 32.43,51,60,63,71,114 Second
surgical risk and indications are largely de-
pendent on the cause of mitral regurgitation
(Table 5). For example, valve surgery is un-
likely to be beneficial in the elderly patient
with mitral regurgitation secondary to a di-
lated and hypokinetic left ventricle. Instead,
medical therapy should be directed at im-
proving ventricular loading conditions and
treating heart failure symptoms.
Similarly, in the patient with ischemic mi-
tral regurgitation, surgical intervention is di-
rected toward relief of myocardial ischemia
rather than toward the mitral valve. It re-
mains controversial whether revasculariza-
tion alone or revascularization plus a mitral
annuloplasty ring is needed in elderly pa-
tients with ischemic mitral reg~rgitati0n.l~ In
the absence of a controlled clinical trial on
this issue, decision making should be individ-
ualized in each patient in consultation with
the surgical team. Of note, surgical interven-
tion for a ruptured papillary muscle has a
mortality rate of about 50%, a factor that may
influence the decision to proceed with aggres-
sive therapy in the elderly patient with this
mechanical complication of acute myocardial
infarction.22* 4y, h6, Even elective surgery for
chronic mitral regurgitation and coronary ar-
tery bypass grafting carries an operative mor-
tality rate as high as 20% to 50% in the el-
derly.33,3% 42
The approach to elderly patients with myx-
omatous valve disease has changed with the
improvement of valve repair procedures. A
major disadvantage of mitral valve replace-
ment is that left ventricular ejection fraction
typically falls 5 to 10 ejection fraction units
after surgery, a decline that may be particu-
larly problematic in the elderly. With mitral
valve repair, preservation of the continuity
between the mitral annulus and papillary
muscles allows preservation of left ventricu-
lar geometry and usually prevents the ex-
pected decline in ventricular function. In the
elderly patient with a reparable valve and
symptoms due to mitral regurgitation, surgi-
cal intervention should be considered.’O Be-
cause our ability to predict valve reparability
is not perfect, the patient needs to be aware
that the surgeon will make the final decision
of repair versus replacement at the time of
surgery.
Surgical Approach
Mitral valve repair is the procedure of
choice whenever possible in the elderly pa-
tient with mitral regurgitation. In two recent
series of septuagenarians undergoing mitral
valve repair, 30-day mortality was as low as
4% to 6% with over 75% alive at 2 years
follow-up.lZ,6o In patients with chronic ische-
mic mitral regurgitation, an annuloplasty ring
alone may be sufficient for relief of mitral
regurgitation. With papillary muscle rupture,
reattachment and use of chordal substitutes
may allow valve preservation. In patients
with myxomatous mitral valve disease, the
most common procedure is quadrilateral re-
section of a section of the posterior leaflet
with placement of an annuloplasty ring.
Other techniques include anterior leaflet re-
pairs, chordal shortening or replacement, and
transfer of a segment of one leaflet to the
 VALVULAR DISEASE IN THE ELDERLY 151

other. Typically, intraoperative transesopha- previous valvuloplasty) is seen rarely in el-

geal echocardiography is performed before
and after the repair procedure to evaluate
for residual mitral regurgitati~n.~~ If excessive
regurgitation persists, the surgeon may elect
to proceed with valve replacement during the
same operation.
If valve repair is not feasible, the choices of
valve substitutes for the mitral position are
limited to mechanical valves and conven-
tional stented porcine valves. Although ho-
mograft mitral valve replacements have been
performed at a few centers, elderly patients
are poor candidates for this procedure. Be-
cause many patients requiring mitral valve
replacement need long-term anticoagulation
for chronic atrial fibrillation, a more durable
mechanical valve should be considered even
in the elderly. In patients with contraindica-
tions to anticoagulation or a shortened life
expectancy for other reasons, a porcine valve
may be a reasonable choice. When valve re-
placement is performed, most surgeons now
will preserve all or part of the mitral appara-
tus to maintain the beneficial effects of mitral
annular-papillary continuity on left ventricu-
lar function.
MITRAL STENOSIS
Rheumatic mitral stenosis typically pres-
ents in young and middle age, so untreated
mitral stenosis (or recurrent obstruction after
derly patients.87Occasionally, severe mitral
annular calcification will involve the leaflets
with some degree of obstruction to
Elderly patients with mitral stenosis most
commonly present with symptoms of conges-
tive heart failure. The typical diastolic rum-
ble, opening snap, and loud first heart tone
of rheumatic mitral stenosis are heard in
fewer than 50% of elderly patients with this
lesion.5oOften only a systolic murmur of aor-
tic sclerosis or stenosis, or no murmur at all,
is heard. The most frequent electrocardio-
graphic finding is atrial fibrillation.
Medical therapy in elderly patients with
mitral stenosis includes diuretics to alleviate
pulmonary congestion symptoms, rate con-
trol of atrial fibrillation, and chronic anticoag-
ulation to prevent left atrial thrombi and em-
bolic events. Endocarditis prophylaxis is
recommended even though endocarditis is
relatively uncommon with isolated mitral ste-
nosis because most patients also have coexist-
ing mitral regurgitation.
Older patients with mitral stenosis often
have additional medical problems that put
them at higher risk for cardiac surgery with
an overall mortality risk of patients over age
70 with mitral valve replacement for mitral
stenosis of about 15%.43,58 Percutaneous mitral
commissurotomy carries significantly higher
risks in the elderly, although the technique
has produced palliative benefit in this popula-
tion at an acceptable risk when surgery is not
an option (Fig. 9).,,, *I5

0 1 2 3 4

Years

Figure 9. Actuarial results after percutaneous mitral commissurotomy (PMC) in 75 patients

