HEADLINE: Valvular heart disease...

Copyright 2003 Gale Group, Inc.
ASAP
Copyright 2003 Advanstar Communications, Inc.
Geriatrics

October 1, 2003

SECTION: No. 10, Vol. 58; Pg. 26 ; ISSN: 0016-867X

IAC-ACC-NO: 109700247

LENGTH: 4571 words

HEADLINE: Valvular heart disease, Part 2: mitral valve disease in older adults;
The Heart

BYLINE: Segal, Bernard L.

AUTHOR-ABSTRACT:
Mitral valve disease is a common cause of morbidity and mortality in patients
over age 65. The etiology, physical findings, and natural history of rheumatic
mitral stenosis, rheumatic mitral regurgitation, chronic non-rheumatic mitral
regurgitation, and acute mitral regurgitation may differ in older and younger
patients. In addition, symptoms of mitral valve disease may be masked or
exacerbated by coexistent coronary artery disease, pulmonary disease,
hypertension, and other systemic disorders that commonly occur in older adults.
The clinical evaluation, along with various non-invasive cardiac procedures, is
important for identifying mitral valve disease as the cause of abnormal signs
and symptoms in older patients. Recognition of mitral valve abnormalities has
important implications, because mitral valve repair or replacement is usually
associated with favorable short- and long-term results, even in patients over
age 65.; Segal BL. Valvular heart disease, part 2: Mitral valve disease in older
adults. Geriatrics 2003; 58(Oct):26-31.; Key words: valve disease * mitral
stenosis * mitral regurgitation

BODY:

Last month, part 1 of this two-part CME article on valvular heart disease
began with a review of aortic valve disease in older adults (Geriatrics 2003;
58(Sept):31-35). For the second installment, the discussion of valvular heart
disease concludes with a look at the diagnosis and management of mitral valve
disease in older adults (age 65 and older).

Rheumatic mitral valve disease

Various autopsy series have reported an incidence of 2.5 to 5% of rheumatic
mitral valve disease in older patients. Between 40 and 65% of older patients
with rheumatic mitral valve disease are able to provide a history of rheumatic
fever during childhood. The valve cusps are involved in an inflammatory reaction
and develop thickening, scarring, and commissural adhesions that reduce the area
of the valve orifice and cause mitral stenosis (MS). Scarring may affect the
chordae tendineae as well as the leaflets, causing thickening, retraction, and
valvular regurgitation.

In older patients, calcification of the leaflets and commissures is almost
always present, whereas in younger patients (age <50), the stenosis is more
often caused by commissural fusion with thin, mobile leaflets. (1) Approximately
one-third of older patients with rheumatic disease have MS, whereas two-thirds
have predominant mitral regurgitation (MR). A combination of the two defects is
common. Patients may also have a myocardial component to the pathology that may
cause a low-output state at rest and an inability to increase cardiac output
with exercise. Pulmonary hypertension is common (approximately 75%). This
pattern of rheumatic involvement seems to be found almost exclusively in older
women. (2-4)

Older patients may exhibit any of the complications of rheumatic disease,
such as atrial fibrillation, cardiac failure, and pulmonary hypertension.
Thromboembolic phenomena are particularly common among older adults, especially
those with atrial fibrillation. Cerebral emboli are most common, with renal,
splenic, and other systemic sites also frequently involved. In some cases, the
embolus may be the first sign of cardiac disease and may be a major cause of
morbidity and mortality. Infective endocarditis is rare in pure MS, but is more
common with combined MS and MR.

Diagnostic clues to mitral valve endocarditis in older patients include
fever with unexplained heart failure, stroke, progressive renal failure, weight
loss and anemia, back pain, confusion or personality disorder, hypotension, and
unexplained systemic embolism.

