VALVULAR HEART DISEASE

Desalew Mekonnen, MD
Consultant Internist and Cardiologist
Associate Professor of Medicine
Surface Anatomy of the Heart

2
3
4
 Introduction
Rheumatic disease is the most common cause of valve
disease worldwide, especially in the young, with an
estimated prevalence of 15.6 to 19.6 million.

In industrially developed regions valve diseases of old

age predominate, particularly calcific aortic stenosis and
functional mitral regurgitation.

Infective endocarditis is increasingly related to medical

devices and intravenous drug use.
Failure of biological replacement valves is a major
burden in all regions of the world.

Substantial variation in access to health care exists in

all countries, including those that are industrially
developed.

The main global challenge is to prevent chronic

rheumatic disease, which will require collaborations
among social, political, and medical programs.
Distribution of the aetiologies of native single-valve diseases in the
Euro Heart Survey on valvular heart disease
Mitral Valve Disease
 The Mitral Valve Apparatus
Mitral Leaflets:
Bileaflet valve
Anterior Leaflet
 In fibrous continuity w/ non-coronary
cusp
 Dual Blood Supply

Posterior Leaflet
 Single blood supply
Chordae Tendineae
Papillary Muscles
Anteriormedial
Posterior lateral
Mitral Annulus
Time-course analysis (by decades) of the relative prevalence of mitral valve disease
 MITRAL STENOSIS (ETIOLOGY)
 Rheumatic fever is the leading cause of mitral stenosis (MS) although only
50 to 70 percent of patients report a history of rheumatic fever

o In rheumatic MS, the valve leaflets are diffusely thickened by fibrous tissue
and/or calcific deposits. The mitral commissures fuse, the chordae tendineae
fuse and shorten, the valvular cusps become rigid, and these changes, in
turn, lead to narrowing at the apex of the funnel-shaped ("fish-mouth") valve

o Calcification of the stenotic mitral valve immobilizes the leaflets and narrows
the orifice further
 MITRAL STENOSIS (ETIOLOGY)
Other less common causes
o Congenital mitral valve stenosis
o Cor triatriatum
o Mitral annular calcification with extension onto the leaflets
(degenerative)
o Left atrial myxoma
o Infective endocarditis with large vegetations
o Carcinoid heart disease
o Endomyocardial fibrosis
o Systemic lupus erythematosus
o Rheumatoid arthritis
 PATHOPHYSIOLOGY OF MS
The primary hemodynamic consequence of MS is a pressure gradient
between the left atrium and left ventricle in diastole
The elevated left atrial pressure is reflected backward, causing an increase
in pulmonary venous, capillary, and arterial pressures and resistance
With mild to moderate MS, these abnormalities are often only apparent
with exercise or other conditions that increase heart rate; they eventually
are seen at rest as the severity of the stenosis increases
An increase in heart rate shortens diastole proportionately more than
systole and diminishes the time available for flow across the mitral valve.
Therefore, at any given level of CO, tachycardia including that associated
with AF augments the transvalvular pressure gradient and elevates further
the LA pressure
The LV diastolic pressure and ejection fraction (EF) are normal in isolated
MS
 CARDIAC OUT PUT AND PULMONARY HYPERTENSION IN MS
In patients with moderate MS (mitral valve orifice 1.0 cm2–1.5 cm2), the
CO is normal or almost so at rest but rises subnormally during
exertion. In patients with very severe MS (valve area <1.0 cm2),
particularly those in whom pulmonary vascular resistance is markedly
elevated, the CO is subnormal at rest and may fail to rise or may even
decline during activity
Pulmonary hypertension results from:
1. Passive backward transmission of the elevated LA pressure
2. Pulmonary arteriolar constriction, which presumably is triggered by
LA and pulmonary venous hypertension (reactive pulmonary
hypertension)
3. Interstitial edema in the walls of the small pulmonary vessels
4. Organic obliterative changes in the pulmonary vascular bed
 MS: Natural History
Chronic Slow but Progressive Narrowing of MV Orifice
RHD
(MS)