270-years-old. (Actuarial survival curves with 95% confidence interval.) The numbers at the
bottom of the table indicate the number of surviving patients who did not undergo surgery and
in NYHA class I or 11, at the corresponding time after PMC. Solid line = survival (cardiac
deaths); uneven dashed line = survival (all deaths); dashed line = not operated on; dotted
line = good functional results. (From lung 8,Cormier B, Farah B, et al: Percutaneous mitral
commissurotomy in the elderly. Eur Heart J 16:1092, 1995; with permission.)
152 HINCHMAN & OTTO
If surgery is needed, surgical commissurot-
omy may be possible if there is no significant
calcification of valve cusps and no major con-
comitant mitral regurgitation. If relief of the
hemodynamic obstruction cannot be achieved
with commissurotomy, however, mitral valve
replacement should be considered.
AORTIC REGURGITATION
Aortic regurgitation is seen in 20% to 29%
of people over age 65 with the cause most
often being aortic valve sclerosis or aortic root
dilation due to hypertension or atherosclero-
sis. The severity of aortic regurgitation in the
elderly is nearly always and surgical
intervention is rarely needed for aortic regur-
gitation in the elderly.
In younger patients with severe aortic re-
gurgitation, afterload reduction with nifedi-
pine has been shown to prevent progressive
left ventricular dilation and systolic dysfunc-
tion and reduce the need for surgical inter-
vention.”O Not only do few elderly adults
have severe enough regurgitation to warrant
medical therapy, but outcomes from these
studies in younger patients may not be gener-
alizable to the elderly, who have been re-
ported to have poor tolerance of this agent
when used for other indication^.^^, 99 Afterload
reduction with angiotensin-converting en-
Figure 10. Transesophageal echocardiographic image showing an
aortic dissection flap (arrow) in association with a murmur of aortic
regurgitation. LA = left atrium; LV = left ventricle; Ao = aorta
zyme inhibitors may be a reasonable alterna-
tive if medical therapy is needed.74
Most patients with aortic regurgitation are
asymptomatic for a prolonged period (if not
for life), especially if the regurgitant severity
is mild. Some patients, however, develop left
ventricular systolic dysfunction in the ab-
sence of symptoms. Although the earliest
signs of ventricular dysfunction are contro-
versial, there is growing acceptance that in
younger adults a left ventricular end-diastolic
dimension of greater than 55 mm or a left
ventricular systolic ejection fraction less than
55% suggests impending deterioration so that
aortic valve replacement is warranted.2o,25, 37* 52
It is unclear, however, whether the potential
benefit of surgical intervention can be justi-
fied in asymptomatic elderly patients.
In the elderly, management of aortic regur-
gitation typically includes endocarditis pro-
phylaxis, consideration of afterload reduction
therapy if regurgitation is moderate or severe,
and careful evaluation of the cause of regurgi-
tation. In a patient with chest pain, a new
finding of aortic regurgitation on auscultation
or echocardiography should prompt consid-
eration of aortic dissection in the differential
diagnosis (Fig. 10).
RIGHT-SIDED VALVULAR DISEASE
A minimal degree of both tricuspid and
pulmonic regurgitation can be detected by

Doppler echocardiology in a majority of
adults with an increasing prevalence of mild
(or physiologic) regurgitation with age. He-
modynamically significant right-sided regur-
gitant lesions, however, are rare in the el-
derly.' In a series of octogenarians, tricuspid
regurgitation was present in 24%, but was
significant in only 6%.129Right-sided valvular
disease is usually secondary to pulmonary
hypertension from left heart failure or lung
disease. The new onset of elevated pulmo-
nary pressures, decreased right ventricular
function or tricuspid regurgitation on echo-
cardiography raises the possibility of in-
tercurrent pulmonary emboli.
INFECTIVE ENDOCARDITIS
Several decades ago, only 5% to 20% of
patients with infective endocarditis were
older than 60 years, but the number of elderly
patients with infective endocarditis has been
increa~ing,5~,'~~ with the mean age of patients
with endocarditis now being about 55 to 60
years. This increase has been attributed to the
aging of the population and the increasing
number of elderly patients with prosthetic
valves.
The diagnosis of infective endocarditis is
difficult in the elderly because the symptoms
of fatigue, weight loss, and a murmur are
often attributed to old age. The more insidi-
ous clinical course may contribute to the more
severe prognosis in the elderly because the
diagnosis often is not considered until after
irreversible complications have occurred. The
recently proposed Duke riter ria,'^ however,
(Table 6) have greatly increased our ability to
accurately diagnose endocarditis by including
echocardiographic findings in the clinical de-
cision-making process, and these criteria are
applicable to the elderly.Il2 Even with trans-
thoracic echocardiography, diagnosis may be
problematic if calcified valves and comorbid
conditions such as obesity and obstructive
lung disease limit image quality.109Further,
elderly patients more often have small vege-
tations or prosthetic valve infection. Trans-
esophageal echocardiography offers im-
proved image quality and should be strongly
considered when endocarditis is sus-
pected.109, 112, 125
The causative organisms are usually Stuph-
ylococcus uureus, group D streptococci, and
enterococcus, and they more frequently arise
from a gastrointestinal or genitourinary
source.112 A lower incidence of embolic events
VALVULAR DISEASE IN THE ELDERLY 153
Table 6. SIMPLIFIED SUMMARY* OF THE DUKE
CRITERIA FOR THE CLINICAL DIAGNOSIS OF
DEFINITE INFECTIVE ENDOCARDITIS
Clinical Diagnosis
2 major criteria or
1 major and 3 minor criteria or
5 minor critria
Major Criteria
Positive blood culture for infective endocarditis
Typical microorganism for infective endocarditis
from two separate blood cultures
Persistently positive blood cultures
Evidence of endocardia1 involvement
Positive echocardiogram for infective endocarditis
OR
New valvular regurgitation
Minor Criteria
Predisposition: predisposing heart condition or
intravenous drug use
Fever: 238.0"C
Vascular phenomena
Immunologic phenomena
Microbiologic evidence: positive blood culture but not
meeting major criterion or serologic evidence of
active infection with organism consistent with
infective endocarditis
Echocardiogram: consistent with infective
endocarditis but not meeting major criterion as
noted previously
From Durack DT, Lukes AS, Bright DK: New criteria for diag-
nosis of infective endocarditis utilization of specific echocardio-
graphic findings. The Duke Endocarditis Series. Am J Med 96200,
1994; with permission.
in patients over age 70 has been observed in
several ~tudies'"~,112, and may be due to the
fact that vegetations develop less frequently
with S. uureus, group D streptococci, and en-
terococcus."h
Currently, surgical intervention is used less
frequently in the elderly, and mortality rates
are higher compared to younger patients
(28% versus 13%)."*Despite higher operative
risk, earlier surgical intervention should be
considered in elderly adults with endocardi-
tis. Indications for surgery include evidence
of persistent infection (fevers, blood cultures,
abscess on echocardiography), significant val-
vular regurgitation (even if responsive to
medical therapy), the presence of a prosthetic
valve, and embolic events. Other relative in-
dications that should be considered include
infection with S. aureus or fungus, a large (>1
cm) vegetation, and conduction abnormali-
ties. When endocarditis is present, trans-
esophageal echocardiography should be con-
sidered for early detection of complication. In
a series of elderly adults with a higher rate of
surgical intervention (65%), hospital survival
has been comparable to younger patients
(25%).lZ5
154 HINCHMAN & OTTO