Mitral stenosis

In normal healthy adults, the cross-sectional area of the mitral valve
orifice is 4 to 6 [cm.sup.2]. Mild MS occurs when the mitral valve orifice is
reduced to 2 [cm.sup.2]. A small pressure gradient is present. When the mitral
valve orifice is reduced to 1 [cm.sup.2], severe MS is present, and a gradient
of at least 20 mm Hg is typically required to maintain normal cardiac output at
rest. Elevated left atrial pressures in turn increase pulmonary venous and
capillary pressures resulting in symptoms of effort dyspnea. In MS, the first
bouts of dyspnea usually occur with exercise or with conditions that produce
rapid heart rates such as infection, fever, and new onset rapid atrial
fibrillation. All of these conditions increase blood flow across the mitral
valve and cause further elevation of left atrial pressures. To assess the
severity of obstruction across the mitral valve, it is essential to measure the
transvalvular pressure gradient and the flow rate. The latter depends on cardiac
output and heart rate. In time, severe pulmonary hypertension, whether fixed or
reactive, may lead to right-sided heart failure and pulmonary and tricuspid
regurgitation. (7)

Clinical findings. Dyspnea may occur with exercise or at rest and is the
result of reduced compliance of the lungs; vital capacity is reduced due to
interstitial edema and pulmonary congestion. Orthopnea and frank pulmonary edema
may be precipitated by rapid ventricular response as in rapid atrial
fibrillation. Mitral stenosis typically develops between ages 30 and 50; so
patients who exhibit MS after age 65 typically had a mild-to-moderate form of
disease at a younger age that became severe in late life as the valve developed
heavy calcification. Patients most likely had rheumatic fever as children, but
often do not remember having it. Women are twice as likely to develop MS as men,
and will start to complain of fatigue and shortness of breath while doing daily
household chores or lifting heavy objects. Additional symptoms include
hemoptysis and palpitations. Symptoms that indicate complications associated
with MS include cardiac arrhythmias, thromboembolism in both pulmonary and
systemic circulation, infective endocarditis, vocal hoarseness due to
compression of the left recurrent laryngeal nerve by a dilated left atrium, and
progressive left- and right-sided failure.

Physical examination. Older patients (usually women) with severe MS and low
cardiac output exhibit the typical mitral facies of pinkish-purple patches on
their cheeks. A loud first heart sound (S1) is palpable at the apex. Most older
patients with MS have pulmonary hypertension. A lift is present over the right
ventricle and pulmonary artery in the second, third, and fourth left interspace.
Auscultatory findings will indicate severe MS (figure 1). The first heart sound
may be loud and sharp if the mitral valve leaflets are still flexible.
Nevertheless, fibrocalcific changes involving the mitral valve leaflets in older
patients reduce the amplitude of excursion of these leaflets so that the
intensity of S1 may be diminished. The second sound is followed by an opening
snap, which is a high frequency sound. In most older patients with MS, severe
calcification involving the mitral leaflets is present, with progressive
pulmonary hypertension. For patients with "silent" MS, the opening snap is
silent and the apical diastolic rumble, which is best heard at the point of
maximal impulse (usually at the apex with the bell of the stethoscope lightly
applied to the chest wall), may not be heard even in the left lateral position.
"Silent" MS is caused by severe fibrocalcification of the mitral valve with
pulmonary hypertension and reduced cardiac output. (5-7)

[FIGURE 1 OMITTED]

ECG. The ECG may show P-wave abnormalities of left atrial enlargement and
right ventricular hypertrophy depending on the degree of right ventricular
pressure elevation.

Chest x-ray. The chest x-ray may show left atrial enlargement on the lateral
and anterior oblique views. Enlargement of the pulmonary artery, right atrium,
and right ventricle are commonly seen in severe MS with pulmonary hypertension.
Calcification of the mitral valve is evident in the older patient. Interstitial
edema produces dense, short, horizontal lines seen at costophrenic angles that
usually suggest severe long-standing MS.

Echocardiography. The echocardiogram is extremely helpful in diagnosing
mitral stenosis and can identify doming of both leaflets as they open into the
left ventricle. Doppler echo studies added to the 2-dimensional echo analysis
provide fairly accurate readings of mitral valve areas.

Cardiac catheterization. Cardiac catheterization provides additional
information regarding the association of coronary artery disease and is used to
evaluate left ventricular (LV) function, determine the degree of mitral
regurgitation, confirm the presence or absence of pulmonary hypertension, and
exclude aortic and tricuspid valve disease.

Coronary arteriography should be performed in older patients who have risk
factors for atherosclerosis.

Medical management. Medical treatment of MS includes the use of prophylactic
antibiotics; appropriate and specific antibiotics after blood cultures for
treating infective endocarditis; digoxin, beta blockers, and calcium channel
blockers to slow atrial fibrillation; and anticoagulation with warfarin to
prevent atrial thrombus and embolism. Balloon valvuloplasty is indicated for
patients with symptomatic MS and pliable, mobile, relatively thin, and minimally
calcified valves. Transesophageal echo ensures that thrombus is absent from the
left atrium prior to the procedure.

