The normal human heart contains 4 valves that regulate blood flow into and out of the heart. The aortic and pulmonic valves are known as the semilunar valves, whereas the tricuspid and mitral valves are referred to as the atrioventricular valves. All the valves are trileaflet, with the exception of the mitral valve, which has 2 leaflets. All 4 cardiac valves are surrounded by fibrous tissue forming partial or complete valvular rings, or annuli. These annuli join the fibrous skeleton of the heart to anchor and support the valvular structures.
Bicuspid aortic valve is the most common congenital lesion of the human heart.Connective tissue disorders that can cause significant AR include the following:Marfan syndromeEhlers-Danlos syndromeFloppy aortic valveAortic valve prolapseSinus of Valsalva aneurysmAortic annular fistula
Hemodynamics of aortic regurgitation. A, Normal conditions. B, The hemodynamic changes that occur in severe acute aortic regurgitation. Although total stroke volume is increased, forward stroke volume is reduced. Left ventricular end-diastolic pressure (LVEDP) rises dramatically. C, Hemodynamic changes occurring in chronic compensated aortic regurgitation are shown. Eccentric hypertrophy produces increased end-diastolic volume (EDV), which permits an increase in total, as well as forward, stroke volume. The volume overload is accommodated, and left ventricular filling pressure is normalized. Ventricular emptying and end-systolic volume (ESV) remain normal. D, In chronic decompensated aortic regurgitation, impaired left ventricular emptying produces an increase in end-systolic volume and a fall in ejection fraction (EF), total stroke volume, and forward stroke volume. There is further cardiac dilation and reelevation of left ventricular filling pressure. E, Immediately following valve replacement, preload estimated by EDV decreases, as does filling pressure. ESV also is decreased, but to a lesser extent. The result is an initial fall in EF. Despite these changes, elimination of regurgitation leads to an increase in forward stroke volume, and with time ejection fraction increases. Aop = aortic pressure; RF = regurgitant fraction.(From Carabello BA: Aortic regurgitation: Hemodynamic determinants of prognosis. In Cohn LH, DiSesa VJ [eds]: Aortic Regurgitation: Medical and Surgical Management. New York, Marcel Dekker, 1986, p 99-101.)
Patients with a projected long life-span generally receive a mechanical valve because of far greater durability and improved patient survival at 15 years .The main indications for a bioprosthesis are patients who cannot or will not tolerate warfarin or for whom compliance is uncertain, and patients ≥65 years of age who do not have risk factors for thromboembolism since valve durability is less of an issue
3rd yr Medicine Resident
• Valve Anatomy
• History & Physical Examination
• Natural History
• Differential diagnosis
• Assessing severity
• Medical Management
• Surgical Management
• Long term monitoring
• Located between the left ventricular outflow tract and
the ascending aorta
• The aortic valve functions to prevent the regurgitation
of blood from the aorta into the left ventricle during
ventricular diastole and to allow the appropriate flow
of blood—the cardiac output —from the left ventricle
into the aorta during ventricular systole.
• The aortic valve has 3 principle components: the
annulus, cusps, and commissures.
• The normal aortic valve area in adults is 3.0 to 4.0
• The aortic valve annulus is a collagenous structure lying at
the level of the junction of the aortic valve and the
ventricular septum, which is the nadir of the aortic valve
complex. This area is also referred to as the aortic ring
and serves to provide structural support to the aortic valve
• There are 3 aortic valve cusps - left, right, and posterior (or
noncoronary), each half-moon shaped or semilunar in
• Each cusp is attached to the wall of the aorta by the
outward edges of its semicircular border. The small
spaces between each cusp's attachment point are called
the aortic valve commissuresvitrag24-www.medicalgeek.com
• In contrast to MR, in which a fraction of the LV stroke
volume is ejected into the low-pressure left atrium, in AR
the entire LV stroke volume is ejected into a high-
pressure chamber (i.e., the aorta), although the low
aortic diastolic pressure does facilitate ventricular
emptying during early systole
• In MR, especially acute MR, the reduction of wall tension
(i.e., reduced afterload) allows more complete systolic
emptying; in AR the increase in LV end-diastolic volume
(i.e., increased preload) provides hemodynamic
Pathophysiology – Acute AR
• Acute AR of significant severity leads to increased blood
volume in the LV during diastole. The LV does not have
sufficient time to dilate in response to the sudden
increase in volume. As a result, LV end-diastolic
pressure increases rapidly, causing an increase in
pulmonary venous pressure and altering coronary flow
dynamics. As pressure increases throughout the
pulmonary circuit, the patient develops dyspnea and
• In severe cases, heart failure may develop and
potentially deteriorate to cardiogenic shock. Decreased
myocardial perfusion may lead to myocardial ischemia.