10yn 12 vrr 15 yrr 17 yrr '

A 535 5 7 6 2 5 9 33726 1 1 1 3 2 5 2
0 2660 6 4 2 ~ 3 95 0 2 2 4 3 2 5 7 2 4 7 166252
C 51 64 7 9 0 ~ 2 26 6 7 2 2 8 45 6 r 4 0 28 9 2 6 2
D 6569 8 4 8 r 3 3 77 724 1 6 0 2 2 7 5 MI2275
E L70s 972-16 923232 62 8 2 12 9
64
D C O 05 C.D.E>A.B D.E>C E>D
J

101 A 535 78 39
204 6 36-50 166 100
508 C 51-64 408 262 185 59

OL
0
195
202
1 2
D 65-69 152
E 270

3
146
4 5 6
1

7
1

8
8 - 195
208
76
208
17
9

9 10 11 12 13 14 15 16 17 18
I
4
'

Year

Figure 11. Freedom from structural deterioration of Carpentier-Edwards porcine bioprostheses, stra-
tified by age group, for all valve positions. (From Jamison WRE: Ann Thorac Surg 60:999-1007,
1995; with permission.)

Of course, the most effective therapy for tients with prior valve surgery survive into
endocarditis in the elderly is prevention by older age groups, clinicians are faced with an
the use of antibiotic prophylaxis per Ameri- increasing number of patients with prosthetic
can Heart Association g ~ i d e l i n e sMany
. ~ ~ el- valves. Unfortunately, although valve replace-
derly patients with a murmur undergo diag- ment prolongs life and relieves symptoms,
nostic and surgical procedures associated the patient with a prosthetic valve still has an
with transient bacteremia. Endocarditis pro- abnormal valve in terms of hemodynamics
phylaxis should be considered whenever a and the risk of endocarditis.128 Many patients
murmur is present. If needed, preprocedure require long-term anticoagulation with the at-
echocardiography allows further definition of tendant risks of hemorrhage and thromboem-
the type and severity of valve disease. bolic events. In addition, valves are subject to
degeneration or malfunction so that repeat
PROSTHETIC VALVES interventions may be needed in the future.
Management of the patient with a pros-
As more elderly patients undergo surgical thetic valve should include periodic echocar-
intervention and as more middle-aged pa- diographic evaluation. A baseline study 3 to
6 months postoperatively should be per-
formed in all patients to serve as a reference
Table 7. RECOMMENDATIONS FOR for future studies and to evaluate the degree
ANTICOAGULATION FOR PROSTHETIC VALVES
of regression of left ventricular dilation and
Anticoagulation hypertrophy and pulmonary hypertension.
Valve Type Regimen After 10 years, tissue valves should be evalu-
Mechanical unlues ated annually as the risk of degenerative
Bileaflet valves Long-term warfarin, INR changes and the potential for valve stenosis
2.5-3.5 or regurgitation increase^.^" Endocarditis pro-
Tilting disk valves Long-term warfarin, INR
3.04.0 phylaxis is essential as the mortality of pros-
Ball-cage valves Long-term warfarin, INR thetic valve endocarditis is substantial (Fig. 11).
4.04.9 Patients on chronic warfarin anticoagula-
Mechanical valve with Add aspirin 100 mg/d tion are optimally followed-up by a pharma-
systemic emboli OR
despite anticoagulation Add dipyridamole 400 mg/d
cist-directed anticoagulation clinic using the
Biologic unlves Warfarin for 3 months post- INR (rather than the traditional PT measure-
OP, INR 2.0-3.0 ment) as the risk of both hemorrhage and
Biologic valves with atrial Long-term warfarin, INR thromboembolism is decreased with this ap-
fibrillation or history of 2.0-3.0 proach compared to physician management
systemic embolization
of antic~agulation.~~ Guidelines for optimal