Normal Mild Moderate Severe

MVO MS MS MS
Strep
Throat Death
< 5 mm Hg 5-10 mm Hg >10 mm Hg
& ARF
4-6 2.0 1.5 1.0
cm2 cm2 cm2 cm2
Asymptomatic phase Symptomatic phase
(lasts decades) (lasts 5 -10 yrs)
 SYMPTOMS OF MS
The interval between the episode of rheumatic fever and the clinical presentation of MS varies
geographically, ranging from as little as a few years in countries with a high prevalence of
rheumatic fever to 20 years in countries where rheumatic fever is rare
Dyspnea, cough,orthopenia and PND
Palpitation (the development of permanent AF often marks a turning point in the patient's
course and is generally associated with acceleration of the rate at which symptoms progress)
Hemoptysis
Hoarsness
Thromboembolism: Systemic embolization, the incidence of which is 10–20%, occurs more
frequently in patients with AF(over 80 percent of patients with MS who have an embolism are
in AF), in older patients, and in those with a reduced CO. However, systemic embolization may
be the presenting feature in otherwise asymptomatic patients with only mild MS
Chest pain: infrequent
Infective endocarditis: this complication is primarily associated with mild mitral stenosis when
the valve is stiff and fibrotic. Endocarditis is uncommon once the valve becomes calcified and
very rigid
Right sided HF
 PHYSICAL FINDINGS (INSPECTION AND PALPATION)
The arterial pulses are reduced in volume due to the decreased stroke volume
When MS is severe and the cardiac output is diminished, there is vasoconstriction,
resulting in pinkish-purple patches on the cheeks (mitral facies)
Pulmonary hypertension and right ventricular hypertrophy can lead to a
prominent "a" wave (atrial contraction or systole) in jugular venous pulsations,
reflecting elevated right atrial pressure. The "a" wave is absent in patients with AF
and only a prominent "v" wave (atrial filling during ventricular systole when the
tricuspid valve is closed) is seen. If present, tricuspid regurgitation can lead to a
prominent "c-v" wave (reflecting regurgitation of blood into the right atrium) and
the neck veins are very pulsatile
Precordial examination reveals an apical impulse that is generally normal, although
it may be reduced in intensity, reflecting the decreased left ventricular filling.
However, if pulmonary hypertension is present, there may be a right ventricular
heave (substernal lift) and a palpable S2
An apical diastolic thrill can be appreciated as well
 PHYSICAL FINDINGS (AUSCULTATION)
 S1 (the first heart sound (S1) is loud, reflecting the increased excursion of the
leaflets . As the leaflets become more rigid and calcified, their motion is limited and S1
becomes soft)
 P2
Opening snap (OS): it is most prominent at the apex and is due to the abrupt halt in
leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the
leaflet tips.The time interval between A2 and OS varies inversely with the severity of
the MS
Diastolic murmur: is a low-pitched diastolic rumble that is most prominent at the
apex. It is heard best in a quiet room with the patient lying on the left side in held
expiration and by using the bell of the stethoscope. Although the intensity of the
diastolic murmur does not correlate with the severity of the stenosis, the duration of
the murmur is helpful since it reflects the transvalvular gradient and the duration of
blood flow across the valve.When the CO is markedly reduced in MS, the typical
auscultatory findings, including the diastolic rumbling murmur, may not be detectable
(silent MS), but they may reappear as compensation is restor
 PHYSICAL FINDINGS (AUSCULTATION)
With severe pulmonary hypertension, a pansystolic murmur
produced by functional TR may be audible along the left sternal
border. This murmur is usually louder during inspiration and
diminishes during forced expiration (Carvallo's sign)
The Graham Steell murmur of PR, a high-pitched, diastolic,
decrescendo blowing murmur along the left sternal border, results
from dilatation of the pulmonary valve ring and occurs in patients
with mitral valve disease and severe pulmonary hypertension
Murmurs of mitral or aortic regurgitation may also be present if
these valve lesions coexist with MS
 DDx FOR MS MURMUR
MR (due to increased flow)

Austin flint murmur

Tricusoid stenosis (rarely in the absence of MS)

Atria septal defect

Atrial myxoma (auscultatory findings may change markedly with

body position and patients will have systemic manifestations)
 ECG FINDINGS IN MS
M-mitrale: P wave that becomes broader (duration in lead
II>0.12 sec), is of increased amplitude, and is notched

