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  • 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.

    References

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    (2.) Wood P. An appreciation of mitral stenosis, part 1: Clinical features.
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    (3.) Waller BF, Howard J, Fess S. Pathology of mitral valve stenosis and
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    (4.) Lachman AS, Roberts WC. Calcific deposits in stenotic mitral valves.
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    (5.) Kotler MN, Mintz GS, Parry WR, Segal BL. Bedside diagnosis of organic
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    (7.) Perloff JK. Auscultatory and phonocardiographic manifestations of
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    (9.) Braunwald E, Moscovitz HL, Amran SS, et al. Hemodynamics of the left
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    (10.) de Bono DP, Warlow CP. Mitral annulus calcification and cerebral or
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    (11.) Roberts WC, Waller BF. Mitral valve "anular" calcium forming a
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    (12.) Perloff JK, Roberts WC. The mitral apparatus. Functional anatomy of
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    (14.) Devereux RB, Brown WT, Kramer-Fox R, Sachs I. Inheritance of mitral
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    (15.) Shell WE, Walton JA, Clifford ME, Willis PW 3rd. The familial
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    (18.) Chatterjee K, Parmley WW, Swan HJ, Berman G, Forrester J, Marcus HS.
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    (22.) Tsai TP, Chaux A, Matloff JM, et al. Ten-year experience of cardiac
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    CME Exam

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    IAC-CREATE-DATE: November 6, 2003

    LOAD-DATE: November 07, 2003

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