INR levels with different types of prosthetic
valves are summarized in Table 7.117,124 When
patients with mechanical valves need noncar-
diac surgical procedures, most clinicians
switch to intravenous heparin in the preoper-
ative and postoperative period to minimize the
time period of subtherapeutic anticoagulation.
When valve dysfunction is suspected, the
initial diagnostic procedure is transthoracic
echocardiography. If images are suboptimal
or if prosthetic mitral regurgitation is sus-
pected, however, transesophageal imaging is
needed for accurate diagnosis.82The indica-
tions for reoperation for prosthetic valve ste-
nosis are similar to those for native valve
stenosis, specifically the onset of new symp-
toms due to valvular obstruction. The excep-
tion is acute valve thrombosis, which may
require emergency surgical intervention.
Prosthetic regurgitation is increasingly rec-
ognized as our diagnostic imaging modalities
have improved. Management again is similar
to that of native valve regurgitation with the
indications for repeat surgical intervention in-
cluding evidence of progressive left ventricu-
lar dilation and systolic dysfunction, increas-
ing pulmonary pressures or significant
symptoms. Hemolytic anemia due to a para-
valvular leak often can be managed medically
but does require surgical intervention when
refractory to conservative management. A
paraprosthetic leak diagnosed soon after sur-
gery may be related to scarring or calcifica-
tion in the annulus leading to suture disrup-
tion. When a new paravalvular leak is
diagnosed late after surgery, the possibility of
infective endocarditis should be considered.
SUMMARY
As the incidence of valvular disease in the
elderly is increasing, understanding of its
pathogenesis and natural progression as well
as surgical approaches and device technolog-
ies are improving. Future studies are needed
to develop medical interventions that slow
or halt the degenerative valvular processes
associated with aging. In addition, mechani-
cal approaches with lower operative risks
should be explored and the search should
continue for a valve substitute that is durable,
hemodynamically efficient, easy to implant,
and does not require anticoagulation. Hope-
fully, future intervention trials will include
quality of life assessments such as symptoms,
functional capacity and perceptions of well
being.
At present, the degenerative valvular pro-
cesses must be followed closely by the clini-
VALVULAR DISEASE IN THE ELDERLY 155
cian, and individual management decisions
for the elderly based on the type and severity
of valve disease, comorbid medical condi-
tions, and the risks and benefits of interven-
tion, along with patient preferences, rather
than on the chronologic age of the patient. It
is becoming clear that both survival and qual-
ity of life outcomes can improve by consider-
ation of surgery at the onset of indications,
before further deterioration eliminates the op-
portunity to provide benefit for the elderly
patient with valvular disease.
References
1. Akasaka T, Yoshikawa J, Yoshida K, et al: Age-
related valvular regurgitation: a study by pulsed
Doppler echocardiography. Circulation 76:262, 1987
2. Akins CW, Daggett WM, Valhakes GJ, et al: Cardiac
operations in patients 80-years-old and older. AM
Thorac Surg 64:606, 1997
3. Aranki SF, Rizzo RJ, Couper GS, et al: Aortic valve
replacement in the elderly. Effect of gender and
coronary artery disease on operative mortality. Cir-
culation 88:1117, 1993
4. Aronow WS, Ahn C, Kronzon I: Prevalence of echo-
cardiographic findings in 554 men and in 1243
women aged >60 years in a long-term health care
facility. Am J Cardiol 79:379, 1997
5. Aronow WS, Ahn C, Kronzon I, Gutstein H: Associ-
ation of mitral annular calcium with new thrombo-
embolic stroke at 44-month follow-up of 2,148 per-
sons, mean age 81 years. Am J Cardiol81:105, 1998
6. Aronow WS, Koenigsberg M, Kronzon I, et al: Associ-
ation of mitral anular calcium with new thrombwm-
bolic stroke and cardiac events at 39-month follow-up
in elderly patients. Am J Cardiol 65:1511, 1990
7. Aronow WS, Kronzon I: Correlation of prevalence
and severity of valvular aortic stenosis determined
by continuous-wave Doppler echocardiography
with physical signs of aortic stenosis in patients
aged 62 to 100 years with aortic systolic ejection
murmurs. Am J Cardiol 60:399, 1987
8. Aronow WS, Kronzon I: Prevalence and severity
of valvular aortic stenosis determined by Doppler
echocardiography and its association with echocar-
diographic and electrocardiographic left ventricular
hypertrophy and physical signs of aortic stenosis in
elderly patients. Am J Cardiol 67776, 1991
9. Aronow WS, Schwartz KS, Koenigsberg M: Correla-
tion of serum lipids, calcium, and phosphorus, dia-
betes mellitus and history of systemic hypertension
with presence or absence of calcified or thickened
aortic cusps or root in elderly patients. Am J Cardiol
59:998, 1987
10. Asimakopoulos G, Edwards MB, Brannan J, et al:
Survival and cause of death after mitral valve re-
placement in patients aged 80 years and over: Col-
lective results from the UK heart valve registry. Eur
J Cardiothorac Surg 11:922, 1997
11. Asimakopoulos G, Edwards MB, Taylor KM: Aortic
valve replacement in patients 80 years of age and
older: survival and cause of death based on 1100
cases: Collective results from the UK Heart Valve
Registry. Circulation 96:3403, 1997
12. Azar H, Szentpetery S: Mitral valve repair in pa-
tients over the age of 70 years. Eur J Cardiothorac
Surg 8:298, 1994
156 HINCHMAN & OTTO
13. Azariades M, Fessler CL, Ahmad A, et al: Aortic
valve replacement in patients over 80 years of age:
A comparative standard for balloon valvuloplasty.
Eur J Cardiothorac Surg 5:373, 1991
14. Baim DS, Grossman W: Cardiac catheterization, an-
giography, and intervention. Baltimore, Williams
and Wilkins, 1996
15. Bayer AS, Ward JI, Ginzton LE, et al: Evaluation of
new clinical criteria for the diagnosis of infective
endocarditis. Am J Med 96:211, 1994
16. Benjamin EJ, Levy D, Anderson KM, et al: Determi-
nants of Doppler indexes of left ventricular diastolic
function in normal subjects (the Framingham heart