Pathophysiology – Chronic AR
• Severe AR may occur with a normal effective forward
stroke volume and a normal ejection fraction ([forward plus
regurgitant stroke volume]/[end-diastolic volume]), together
with an elevated LV end-diastolic volume, pressure, and
• According to Laplace's law, which indicates that wall
tension is related to the product of the intraventricular
pressure and radius divided by wall thickness, LV dilation
also increases the LV systolic tension required to develop
any level of systolic pressure. Thus, in AR, there is an
increase in preload and afterload. LV systolic function is
maintained through the combination of chamber dilation
and hypertrophy. This leads to eccentric hypertrophy. In
compensated AR, there is sufficient wall thickening so that
the ratio of ventricular wall thickness to cavity radius
Pathophysiology – Chronic AR …Cont’d
• During the early phases of chronic AR, the LV ejection
fraction (EF) is normal or even increased (due to the
increased preload and the Frank-Starling mechanism).
Patients may remain asymptomatic during this period.
• As AR progresses, LV enlargement surpasses preload
reserve on the Frank-Starling curve, with the EF falling to
normal and then subnormal levels.
• The LV end-systolic volume rises and is a sensitive
indicator of progressive myocardial dysfunction.
• The severity of AR is dependent on the diastolic valve
area, the diastolic pressure gradient between the aorta
and LV, and the duration of diastole.
Pathophysiology – Chronic AR …Cont’d
• Eventually, the LV reaches its maximal diameter and
diastolic pressure begins to rise, resulting in symptoms
(dyspnea) that may worsen during exercise. Increasing
LV end-diastolic pressure may also lower coronary
perfusion gradients, causing subendocardial and
myocardial ischemia, necrosis, and apoptosis.
• Severe chronic AR pts have the largest EDV of those
with any form of heart disease, resulting in cor bovinum.
• Grossly, the LV gradually transforms from an elliptical to
a spherical configuration.
• Increase in wall tension – Increase in 02 demand
• Decrease in diastolic pressure – coronary perfusion
pressure is reduced
• So increased O2 demand & decreased O2 supply sets
• Approximately three-fourths of patients with pure or
predominant valvular AR are men; women predominate
among patients with primary valvular AR who have
associated rheumatic mitral valve disease.
• Chronic AR often begins in patients when they are in
their late 50s. In general, the prevalence and severity of
AR increase with age.
• However, there are many exceptions to this observation.
Patients with bicuspid aortic valve and, especially, those
with Marfan syndrome tend to present much earlier
History – Acute AR
• Sudden, severe shortness of breath
• Chest pain if myocardial perfusion pressure is decreased
or an aortic dissection is present
• Rapidly developing heart failure, Pulmonary edema &
History – Chronic AR
• Relatively asymptomatic for as long as 10–15 years.
• Palpitations, especially on lying down.
• Sinus tachycardia, during exertion or with emotion, or
VPCs may produce uncomfortable palpitations as well as
head pounding. These complaints may persist for many
years before the development of exertional dyspnea,
usually the first symptom of diminished cardiac reserve.
• The dyspnea is followed by orthopnea, paroxysmal
nocturnal dyspnea, and excessive diaphoresis.
History – Chronic AR
• Anginal chest pain even in the absence of CAD - at rest
as well as during exertion.
• Nocturnal angina may be a particularly troublesome
symptom, and it may be accompanied by marked
• The anginal episodes can be prolonged and often do not
respond satisfactorily to sublingual nitroglycerin.
• Congestive heart failure
• Sudden cardiac death
• Physical Examination
• Chronic AR Acute AR
• Systolic BP Systolic BP =
• Diastolic BP Diastolic BP =
• Aortic Pulse Pressure Aortic Pulse Pressure =
• Heart Rate = Heart Rate
• S1 = (in CHF ) S1
• S2 = S2
• S3 absent(except CHF) S3 present
• S4 usually not present S4 never present
Physical Examination – Acute AR
• Peripheral vasoconstriction
• Pulmonary edema
• Arterial pulsus alternans; normal LV impulse
• Early mitral valve closure
• Early diastolic murmur (lower pitched and shorter than in
chronic AR) may be present.