Chronic rheumatic mitral regurgitation

Pathophysiology. Chronic rheumatic mitral regurgitation is a form of
volume-overload of the left ventricle and left atrium (LA). The condition is
well tolerated for many years, but eventually leads to LV failure. The mitral
valve apparatus involves the mitral annulus, mitral leaflets, chordae, and the
papillary muscles. Abnormalities of any of these structures may cause MR.
Compliance of the LA and the pulmonary venous bed are important determinants of
hemodynamic and clinical findings in MR. Patients with normal LA compliance
exhibit little enlargement of the LA, although marked elevation of mean LA
pressure and a V-wave are conspicuous. Pulmonary congestion is a prominent
symptom. Patients with long-standing chronic MR, however, exhibit massive
enlargement of the LA and normal or slightly elevated LA pressure. In these
patients, pulmonary artery pressures and pulmonary vascular resistance are
normal and only slightly elevated at rest.

Clinical findings. Symptoms usually do not develop in patients with chronic
rheumatic MR until the LV fails. Acute pulmonary edema occurs less often in
chronic rheumatic MR than in MS, presumably because sudden surges in LA pressure
are less common. Dyspnea, hemoptysis, and embolism do occur in MR but are less
common than in MS. Fatigue, weakness, and progressive reduction in exercise
tolerance are attributed to reduced cardiac output. Palpitations are frequent,
particularly in association with intermittent and permanent atrial fibrillation.
Progressive left and right sided failure, thromboembolism, infective
endocarditis, and intermittent arrhythmias may produce characteristic symptoms.

Physical examination. The carotid pulsation is helpful in differentiating
the systolic murmur of MR from aortic stenosis (AS). The carotid upstroke is
brisk in MR, but is delayed and reduced in AS. Pulse volume is increased in
severe MR in the absence of heart failure. The left ventricular impulse is
hyperdynamic and displaced to the left. Systolic expansion of a large LA may
result in a late systolic impulse in the parasternal region that may produce a
"rocking" motion during systole. In patients with pulmonary hypertension, the
second heart sound at the pulmonary area (S2) is accentuated and palpable at the
second left interspace, and the right ventricle and pulmonary artery are both
palpable.

On auscultation, the first heart sound (S1) is usually reduced. Splitting of
the second sound into aortic and pulmonary components (A2 and P2) is usually
wide because of a shortened LV ejection fraction with early A2 as a consequence
of reduced resistance to LV outflow. In patients with pulmonary hypertension, P2
is louder than A2 if splitting of S2 is present. The tumultuous rapid filling of
blood from LA to LV in early diastole will produce a loud third heart sound
(S3).

The holosystolic murmur at the apex is the hallmark of MR (figure 2).

[FIGURE 2 OMITTED]

The murmur starts with a soft S1 and continues through A2. It is usually of
a constant intensity, occupying all of systole, and is loudest at the apex with
transmission to the axilla. The murmur may also be transmitted to the base of
the heart at the aortic area, particularly with posterior leaflet abnormalities.
The holosystolic murmur shows little change in intensity even with beat-to-beat
variation of LV stroke volume, as in atrial fibrillation. The murmur is often
associated with a high-pitched frequency and blowing, and is best heard at the
apex. When the murmur is confined to late systole, MR is usually mild and
generally due to a non-rheumatic etiology, typically mitral valve prolapse
(MVP). Loud early systolic murmurs beginning with S1 and ending in mid- or
late-systole may indicate severe MR. The tumultuous backward regurgitant flow
from the left ventricle into the left atrium will produce a very high pressure
in the LA, and turbulence will be confined to early- and mid-systole. The
characteristic holosystolic murmur of MR is well tolerated for many years. With
aging, progressive heart failure may result.

ECG. Chronic rheumatic MR is associated with left atrial and left
ventricular dilatation, which produces patterns of LA dilatation and LV
hypertrophy. Atrial fibrillation is generally present in long-standing MR.

Chest x-ray. Chest x-ray helps identify LV and LA enlargement. Interstitial
pulmonary edema is observed in patients with overt heart failure.