study). Am J Cardiol 70:508, 1992
17. Beppu S, Suzuki S, Matsuda H, et al: Rapidity of
progression of aortic stenosis in patients with congeni-
tal bicuspid aortic valves. Am J Cardiol 71:322, 1993
18. Block PC, Palacios IF: Clinical and hemodynamic
follow-up after percutaneous aortic valvuloplasty in
the elderly. Am J Cardiol 62:1760, 1988
19. Bolling SF, Deeb GM, Bach DS: Mitral valve recon-
struction in elderly, ischemic patients. Chest 109:35,
1996
20. Bonow RO, Lakatos E, Maron BJ, et al: Serial long-
term assessment of the natural history of asymp-
tomatic patients with chronic aortic regurgitation
and normal left ventricular systolic function. Circu-
lation 84:1625, 1991
21. Brener SJ, Duffy CI, Thomas JD, et al: Progression
of aortic stenosis in 394 patients: Relation to changes
in myocardial and mitral valve dysfunction. J Am
Coll Cardiol 25:305, 1995
22. Buda AJ:The role of echocardiography in the evalu-
ation of mechanical complications of acute myocar-
dial infarction. Circulation 84:1109, 1991
23. Burwash IG, Pearlman AS, Kraft CD, et al: Flow
dependence of measures of aortic stenosis severity
during exercise. J Am Coll Cardiol 24:1342, 1994
24. Bussey HI, Chiquette E, Amato MG: Anticoagula-
tion clinic care versus routine medical care: A re-
view and interim report. J Thrombosis Thrombolysis
2:315, 1996
25. Carabello BA: The changing unnatural history of
valvular regurgitation. Ann Thorac Surg 53:191, 1992
26. Carabello BA: Timing of valve replacement in aortic
stenosis: Moving closer to perfection [editorial]. Cir-
culation 95:2241, 1997
27. Cohn LH, Collins JJ Jr., Disesa VJ, et al: Fifteen-year
experience with 1678 Hancock porcine bioprosthetic
heart valve replacements. Ann Surg 210:435, 1989
28. Craver JM, Weintraub WS, Jones EL, et al: Predictors
of mortality, complications, and length of stay in
aortic valve replacement for aortic stenosis. Circula-
tion 78:85, 1988
29. Dajani AS, Taubert KA, Wilson W, et al: Prevention
of bacterial endocarditis. Recommendations by the
American Heart Association. JAMA 2771794, 1997
30. Dare AJ, Veinot JP, Edwards WD, et al: New obser-
vations on the etiology of aortic valve disease: a
surgical pathologic study of 236 cases from 1990.
Hum Pathol 24:1330, 1993
31. David TE, Armstrong S, Sun Z , et al: Late results of
mitral valve repair for mitral regurgitation due to
degenerative disease. AM Thorac Surg 56:7, 1993
32. Davis EA, Greene PS, Cameron DE, et al: Biopros-
thetic versus mechanical prostheses for aortic valve
replacement in the elderly. Circulation 94:121, 1996
33. Delahaye JP, Gare JP, Viguier E, et al: Natural history
of severe mitral regurgitation. Eur Heart J 9:5, 1991
34. Deutscher S, Rockette HE, Krishnaswami V Diabe-
tes and hypercholesterolemia among patients with
calcific aortic stenosis. J Chron Dis 37407, 1984
35. Devereux RB, Hawkins I, Kramer Fox R, et a 1 Com-
plications of mitral valve prolapse. Disproportionate
occurrence in men and older patients. Am J Med
81:751, 1986
36. Devereux RB, Kramer Fox R, Kligfield P: Mitral
valve prolapse: causes, clinical manifestations, and
management. Ann Intern Med 111:305, 1989
37. Donovan CL, Starling MR: Role of echocardiogra-
phy in the timing of surgical intervention for chronic
mitral and aortic regurgitation. In Otto CM (ed): The
Practice of Clinical Echocardiography, Philadelphia,
W.B. Saunders, 1997, p 327
38. Elayda MA, Hall RJ, Reul RM, et al: Aortic valve
replacement in patients 80 years and older. Operative
risks and long-term results. Circulation 88:11, 1993
39. Faggiano P, Ghizzoni G, Sorgato A, et al: Rate of
progression of valvular aortic stenosis in adults. Am
J Cardiol 70:229, 1992
40. Fann JI, Miller DC, Moore KA, et al: Twenty-year
clinical experience with porcine bioprostheses. Ann
Thorac Surg 62:1301, 1996
41. Freeman WK, Hartzell HV, Schaff HV, et al: Ultra-
sonic aortic valve decalcification: serial Doppler
echocardiographic follow-up. J Am Coll Cardiol
16:623, 1990
42. Freeman WK, Schaff HV, OBrien PC, et al: Cardiac
surgery in the octogenarian: perioperative outcome
and clinical follow-up. J Am Coll Cardiol 18:29,1991
43. Fremes SE, Goldman BS, Ivanov J, et al: Valvular
surgery in the elderly. Circulation 8O(suppl II):77, 1989
44. Gehlot A, Mullany CJ, Ilstrup D, et al: Aortic valve
replacement in patients aged eighty years and older:
Early and long-term results. 1 Thorac Cardiovasc
Surg 111:1026,7996
45. Georeeson S. Mever KB. Pauker SG: Decision analv-
sis ilclinical cardiology: When is coronary angiig-
raphy required in aortic stenosis. J Am Coil CGdiol
15:751, 1990
46. Gorlin R, Gorlin WB: Further reconciliation between
pathoanatomy and pathophysiology of stenotic car-
diac valves. J Am Coll Cardiol 15:1181, 1990
47. Gotoh T, Kuroda T, Yamasawa M, et al: Correlation
between lipoprotein(a) and aortic valve sclerosis as-
sessed by echocardiography (the JMS cardiac echo
and cohort study). Am J Cardiol 76:928, 1995
48. Gould KL: Why angina pectoris in aortic stenosis
[editorial]. Circulation 95:790, 1997
49. Gula G, Yacoub MH: Surgical correction of complete
rupture of the anterior papillary muscle. Ann
Thorac Surg 32:88, 1981
50. Hammer WJ, Roberts WC, deLeon AC: "Mitral ste-
nosis" secondary to combined "massive" mitral an-
ular calcific deposits and small, hypertrophied left
ventricles. Hemodynamic documentation in four
patients. Am J Med 64:371, 1978
51. Hendren WG, Nemec JJ, Lytle BW, et al: Mitral
valve repair for ischemic mitral insufficiency. AM
Thorac Surg 52:1246, 1991
52. Henry WL, Bonow RO, Borer JS, et al: Observations
on the optimal time for operative intervention for
aortic regurgitation. 11. Serial echocardiographic
evaluation of asymptomatic patients. Circulation
61:484, 1980
53. Hoagland PM, Cook EF, Flatley M, et al: Case-con-
trol analysis of risk factors for presence of aortic
stenosis in adults (age 50 years or older). Am J
Cardiol55:744, 1985
54. Hogevik H, Olaison L, Andersson R, et al: Epidemi-
ologic aspects of infective endocarditis in an urban
population. A 5-year prospective study. Medicine
Baltimore 74:324, 1995
55. Horstkotte D, Loogen F: The natural history of aor-
tic valve stenosis. Eur Heart J 9:57, 1988