• A murmur at the right sternal border is associated more
often with dissection than it is with any other cause of
Physical Examination – Chronic AR
• Manifestations of severe chronic AR are often the result
of widened pulse pressure because (1) elevated stroke
volume exists during systole and (2) the incompetent
aortic valve allows the diastolic pressure within the aorta
to fall significantly.
• On palpation, the point of maximal impulse may be
diffuse or hyperdynamic but is often displaced inferiorly
and toward the axilla. Peripheral pulses are prominent or
bounding. Auscultation may reveal an S3 gallop if LV
dysfunction is present.
• A diastolic thrill may be palpable along the left sternal
border in thin-chested individuals, and a prominent
systolic thrill may be palpable in the suprasternal notch
and transmitted upward along the carotid arteries.vitrag24-www.medicalgeek.com
• Early-Holo diastolic murmur, immediately after A2, usually as a
high-pitched blowing sound that is loudest at the left sternal border,
decrescendo, best heard in at end-expiration & in sitting & leaning
forward position. The duration of the murmur correlates better with
the severity of AR than does the loudness of the murmur.
• When the murmur is musical (cooing dove murmur), it usually
signifies eversion or perforation of an aortic cusp.
• The diastolic murmur of AR when well or predominantly heard in the
left axilla – Cole-Cecil murmur
• Harvey sign - When regurgitation is caused by primary valvular
disease, the diastolic murmur is heard best along the left sternal
border in the 3rd and 4th ICS. When it is caused mainly by dilation
of the ascending aorta, the murmur is often more readily audible
along the right sternal border.vitrag24-www.medicalgeek.com
• A functional systolic flow murmur may also be
present because of increased stroke volume, although
concurrent AS may also be present.
• An Austin-Flint murmur may be present at the cardiac
apex in severe AR; it is a low-pitched, mid-diastolic
rumbling murmur due to blood jets from the AR striking
the anterior leaflet of the mitral valve, which results in
premature closure of the mitral leaflets.
• A2 may be normal or accentuated when AR is caused by
disease of the aortic root but is soft or absent when the
valve is causing AR. P2 may be obscured by the early
diastolic murmur. Thus, S2 may be absent or single or
exhibit narrow or paradoxical splitting.
• A systolic ejection sound, presumably related to abrupt
distention of the aorta by the augmented stroke volume,
is frequently audible.
• A third heart sound (S3) correlates with an increased LV
end-diastolic volume. Its development may be a sign of
impaired LV function, which is useful in identifying
patients with severe AR who are candidates for surgical
• The auscultatory features of AR are intensified by
strenuous and sustained handgrip, which augments
systemic vascular resistance.
• Becker sign - Visible systolic pulsations of the retinal
• Corrigan pulse ("water-hammer" pulse) - Abrupt
distention and quick collapse on palpation of the
peripheral arterial pulse
• de Musset sign - Bobbing motion of the patient's head
with each heartbeat
• Hill sign – (Popliteal cuff systolic blood pressure 20 mm
Hg higher than brachial cuff systolic blood pressure) is
an artifact of sphygmomanometric measurements and is
no longer considered a sign of severe AR.
• Duroziez sign - Systolic murmur over the femoral artery
with proximal compression of the artery, and diastolic
murmur (Duroziez murmur) over the femoral artery with
distal compression of the arteryvitrag24-www.medicalgeek.com
• Müller sign - Visible systolic pulsations of the uvula
• Light-house sign – Alternate flushing & blanching of
• Landolfi’s sign - Change in pupil size with each systole
• Gerhardt’s sign - Visible systolic pulsations of spleen
• Rosenbach’s sign - Visible systolic pulsations of liver
• Corrigan’s sign – Dancing carotid in neck
• Quincke sign - Visible pulsations of the fingernail bed
with light compression of the fingernail
• Traube sign ("pistol-shot" pulse) - Booming systolic
and diastolic sounds auscultated over the femoral artery
• A bisferiens pulse in AS + AR – readily recognized in
the brachial and femoral arteries than in the carotid
arteries.(Two systolic waves separated by a trough )
Physical Examination …Cont’d
As heart failure develops, peripheral vasoconstriction
may occur and arterial diastolic pressure may rise, even
though severe AR is present, so pulse pressure can be
normal or narrow in severe AR.