P-pulmonale

Right axis deviation and right ventricular hypertrophy:

the frontal axis shifts to the right (S>R in lead I and aVL) and a
tall R wave develops in V1 and V2 (R>S or R/S ratio >1)
 CXR FINDINGS IN MS
 Left atrial enlargement
o A "double density"
o The left heart border becomes straightened
o The left bronchus is elevated
o On the lateral projection, the left atrium is displaced posteriorly, impinging
on the esophagus
 Pulmonary vascular congestion
o Redistribution or "cephalization" of pulmonary blood flow to the upper lobes
o Dilated pulmonary vessels,
o Kerley B lines at the bases, and interlobar effusions (Kerley C lines)
o In more severe cases, Kerley A lines (straight dense lines running toward the
hilum)
CXR: LA enlargement and pulmonary
congestion
 ECHOCARDIOGRAPHY IN MS
The mitral leaflets are thickened, have reduced motion during
diastole, and show doming
The mitral valve area can be accurately measured by planimetry in
short axis views
Estimates of leaflet motion, the degree of calcification and fibrosis
of the leaflets, and assessment of the subvalvular apparatus can
help establish the role for surgical or balloon valvotomy
Left atrial size, and left and right ventricular size and systolic
function can be assessed
Vegetations
Left atrial thrombus
ECHOCARDIOGRAPHY IN MS
Mitral Stenosis Doming
MS Planimetry
ECHOCARDIOGRAPHIC ASSESSEMENT OF SEVERITY OF
MS IN ADULTS
New Severity Assessment
 Assessment of mitral valve anatomy according to the
Wilkins score

The total score is the sum of the four items and ranges between 4 and 16. A score of 8 or less
is usually associated with an excellent immediate and long-term result, whereas scores
exceeding 8 are associated with less impressive results including the risk of development of
MR
 OTHER INVESTIGATIONS IN MS
Stress ECHO

Cardiac catheterization

MRI

Base line investigations (CBC, RFT, electrolytes)

Coagulation profile
 MEDICAL MANAGEMENT OF MS
Avoid strenous exercise and physical activity
Diuretcs: in combination with salt restriction, is appropriate
when there are manifestations of pulmonary vascular congestion
and right sided HF
Digoxin: indicated if and only if there is atrial fibrilation with
fast ventricular responce and right sided HF
Secondary prevention of rheumatic fever
Prevention of endocarditis
Prevention of thromboembolism
Management of AF
 SURGICAL MANAGEMENT OF MS

Unfavourable clinical characteristics: old age,history of commissurotomy,NYHA class IV,atrial fibirilation,severe

pulmonary hypertension
High risk of embolism or hemodynamic decompensation: previous history of embolism,dense spontaneous
contrast in the LA,recent or paroxysmal AF,PAP>50 at rest,need for non-major cardiac surgery and desire of
pregnancy
CONTRAINDICATIONS TO PERCUTANEOUS MITRAL
COMMISSUROTOMY (PMC)
Long term prediction after PMBC in different patient scenario
 VALVULAR HEART DISEASE
MITRAL REGURGITATION
MITRAL VALVE ANATOMY
 ETHIOLOGY OF MR