56. Iung B, Cormier B, Farah B, et al: Percutaneous
mitral commissurotomy in the elderly. Eur Heart J
16:1092, 1995
57. Jaeger AA, Hlatky MA, Paul SM, et a1 Functional
capacity after cardiac surgery in elderly patients. J
Am Coll Cardiol 24:104, 1994
58. Jamieson WR, Burr LH, Munro AI, et al: Cardiac
valve replacement in the elderly: clinical perfor-
mance of biological prostheses. AM Thorac Surg
48:173, 1989
59. Jamieson WR, Tyers GF, Janusz MT, et al: Age as a
determinant for selection of porcine bioprostheses
for cardiac valve replacement: experience with Car-
pentier-Edwards standard bioprosthesis. Can J
Cardiol 7181, 1991
60. Jebara VA, Dervanian P, Acar C, et a1 Mitral valve
repair using Carpentier techniques in patients more
than 70 years old. Early and late results. Circulation
86:53, 1992
61. Johnson AM: Aortic stenosis, sudden death, and the
left ventricular baroceptors. Br Heart J 33:1, 1971
62. Julius BK, Spillmann M, Vassalli G, et al: Angina
pectoris in patients with aortic stenosis and normal
coronary arteries. Mechanisms and pathophysiolog-
ical concepts. Circulation 95392, 1997
63. Kay GL, Kay JH, Zubiate P, et al: Mitral valve repair
for mitral regurgitation secondary to coronary ar-
tery disease. Circulation 74:88, 1986
64. Kelly TA, Rothbart RM, Cooper CM, et al: Compari-
son of outcome of symptomatic to symptomatic pa-
tients older than 20 years of age with valvular aortic
stenosis. Am J Cardiol 61:123, 1988
65. Kennedy KD, Nishimura RA, Holmes DRJ, et al:
Natural history of moderate aortic stenosis. J Am
Coll Cardiol 17313, 1991
66. Killen DA, Reed WA, Wathanacharoen S, et a1 Sur-
gical treatment of papillary muscle rupture. AM
Thorac Surg 35:243, 1983
67. Kocemba J, Kawecka JK, Grodzicki T, et al: Influence
of long-term treatment with nifedipine on blood
pressure, left ventricular mass and cardiac arrhyth-
mias in elderly hypertensive patients. J Hum Hyper-
tens 8:279, 1994
68. Kono T, Sabbah HN, Rosman H, et al: Mechanism
of functional mitral regurgitation during acute myo-
cardial ischemia. J Am Coll Cardiol 19:1101, 1992
69. Krayenbuehl HP, Hess OM, Monrad ES, et al: Left
ventricular myocardial structure in aortic valve dis-
ease before, intermediate, and late after aortic valve
replacement. Circulation 79:744, 1989
70. Labovitz AJ, Nelson JG, Windhorst DM, et al: Fre-
quency of mitral valve dysfunction from mitral anu-
lar calcium as detected by Doppler echocardiogra-
phy. Am J Cardiol55:133, 1985
71. Lee EM, Shapiro LM, Wells FC: Importance of sub-
valvular preservation and early operation in mitral
valve surgery. Circulation 94:2117, 1996
72. Lee EM, Shapiro LM, Wells FC: Echocardiography
in mitral valve repair for mitral regurgitation: The
surgeon’s needs. J Heart Valve Dis 6:228, 1997
73. Levine HJ, Gaasch WH: Vasoactive drugs in chronic
regurgitant lesions of the mitral and aortic valves. J
Am Coll Cardiol 28:1083, 1996
74. Lin M, Chiang HT, Lin SL, et al: Vasodilator therapy
in chronic asymptomatic aortic regurgitation: enala-
pril versus hydralazine therapy. J Am Coll Cardiol
14:1046, 1994
75. Lindroos M, Kupari M, Heikkila J, et al: Prevalence
of aortic valve abnormalities in the elderly: An echo-
cardiographic study of a random population sam-
ple. J Am Coll Cardiol 21:1220, 1993
76. Litvack F, Jakubowski AT, Buchbinder NA, et al:
VALVULAR DISEASE IN THE ELDERLY 157
Lack of sustained clinical improvement in an elderly
population after percutaneous aortic valvuloplasty.
Am J Cardiol 62:270, 1988
77. Logeais Y, Langanay T, Roussin R, et al: Surgery for
aortic stenosis in elderly patients. A study of surgical
risk and predictive factors. Circulation 902891, 1994
78. Lombard JT, Selzer A: Valvular aortic stenosis. A
clinical and hemodynamic profile of patients. Ann
Intern Med 106:292, 1987
79. Lytle BW, Cosgrove DM, Loop FD, et al: Replace-
ment of aortic valve combined with myocardial re-
vascularization: determinants of early and late risk
for 500 patients, 1967-1981. Circulation 68:1149,1983
80. Nair CK, Sketch MH, Ahmed I, et al: Calcific valvu-
lar aortic stenosis with and without mitral anular
calcium. Am J Cardiol 60:865, 1987
81. Nair CK, Thomson W, Ryschon K, et al: Long-term
follow-up of patients with echocardiographically
detected mitral anular calcium and comparison with