Causes of AR with normal/low pulse pressure:
• Acute AR
• AR with AS or severe MS
• AR with CHF
• AR with systemic hypertension
• Assess severity by impact on peripheral signs and LV
• peripheral signs = severity
• LV = severity
• Long duration of diastlic murmur
• Austin –Flint murmur
• radiological cardiomegaly
Features AS > AR AR > AS
Anginal pain, blackout
Pulse Low volume
Pulse pressure Normal to low Wide
Peripheral signs +/- +
Apex Heaving Hyperdynamic
Thril Always systolic Rarely
S3 Absent May be present
S4 May be present Absent
Ejection click Present Rare
Diastolic murmur Very short Classic murmur of AR
Systolic murmur Classic murmur of AS Function systolic murmur
Chest X-Ray Calcification + Cardiomegaly
ECG Pressure overload Volume overloadvitrag24-www.medicalgeek.com
Hyperdynamic circulation (wide pulse pressure),
including the following:
• Severe anemia
• Thiamine deficiency (wet beriberi)
• Arteriovenous fistula - Such as patent ductus arteriosus
or peripheral arteriovenous malformations
• Volume depletion
• Sympathetic overdrive
• LV hypertrophy
• Left axis deviation
• Left atrial enlargement
• LV volume overload pattern - Prominent Q waves in
leads I, aVL, and V3 to V6 and relatively small r waves in
• LV conduction defects - Typically late in the disease
• Left-axis deviation and/or QRS prolongation denote
diffuse myocardial disease, generally associated with
patchy fibrosis, and usually signify a poor prognosis.
The patient’s 12-lead electrocardiogram shows normal sinus rhythm and a rate of 55
beats per minute. The frontal-plane QRS complex vector is deviated leftward. Left
atrial abnormality is present, given the terminally negative P wave in lead V1 and the
bifid P wave in lead II. Left ventricular volume overload is supported by the following
findings: increased QRS complex voltage, best seen in the precordial (chest) leads,
indicative of increased left ventricular mass; prominent septal depolarization, as
reflected by Q waves in leads V4 to V6; the absence of an ST-segment or T-wave
abnormality; and negative U waves in leads V4 to V6 (arrows).
Normal size LV with pulmonary
LVE with normal pulmonary
• In acute AR, there may be minimal cardiac enlargement,
but marked enlargement is a common finding in chronic
• The apex is displaced downward and to the left in the
frontal projection. In the left anterior oblique and lateral
projections, the LV is displaced posteriorly and
encroaches on the spine.
• Distinct left atrial enlargement in the absence of heart
failure suggests associated mitral valve disease.
• When AR is caused by primary disease of the aortic root,
aneurysmal dilation of the aorta may be noted, and the
aorta may fill the retrosternal space in the lateral view.
• Aortic valve structure and morphology - Bileaflet versus
trileaflet, flail, thickening
• Presence of vegetations or nodules - May require
transesophageal echocardiography in selected cases
• Severity of AR
• Color Doppler central jet width & Vena contracta
(narrowest portion of the jet located at or just distal to its
orifice) width - In severe AR, the vena contracta width is
usually more than 65% of the width of the LV outflow tract
• Regurgitant volume, fraction, and orifice area
• Premature closure of the mitral valve (seen in severe AR)
and opening of the aortic valve (with severely elevated LV
• Holodiastolic flow reversal in the descending thoracic or
• Pressure half-time - Usually less than 300-350 ms with
• Associated lesions of the aorta - Including dilation,
aneurysm, dissection, or ectasia
• A rapid, high-frequency diastolic fluttering of the anterior
mitral leaflet produced by the impact of the regurgitant jet
is a characteristic finding - it does not develop when the
mitral valve is rigid, as occurs with rheumatic
involvement. & unlike the Austin Flint murmur, occurs
even in mild AR
• LV structure and function, LV hypertrophy and dilation
• Ejection fraction (EF) and end-systolic dimension -
These are key determinants of outcome; surgery is
recommended if the EF is 50% or less or if the end-
systolic dimension is more than 55 mm
Color Flow – top mild, bottom moderate
Continuous Wave Doppler
Regurgitant jet width/LVOT diameter ratio
greater than or equal to 60 percent
Vena contracta greater than 6 mm
Regurgitant jet area/LVOT area ratio greater
than or equal to 60 percent
Class I indications for cardiac catheterization under
current ACC/AHA guidelines:
• Assessment of coronary anatomy prior to aortic valve
surgery in patients with risk factors for coronary artery
• Assessment of severity of AR, LV function, or aortic root
size when noninvasive tests are inconclusive or are
discordant with clinical findings
• Mild (1+) - A small amount of contrast enters the LV
during diastole and clears with each systole
• Moderate AR (2+) - Contrast enters the LV with each
diastole, but the LV chamber is less dense than the aorta
• Moderately severe AR (3+) - The LV chamber is equal in
density to the ascending aorta.