Echocardiography. Doppler echo studies are useful for determining
abnormalities of valve structure, left atrial and left ventricular size and
function, semi-quantitative estimates of severity of MR, size and function of
the right ventricle, and estimates of pulmonary arterial systolic pressure.
Systolic posterior displacement of one or both leaflets of the valve into the LA
is common in patients with MVP and MR. In mild MR, prolapse is confined to mid-
and late-systole. With progression of MR, the prolapse may be demonstrated
throughout systole beginning with the first sound associated with dilatation of
the annulus, chordal elongation, or leaflet thickening.

Cardiac catheterization. Cardiac catheterization in older patients confirms
the status of LV function, the degree of mitral regurgitation, the presence of
associated coronary heart disease, the presence of other valvular disease, and
the degree of pulmonary hypertension. This information has important
considerations in defining the risk of mitral valve surgery for MR. (9)

Clinical management. In patients with chronic rheumatic MR, the use of
diuretics, digoxin therapy, and LV unloading agents along with restriction of
activities will improve function, avoid fluid retention, and improve symptoms.

Chronic non-rheumatic mitral regurgitation

The normal mitral valve changes with age. Older patients exhibit thickening
of the atrial aspects of the endocardium that primarily involves the anterior
leaflet as well as thickening and nodularity along the approximating edge of the
chordae tendineae. Microscopically, collagen fibers become disorganized, denser,
and contain fewer nuclei. Fibroelastic hyperplasia of the posterior leaflet and
microscopic calcification of both valve leaflets is evident. Mitral
regurgitation may result in progressive mitral annular calcification and mucoid
or myxomatous mitral leaflet degeneration.

Other disorders that produce chronic non-rheumatic MR include
cardiomyopathy, papillary muscle dysfunction and rupture associated with
coronary heart disease, infective endocarditis, and mitral valve prolapse.

Mitral annular calcification

The incidence of mitral annular calcification (MAC) is 8.5 to 10% in various
autopsy series of patients older than age 50 and is 2 to 3.5 times more common
in women than in men. MAC occurs with increasing age, and appears to be
associated with calcific aortic stenosis, hypertrophic cardiomyopathy, MVP, and
type 2 diabetes mellitus. (10-11)

Pathology. Mitral annular calcification involves the mitral annulus and may
extend to the posterior subvalvular areas adherent to the ventricular side of
the posterior leaflet and adjacent to the ventricular wall. Rarely, the
calcified mass may erode through the leaflet into the left atrium to form a
nidus for infective or marantic endocarditis.

Clinical manifestations. Most patients are asymptomatic, and MAC is often an
incidental finding. When symptoms develop, they are the result of mitral valve
dysfunction (usually MR), arrhythmias, or conduction disturbances. Heart block
is common. The mitral annulus is close to the bundle of His, and calcification
can erode into the conduction system. Bundle branch block, AV block, and atrial
fibrillation are found in up to 30% of patients with severe MAC. Complications
of MAC include mitral regurgitation, mitral valve obstruction, arrhythmias,
conduction problems, calcific thromboembolism, and infective endocarditis.
(10,11)

Myxomatous leaflet degeneration

Since its recognition as a mid-systolic click and late systolic murmur,
myxomatous mitral leaflet degeneration causing MVP generally has been considered
a common benign condition found most often in young (age <40) women. (12-15) In
older patients, however, myxomatous leaflet degeneration may not be benign
because the lesion or its consequence, ruptured chordae, is probably the most
common cause of mitral regurgitation requiring surgery. The etiology of
myxomatous mitral leaflet degeneration is not known. All of the major components
of mitral valvular connective tissue are abnormal in MVP. The posterior leaflet
is affected more often and more severely than the anterior leaflet. Myxomatous
chordae are prone to spontaneous rupture resulting in severe MR. Some older
patients may develop end-systolic MVP caused by elongated chordae, papillary
muscles, or both. End-systolic MVP may occur in older men with progressive
mitral regurgitation.