Rheumatic heart disease is the cause of chronic MR in only about one-third of cases
and occurs more frequently in males. The rheumatic process produces rigidity,
deformity, and retraction of the valve cusps and commissural fusion, as well as
shortening, contraction, and fusion of the chordae tendineae
"mitral regurgitation begets mitral regurgitation’’
 PATHOPHYSIOLOGY OF MR
The resistance to LV emptying (LV afterload) is reduced in patients with
MR. As a consequence, the LV is decompressed into the LA during
ejection, and with the reduction in LV size during systole, there is a
rapid decline in LV tension
The initial compensation to MR is more complete LV emptying.
However, LV volume increases progressively with time as the severity of
the regurgitation increases and as LV contractile function deteriorates
This increase in LV volume is often accompanied by a reduced forward
CO, though LV compliance is often increased and thus LV diastolic
pressure does not elevate until late in the course
Since ejection fraction (EF) rises in severe MR in the presence of normal
LV function, even a modest reduction in this parameter (<60%) reflects
significant dysfunction
 PATHOPHYSIOLOGY OF MR
In acute severe MR, the regurgitant volume is delivered into a
normal-sized LA having normal or reduced compliance. As a
result, LA pressures rise markedly for any increase in LA volume.
LA and pulmonary venous pressures are markedly elevated, and
pulmonary edema is common
Patients with chronic severe MR, on the other hand, develop
marked LA enlargement and increased LA compliance with little
if any increase in LA and pulmonary venous pressures for any
increase in LA volume. These patients usually complain of severe
fatigue and exhaustion secondary to a low CO, while symptoms
resulting from pulmonary congestion are less prominent initially
 SYMPTOMS OF MR
Patients with chronic mild-to-moderate isolated MR are usually
asymptomatic
Fatigue, exertional dyspnea, and orthopnea are the most
prominent complaints in patients with chronic severe MR.
Palpitations are common and may signify the onset of AF
Right-sided heart failure, with painful hepatic congestion, ankle
edema, distended neck veins, ascites, and secondary TR, occurs
in patients with MR who have associated pulmonary vascular
disease and marked pulmonary hypertension
On the other hand, acute pulmonary edema is common in
patients with acute severe MR
 PHYSICAL FINDINGS IN ACUTE MR
The patient with acute MR is often in pulmonary edema and there is evidence of poor tissue
perfusion with peripheral vasoconstriction, pallor, and diaphoresis
The arterial pulse is often rapid and of low amplitude or thready due to the reduction in
forward output. When there is an associated increase in right-sided pressure, the neck veins
become distended; they may also become pulsatile with a marked "v" wave if the elevated
right ventricular pressure leads to tricuspid regurgitation
The cardiac impulse is hyperdynamic but is usually normal in location because left
ventricular size is normal. If, however, acute regurgitation is superimposed upon chronic MR,
the cardiac impulse may be displaced due to the underlying left ventricular enlargement
There is often a hyperdynamic precordium with a right ventricular lift due to the acute
increase in pressure within this chamber
The murmur of acute mitral regurgitation may be early, midsystolic, or holosystolic. However,
since the pressure within the left atrium markedly increases during ventricular systole and
the pressure gradient between the left atrium and ventricle diminishes or disappears by the
end of systole, the systolic murmur is often soft, low pitched and decrescendo, ending before
well before S2.When present, the murmur is often best heard along the left sternal border
and base of the heart, generally without a thrill, and may radiate to the back
 PHYSICAL FINDINGS IN ACUTE MR
An S3 is commonly heard but may be difficult to appreciate if tachycardia
is present
With the development of pulmonary hypertension, P2 is increased in
intensity and the murmurs of pulmonary and tricuspid regurgitation may
be appreciated
Approximately 50 percent of patients with moderate to severe MR have no
audible murmur, particularly those with acute ischemic MR
The presumed mechanism of silent MR is a relatively low pressure
gradient in systole between the left ventricle and left atrium due to the
combination of a low systemic blood pressure and elevated left atrial
pressure. In addition, acoustic transmission of the murmur may be
obscured by obesity and respiratory distress. Thus, the absence of a
systolic murmur does not reliably exclude the diagnosis of acute severe
MR
 PHYSICAL FINDINGS IN CHRONIC MR
In chronic MR, the arterial pulse may be reduced in volume, but is usually brisk in upstroke,
reflecting the increased ejection rate and normal ejection fraction. Since there is a rapid
reduction in the volume of forward flow late in systole and therefore a decrease in ejection time,
the arterial pulse falls off rapidly, giving the impression of a bounding pulse, similar to that seen
with aortic regurgitation. However, the pulse pressure is normal with mitral regurgitation
Enlargement of the left ventricle results in a leftward displacement of the apical impulse; it is
usually brisk or hyperdynamic. When the mitral regurgitation is severe or when there has been
an acute exacerbation of the regurgitation as a result of a chordal rupture, a thrill and an S3 may
be palpable. Signs of right-sided congestive heart failure are typically absent unless there is
associated mitral stenosis or the MR is of long standing and is very severe
S1 is diminished, reflecting failure of the mitral leaflets to close properly
Wide splitting of S2 is not infrequent because the decrease in left ventricular ejection time
results in an early A2.Furthermore, if pulmonary hypertension is present, P2 will be increased
and delayed, further widening the splitting of S2.
The augmented flow rate across the mitral valve orifice into a dilated left ventricle produces an
S3 gallop, which becomes particularly prominent if left ventricular failure occurs (it is a sign of
severe MR)
 PHYSICAL FINDINGS IN CHRONIC MR