age- and sex-matched control subjects. Am J Cardiol
63:465, 1989
82. Nottestad SY, Zabalgoitia M: Echocardiographic rec-
ognition and quantitation of prosthetic valve dys-
function. In Otto CM (ed): The Practice of Clinical
Echocardiography, Philadelphia, W.B. Saunders,
1997, p 797
83. OBrien KD, Kuusisto J, Reichenbach DD, et al: Os-
teopontin is expressed in human aortic valvular le-
sions. Circulation 92:2163, 1995
84. OBrien KD, Reichenbach DD, Marcovina SM, et
al: Apolipoproteins B, (a) and E accumulate in the
morphologically early lesion of ”degenerative” val-
vular aortic stenosis. Arterio and Thrombosis
16:523, 1996
85. O’Keefe JHJ, Vlietstra RE, Bailey KR, et al: Natural
history of candidates for balloon aortic valvu-
loplasty. Mayo Clin Proc 62:986, 1987
86. Oh JK, Taliercio CP, Holmes DRJ, et al: Prediction
of the severity of aortic stenosis by Doppler aortic
valve area determination: prospective Doppler-cath-
eterization correlation in 100 patients. J Am Coll
Cardiol 11:1227, 1988
87. Olesen KH: The natural history of 271 patients with
mitral stenosis under medical treatment. Br Heart J
24:349, 1962
88. Olsson M, Granstrom L, Lindblom D, et al: Aortic
valve replacement in octogenarians with aortic ste-
nosis: a case-control study. J Am Coll Cardiol
20:1512, 1992
89. Otto CM: Aortic stenosis: echocardiographic evalua-
tion of disease severity, disease progression, and the
role of echocardiography in clinical decision mak-
ing. In Otto CM (ed): The Practice of Clinical Echo-
cardiography, Philadelphia, W.B. Saunders, 1997
90. Otto CM, Burwash IG, Legget ME, et al: A prospec-
tive study of asymptomatic valvular aortic stenosis:
Clinical, echocardiographic, and exercise predictors
of outcome. Circulation 95: 2262, 1997
91. Otto CM, Kuusisto J, Reichenbach DD, et al: Charac-
terization of the early lesion of ’degenerative’ valvu-
lar aortic stenosis: histologic and immunohisto-
chemical studies. Circulation 90:844, 1994
92. Otto CM, Munt BI, Legget ME, et al: Correlation
between physical examination findings and Doppler
echocardiography in adults with aortic stenosis. Cir-
culation 96157, 1997 (abstract)
93. Otto CM, Pearlman A S Valvular stenosis: diagnosis,
quantitation, and clinical approach. In Otto CM,
Pearlman AS (eds): Textbook of Clinical Echocardi-
ography, Philadelphia, W.B. Saunders Company,
1995, p 209
94. Otto CM, Pearlman AS, Gardner C L Hemodynamic
158 HINCHMAN & OTTO
progression of aortic stenosis in adults assessed by
Doppler echocardiography. J Am Coll Cardiol
13:545, 1989
95. Otto CM, Pearlman AS, Comess KA, et al: Determi-
nation of the stenotic aortic valve area in adults
using Doppler echocardiography. J Am Coll Cardiol
7509, 1986
96. Otto CM, Pearlman AS: Doppler echocardiography
in adults with asymptomatic aortic stenosis: Diag-
nostic utility and cost-effectiveness. Arch Intern
Med 148:2553, 1988
97. Otto CM, Pearlman AS, Kraft CD, et al: Physiologic
changes with maximal exercise in asymptomatic
valvular aortic stenosis assessed by Doppler echo-
cardiography. J Am Coll Cardiol 20:1160, 1992
98. Pachulski RT, Chan KL: Progression of aortic valve
dysfunction in 51 adult patients with congenital
bicuspid aortic valve: assessment and follow up by
Doppler echocardiography. Br Heart J 69:237, 1993
99. Pahor M, Guralnik JM, Corti MC, et al: Long-term
survival and use of antihypertensive medications in
older persons. J Am Geriatr SOC43:1191, 1995
100. Peter M, Hoffmann A, Parker C, et al: Progression
of aortic stenosis. Role of age and concomitant coro-
nary artery disease. Chest 103:1715, 1993
101. Pini R, Devereux RB, Greppi B, et al: Comparison
of mitral valve dimensions and motion in mitral
valve prolapse with severe mitral regurgitation to
uncomplicated mitral valve prolapse and to mitral
regurgitation without mitral valve prolapse. Am J
Cardiol 62:257, 1988
102. Rankin JS, Hickey MS, Smith LR, et al: Ischemic
mitral regurgitation. Circulation 79(suppl lI):116, 1989
103. Richards AM, Nicholls MG, Ikram H, et al: Syncope
in aortic valvular stenosis. Lancet 2:1113, 1984
104. Roberts WC: The senile cardiac calcification syn-
drome. Am J Cardiol 58:572, 1986
105. Roger VL, Tajik AJ, Bailey KR, et al: Progression of
aortic stenosis in adults: new appraisal using Dopp-
ler echocardiography. Am Heart J 119:331, 1990