Acute mitral regurgitation

Acute MR may occur in patients with acute and chronic coronary artery
disease, with partial rupture of papillary muscles. Total rupture generally
leads to sudden death. Other causes of acute MR include endocarditis with
abscess formation and leaflet rupture, progressive prosthetic valve malfunction,
and acute chordal rupture associated with myxomatous degeneration of the mitral
valve. In the acute form of MR, patients often have acute pulmonary edema, and
cardiogenic shock may ensue. These patients should be initially treated with LV
unloading agents and then undergo urgent mitral valve repair or replacement. In
acute MR, IV vasodilator therapy will reduce LV cavity dilatation, reduce
diastolic filling pressures, and thereby reduce the degree of MR. Patients
should be stabilized before mitral valve repair or replacement. (17-19)

Papillary muscle dysfunction and rupture

The incidence of papillary muscle dysfunction following MI is difficult to
assess. Frank papillary muscle rupture occurs in approximately 1% of patients.
Untreated papillary muscle rupture has a reported mortality rate of 80 to 90%.
It develops most often 2 to 7 days after an acute MI. The prognosis depends on
the site and extent of rupture. With rupture of the entire trunk, one-half of
valvular support is lost, causing overwhelming acute mitral regurgitation and
most likely death. If one or several of the apical heads rupture, there is less
mitral regurgitation, and survival depends on the state and amount of the
functioning myocardium. Patients with mild-to-moderately impaired ventricular
function may survive, although heart failure is common. The development of a
harsh, apical systolic murmur is the most frequent finding following acute MI.
The murmur may vary in timing, intensity, pitch, and duration.

Surgical management

Mitral valve repair is preferred, if possible, for patients with MS. The
ability to successfully repair the mitral valve depends on the severity of the
pathology as well as the experience and skill of the surgeon. Mitral valvotomy
is typically successful for repairing rheumatic mitral stenosis. Repair of the
mitral valve for MS is associated with a mortality rate of less than 2 to 3% for
the uncomplicated patient, with a 10-year survival rate of at least 95%. Early,
rather than late mitral valve repair for MS improves operative mortality and
long-term outcome. (8)

The ability to perform successful mitral valve repair for MR also depends on
the degree of pathology and the experience of the surgical team. (20) Myxomatous
mitral valves typically require repair rather than replacement. The operative
mortality rate for repair is less than the rate for valve replacement. This is
true for degenerative MR and less so for ischemic MR. The lower risk is
attributed to improved LV function, probably because the entire native
subvalvular apparatus is preserved at the time of surgery. Long-term results for
mitral valve repair for MR have been encouraging. Five-year survival rates of 86
to 91% have been reported, and the rates of re-operation for structural valve
failure at 5 years have been reported to be 5 to 17%. Inclusion of a ring
annuloplasty at the time of mitral valve repair improves long-term success.
(8,22,23)

Mechanical or bioprosthetic valves are used for mitral valve replacement.
Mechanical valves will require lifetime anticoagulation therapy with warfarin to
prevent thromboembolism. Bioprosthetic valves lack the long-term durability of
mechanical valves. Patients with bioprosthetic valves who are in sinus rhythm
may not require anticoagulation. Nevertheless, most older patients with
long-term chronic mitral valve disease have large atria and atrial fibrillation.
These patients do require lifetime warfarin therapy.

The major drawback of the bioprosthetic valve in younger patients is that 20
to 40% of these valves will fail during 10-year follow-up as the result of
progressive deterioration. Structural deterioration of bioprosthetic valves is
rare in patients age 70 and older. Valve selection requires the weighing of
complications of long-term anticoagulation against the disadvantages of mild
deterioration. Mechanical valves are usually selected for patients less than age
60 who have no contraindications to anticoagulation. Patients who have
contraindications because of bleeding tendencies will require bioprosthetic
valve replacement.

LV function is preserved following mitral valve replacement if the mitral
leaflets and chordae are preserved. Preserving mitral valve chordae during
mitral valve replacement results in improved LV function after operation with
reduced operative and long-term mortality. (21) The operative mortality in
patients with preserved pre-operative LV function is less than 3%. In some
patients with severe LV dysfunction, operative mortality may exceed 25%.
Long-term survival rates generally depend upon pre-operative LV function. In
general, 5-year survival following mitral valve replacement in patients with
adequate LV function is [greater than or equal]80%. Mitral valve surgery should
be performed before LV function becomes severely depressed.

Two to 4% of patients with mechanical valves will have thromboembolic
complications per year. Patients with bioprosthetic valves and atrial
fibrillation who do not receive anticoagulation therapy have a yearly
thromboembolic rate of 1 to 3%. (8)

The conclusions reached by Mayo Clinic researchers in a recent editorial
suggest that mitral valve repair is beneficial in all subsets of patients with
non-ischemic MR. (24) Age and associated coronary artery bypass grafting should
not contraindicate valve repair, as long as the valve is repairable. For those
patients with severe valvular and subvalvular pathology, valve replacement is an
acceptable option.

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