The murmur of chronic MR is holosystolic, commencing immediately after S1 and continuing up to and
sometime beyond and obscuring A2, a result of the persistent pressure gradient between the left ventricle
and atrium

The murmur is heard best over the apex, radiating to the axilla and when very loud may often radiate to the
back. It is most often blowing and high pitched in quality

However, in patients with ruptured chordae tendineae or primary involvement of the posterior mitral leaflet
with prolapse or flail, the regurgitant jet is eccentric, directed anteriorly, and strikes the LA wall adjacent to
the aortic root. In this situation, the systolic murmur is transmitted to the base of the heart and therefore
may be confused with the murmur of AS

There is a variable correlation between murmur grade and regurgitant severity with primary mitral valve
disease. A loud murmur associated with a thrill (grade 4 or greater) has a specificity of 91 percent for
severe regurgitation, but a sensitivity of only 24 percent . Conversely, severe regurgitation is rarely present
with a grade 1-2 murmur. However, there is a wide range of regurgitant severity with a grade 3 murmur
(which is common)

In contrast, the loudness of the murmur does not necessarily correlate with severity in secondary
(functional) MR. In addition, among patients acute MR due to ischemia, moderate to severe regurgitation is
often silent or associated with only a soft murmur due to equalization of left ventricular and left atrial
pressure

Infrequently, the large diastolic volume across the mitral valve produces an early diastolic murmur

In patients with ruptured chordae tendineae, the systolic murmur may have a cooing or "sea gull" quality,
while a flail leaflet may cause a murmur with a musical quality
 INVESTIGATIONS
ECG: LA enlaregement,LVH and if they develop
pulmonary hypertension RA enlargement and RVH
can be seen
CXR: the most common finding on the chest radiograph is
cardiomegaly, resulting from enlargement of the left ventricle
and left atrium
ECHO: echocardiography is essential for establishing the
etiology and hemodynamic consequences of mitral regurgitation
.Other important features on echocardiography are evaluation of
the left atrium, left ventricle, and pulmonary artery pressures
Cardiac catheterization and angiography 
Mitral Regurgitation
 MEDICAL MANAGEMENT OF MR
The management of chronic severe MR depends to some degree on its cause
There are no published studies that support the hypothesis that vasodilator therapy is beneficial
in asymptomatic patients with isolated chronic MR
In symptomatic patients with primary MR (eg, myxomatous or rheumatic), there is little
potential to induce a change in the regurgitant orifice area via preload reduction and the
therapeutic goal should be a reduction in systolic pressure. Thus, a beta blocker, diuretic,
hydralazine, or calcium channel blocker should be used. However, medical therapy is not a
substitute for surgical intervention in patients with chronic symptomatic MR.
Chronic vasodilator therapy is indicated in symptomatic patients who are not candidates for
surgery. The evidence of benefit is best in patients with secondary (functional) MR due to left
ventricular dysfunction. Treatment of such patients should consist of optimal medical therapy of
heart failure and, in appropriate patients, cardiac resynchronization therapy. With respect to ACE
inhibitors and/or angiotensin II receptor blockers, the dose titration and monitoring schedules are
the same as for heart failure due to left ventricular systolic dysfunction in the absence of
moderate to severe MR
Patients with acute severe MR require urgent stabilization and preparation for surgery. Diuretics,
intravenous vasodilators (particularly sodium nitroprusside), and even intraaortic balloon
counterpulsation may be needed for patients with post-MI papillary muscle rupture or other
forms of acute severe MR
SURGICAL MANAGENET OF CHRONIC SEVERE MR
Aortic Valve
Semilunar Valvular
Disorders
Disorders
Grant’s Atlas of Anatomy 9th edition 1991
-The noncoronary cusp is in fibrous continuity with the anterior leaflet of the mitral valve
Each cusp has:
Fibrous nodule at the free edge
Thin connective tissue area, the lunula, to each side
Closed valve: nodules and lunulae meet