• Severe AR (4+) - Complete, dense opacification of the
LV chamber occurs on the first beat, and the LV is more
densely opacified than the ascending aorta
• CMR provides accurate measurements of regurgitant
volumes and the regurgitant orifice in AR. It is the most
accurate noninvasive technique for assessing LV end-
systolic volume, diastolic volume, and mass
• Provides AR regurgitant fraction and the LV/right
ventricular (RV) stroke volume ratio
• In the absence of mitral regurgitation and tricuspid
regurgitation, an LV/RV stroke volume ratio of 2.5 or
more denotes severe aortic regurgitation.
Management – Acute AR
• Prompt surgical intervention is indicated
• Administer a positive inotrope (eg, dopamine,
dobutamine) and a vasodilator (eg, nitroprusside).
• Administration of vasodilators may be appropriate to
improve systolic function and to decrease afterload.
• The administration of cardiac glycosides (eg, digoxin) for
rate control may in rare cases be necessary.
• Beta-blocking agents and intra-aortic balloon
counterpulsation are contraindicated, because either
lowering the heart rate or augmenting peripheral
resistance during diastole can lead to rapid
Management – Chronic MR
The current ACC/AHA guidelines say the following about
vasodilator therapy (Nifedipine, ACE Inhibitors):
• Vasodilator therapy is indicated for long-term treatment
in patients who have severe chronic AR and
symptoms of LV dysfunction but who are not
candidates for surgery.
• Vasodilator therapy is reasonable for short-term therapy
in patients with severe LV dysfunction and heart
failure symptoms, in order to improve their
hemodynamic profile before surgery
• Vasodilator therapy is acceptable for long-term therapy
in asymptomatic patients with severe AR and LV
dilation with normal EF
(To control diastolic BP)
• Chronic medical therapy for some patients who refuse
surgery or are considered to be inoperable because of
comorbid conditions - These patients should receive an
aggressive heart failure regimen with ACE inhibitors
(and perhaps other vasodilators), digoxin, diuretics,
and salt restriction; beta blockers may also be
• Although nitroglycerin and long-acting nitrates are not as
helpful in relieving anginal pain as they are in patients
with ischemic heart disease, they are worth a trial.
• Beta blockers (contraindicated in Valvular AR) and the
angiotensin receptor blocker, losartan, may be useful to
retard the rate of aortic root enlargement in young
patients with Marfan's syndrome and aortic root dilation.
• Avoid isometric exercises
• Avoidance of atrial fibrillation and bradycardia are
important as these are poorly tolerated
The prophylactic use of antibiotics prior to dental
procedures is no longer routinely recommended for all
patients with AR. Select patient groups for whom
prophylactic antibiotic therapy prior to dental procedures
may be reasonable include the following:
• Patients with prosthetic material in their heart - Such as
an artificial valve or a valve repaired with prosthetic
• Patients with prior infective endocarditis
• Patients who, following cardiac transplantation, have
valve regurgitation due to a structurally abnormal valve
• Patients with congenital heart disease (CHD) who meet
any of the following criteria: (1) Cyanotic CHD that has
not been repaired or has been incompletely repaired
(including patients with palliative shunts and conduits);
(2) repaired CHD using prosthetic material, for the first 6
months postprocedurally (ie, prior to endothelialization of
the material); or (3) repaired CHD but the patient is at
risk for inhibited endothelialization (ie, with residual
defects at or adjacent to the site of the prosthetic
Surgical treatment – ACC/AHA guideline summary
Class I - There is evidence and/or general agreement that aortic
valve replacement or repair (AVR) is indicated in patients with
chronic AR in the following settings
• Symptomatic patients with severe chronic AR, irrespective of left
ventricular ejection fraction (LVEF).
• If the presence of symptoms in patients with severe chronic AR is
equivocal, the development of symptoms during an exercise test.
• Asymptomatic patients with severe chronic AR and an LVEF ≤50
percent at rest.
• Patients with severe chronic AR who undergo coronary artery bypass
graft surgery (CABG) or surgery on the aorta or other heart valves.