106. Roijer A, Lindgren A, Rudling 0, et al: Potential
cardioembolic sources in an elderly population
without stroke. A transthoracic and transoesopha-
geal echocardiographic study in randomly selected
volunteers. Eur Heart J 171103, 1996
107. Sanfilippo AJ, Picard MH, Newel1 JB, et al: Echocar-
diographic assessment of patients with infectious
endocarditis: prediction of risk for complications. J
Am Coll Cardiol 18:1191, 1991
108. Sauren AAHJ, Kuijpers W, Van Steenhoven AA, et
al: Aortic valve histology and its relation with me-
chanics:preliminary report. J Biomechanics 13:97,1980
109. Schiller NB: Clinical decision making in patients
with endocarditis: the role of echocardiography. In
Otto CM (ed): The Practice of Clinical Echocardiog-
raphy, Philadelphia, W.B. Saunders, 1997
110. Scbgnamiglio R, Rahimtoola SH, Fasoli G, et al:
Nifedipine in asymptomatic patients with severe
aortic regurgitation and normal left ventricular
function. N Engl J Med 331:689, 1994
111. Scott WJ, Neumann AL, Karp RB: Ultrasonic de-
bridement of the aortic valve with six-month echo-
cardiographic follow-up. Am J Cardiol64:1206,1989
112. Selton-Suty C, Hoen B, Grentzinger A, et al: Clinical
and bacteriological characteristics of infective endo-
carditis in the elderly. Heart 77260, 1997
113. Selzer A: Changing aspects of the natural history of
valvular aortic stenosis. N Engl J Med 31791, 1987
114. Shapira OM, Kelleher RM, Zelingher J, et al: Progno-
sis and quality of life after valve surgery in patients
older than 75 years. Chest 112:885, 1997
115. Shaw TR, Elder AT, Flapan AD, et al: Mitral balloon
valvuloplasty for patients aged over 70 years: An
alternative to surgical treatment. Age Ageing
20:299, 1991
116. Steckelberg JM, Murphy JG, Ballard D, et al: Emboli
in infective endocarditis: the prognostic value of
echocardiography. Ann Intern Med 114:635, 1991
117. Stein PD, Alpert JS, Copeland J, et al: Antithrom-
botic therapy in patients with mechanical and bio-
logical prosthetic heart valves [published erratum
appears in Chest 1996 109(2):592, 19961. Chest
108:371S, 1995
118. Stewart BF, Siscovick D, Lind BK, et al: Clinical
factors associated with calcific aortic valve disease.
J Am Coll Cardiol 29:630, 1997
119. Tepe NA, Edmunds LH Jr.: Operation for acute post-
infarction mitral insufficiency and cardiogenic
shock. J Thorac Cardiovasc Surg 89:525, 1985
120. Thubrikar MJ, Aouad J, Nolan SP: Patterns of
calcific deposits in operatively excised stenotic or
purely regurgitant aortic valves and their relation
to mechanical stress. Am J Cardiol58:304, 1986
121. Torsher LC, Shub C, Rettke SR, et al: Risk of patients
with severe aortic stenosis undergoing noncardiac
surgery. Am J Cardiol 81948, 1998
122. Turina J, Hess 0, Sepulcri F, et al: Spontaneous
course of aortic valve disease. Eur Heart J 8:471, 1987
123. Villari B, Hess OM, Kaufmann P, et al: Effect of
aortic valve stenosis (pressure overload) and regur-
gitation (volume overload) on left ventricular sys-
tolic and diastolic function. Am J Cardiol69927,1992
124. Vongpatanasin W, Hillis LD, Lange RA: Prosthetic
heart valves. N Engl J Med 335:407, 1996
125. Werner GS, Schulz R, Fuchs JB, et al: Infective endo-
carditis in the elderly in the era of transesophageal
echocardiography: Clinical features and prognosis
compared with younger patients. Am J Med
100:90, 1996
126. Westaby S, Huysmans HA, David TE: Stentless aortic
bioprostheses: compelling data from the Second Inter-
national Symposium. Ann Thorac Surg 65235, 1998
127. Wilcken DE, Hickey AJ: Lifetime risk for patients
with mitral valve prolapse of developing severe
valve regurgitation requiring surgery. Circulation
78:10, 1988
128. Yoganathan AP, Heinrich RS, Fontaine AA: Fluid
dynamics of prosthetic valves. In Otto CM (ed): The
Practice of Clinical Echocardiography, Philadelphia,
W.B. Saunders. 1997, v 773
129. Zavitsanos JP, Goldmk AP, Kotler MN, et al: The
echo Doppler spectrum of valvular abnormalities in
the hospitalized octogenarian. Clin Cardiol11:683, 1988
130. Zoghbi WA, Galan A, Quinones MA: Accurate as-
sessment of aortic stenosis severity by Doppler
echocardiography independent of aortic jet velocity.
Am Heart J 116:855, 1988
Address reprint requests to
Catherine M. Otto, MD
Division of Cardiology
Box 356422
University of Washington
Seattle, WA 98195