The indications for surgery for patients with severe AR secondary to aortic
root disease are similar to those with primary valvular disease. However,
progressive expansion of the aortic root and/or a diameter more than 50 mm
by echocardiography with any degree of regurgitation in patients with a
bicuspid valve (or other connective tissue disorder) or with a diameter more
than 55 mm in other patients is also an indication for aortic root replacement
Class IIa - The weight of evidence or opinion is in favor of the
usefulness of AVR in patients with chronic AR in the following
• Asymptomatic patients with severe chronic AR and a normal LVEF
(LVEF >50 percent) who have severe left ventricular dilatation (end-
diastolic dimension >75 mm or end-systolic dimension >55 mm).
Lower threshold values can be considered for patients of small stature.
Class IIb - The weight of evidence or opinion is less well
established for the usefulness of AVR in patients with chronic AR
in the following settings
• Patients with moderate chronic AR who undergo CABG or surgery
on the ascending aorta.
• Asymptomatic patients with severe chronic AR and an LVEF >50
percent in whom the end-diastolic dimension is >70 mm or the end-
systolic dimension is >50 mm, and there is evidence of progressive left
ventricular dilatation, declining exercise tolerance, or an abnormal
hemodynamic response to exercise.
ACC/AHA guideline summary: Criteria for selection of an aortic valve in
patients undergoing aortic valve replacement (AVR)
• A mechanical valve in patients who already have a mechanical valve in the
mitral or tricuspid position.
• A bioprosthetic valve in patients who will not take or are incapable of taking
warfarin or have a major contraindication to warfarin therapy.
• A bioprosthesis in patients ≥65 years of age who do not have risk factors for
• Patient preference can be considered in patients less than 65 years of age:
1. A mechanical valve is reasonable in patients who do not have a contraindication
to warfarin therapy.
2. A bioprosthetic valve may be chosen after a detailed discussion of the risks of
warfarin therapy compared to the likelihood of repeat valve replacement in the
• A homograft when aortic valve re-replacement is performed for active prosthetic
• A bioprosthesis in women of child-bearing age to avoid the problems associated
anticoagulation during pregnancy.
Figure 29-15 A. Björk-Shiley Monostrut
mechanical prosthesis. B. Sorin Allcarbon
monoleaflet mechanical prosthesis.
C. Medtronic-Hall mechanical prosthesis.
D. Omnicarbon mechanical prosthesis.
Figure 29-16 A. Carpentier-Edwards Supra-
annular porcine bioprosthesis. B. Hancock II
porcine bioprosthesis. C. Hancock modified
orifice porcine bioprosthesis. D. St. Jude
Medical Bioimplant porcine bioprosthesis.vitrag24-www.medicalgeek.com
Surgery – Primary Root disease
• Annuloplasty or other valve sparing surgery
Transcatheter aortic valve replacement
• TAVR involves the implantation of a bioprosthetic aortic
valve using a catheter that is inserted peripherally,
typically through the femoral artery, and implanted
without requiring a median sternotomy (ie, without ―open
heart surgery‖). Initial reports are promising but further
studies are needed before TAVR becomes clinically
• If MS + AR, first go for AR as correcting MS will increase
LV load LVF.
Long term monitoring
• All patients with an artificial heart valve should receive
antibiotic prophylaxis prior to dental procedures. For
antithrombotic therapy, all patients with an artificial heart
valve should receive daily aspirin, and many should also
receive oral anticoagulation therapy with warfarin
according to the ACC/AHA guidelines.
• After the initial study, clinical evaluation and a repeat
echocardiogram are recommended in 3 months. The
recommended frequency of subsequent follow-up
evaluations is based on the stability of the LVESD and
LVEDD – every 3 to 12 months.
• Death usually occurs within 4 yrs after onset of angina
pectoris and within 3 yrs of onset of heart failure
• It is imperative to intervene before irreversible LV
• After AVR, Long term results reveal 80-90% three year
survival in patients with preserved LV function, and 40-
60% three year survival in patients with poor LV function
• Mortality rate of AVR ranges from 3-8%
American Heart Association & American College of
Cardiology Guidelines (http://www.cardiosource.org)
Harrison’s PRINCIPLES OF INTERNAL MEDICINE :
Braunwald's Heart Disease : A Textbook of
Cardiovascular Medicine : Ninth Edition
Hurst's the Heart Manual of Cardiology, Thirteenth