Grant’s Atlas of Anatomy 9th edition 1991

VALVULAR HEART DISEASE
AORTIC STENOSIS
 ETIOLOGY
Rheumatic heart disease
o Rheumatic AS is almost always associated with involvement of the
mitral valve and with AR
o Worldwide, rheumatic valve disease is the most common cause of AS
• Congenital (bicuspid,unicaspid)
o The congenitally affected valve may be stenotic at birth and may
become progressively more fibrotic, calcified, and stenotic
o In other cases the valve may be congenitally deformed, usually
bicuspid [bicuspid aortic valve (BAV)], without serious narrowing of
the aortic orifice during childhood; its abnormal architecture makes
its leaflets susceptible to otherwise ordinary hemodynamic stresses,
which ultimately lead to valvular thickening, calcification, increased
rigidity, and narrowing of the aortic orifice
 ETIOLOGY
 Age-related degenerative calcific AS (also known as senile or sclerocalcific AS)
o It is now the most common cause of AS in adults in North America and Western
Europe
o About 30% of persons >65 years exhibit aortic valve sclerosis; many of these
have a systolic murmur of AS but without obstruction, while 2% exhibit frank
stenosis
o Aortic sclerosis appears to be a marker for an increased risk of coronary heart
disease events
o On histologic examination these valves frequently exhibit changes similar to
those seen with atherosclerosis and vascular inflammation
o Interestingly, risk factors for atherosclerosis, such as age, male sex, smoking,
diabetes mellitus, hypertension, chronic kidney disease, increased LDL, reduced
HDL cholesterol, and elevated C-reactive protein are all risk factors for aortic
valve calcification
 PATHOPHYSIOLOGY
When AS becomes hemodynamically significant, it results in obstruction to left
ventricular ejection
The stenotic process is gradual in onset and progression, resulting in adaptive changes in
the left ventricle
The increased systolic pressure in the ventricular chamber, leads to concentric
hypertrophy as a mechanism to maintain normal wall stress
AS is rarely of clinical importance until the valve orifice has narrowed to approximately 1.0
cm2. Even severe AS may exist for many years without producing any symptoms because
of the ability of the hypertrophied LV to generate the elevated intraventricular pressures
required for a normal stroke volume
However, as stenosis severity and hypertrophy continue to progress, the left ventricle
becomes less compliant and left ventricular end-diastolic pressure can become elevated
even though the ventricular size remains normal. Abnormal diastolic function contributes
to symptom onset and may persist after relief of stenosis due to persistent interstitial
fibrosis. Another contributing factor to the reduction in ventricular function is
incoordinate contraction, resulting from regional wall motion abnormalities, fibrosis, or
subendocardial ischemia
 SYMPTOMS OF AS
Dyspnea: results primarily from elevation of the pulmonary capillary
pressure caused by elevations of LV diastolic pressures secondary to
reduced left ventricular compliance
Diziness and Syncope
o Exercise-induced vasodilation in the presence of an obstruction with
fixed cardiac output can result in hypotension
o A transient bradyarrhythmia that can occur during or immediately
after exertion
o Abnormalities in the baroreceptor response with an ensuing failure
to appropriately increase the blood pressure
o An arrhythmia, such as atrial fibrillation; ventricular arrhythmias
are uncommon
 SYMPTOMS OF AS
 Angina
o Increased left ventricular oxygen demand as a result of increased left ventricular
o Compression of intramyocardial coronary arteries from prolonged contraction and impaired
myocardial relaxation
o Reduced diastolic coronary perfusion time during tachycardia
o Accompaning coronary artery disease
 Since the CO at rest is usually well maintained until late in the course, marked fatigability,
weakness, peripheral cyanosis, cachexia, and other clinical manifestations of a low CO are usually
not prominent until this stage is reached.
 Orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema, i.e., symptoms of LV failure,
also occur only in the advanced stages of the disease.
 Severe pulmonary hypertension leading to RV failure and systemic venous hypertension,
hepatomegaly, AF, and TR are usually late findings in patients with isolated severe AS
 When AS and MS coexist, the reduction in CO induced by MS lowers the pressure gradient across
the aortic valve and thereby masks many of the clinical findings produced by AS
 Atrial fibrillation (AF), which is uncommon in isolated AS, often accompanies HF. AF can be life-
threatening in severe AS because the loss of atrial contraction and the rapid heart rate both limit
diastolic filling of the small, stiff left ventricle
 PHYSICAL FINDINGS IN AS
Pulse character: "parvus et tardus“
Carotid thrill
The cardiac impulse at the apex is sustained and is initially
normal in location. However, it becomes displaced late in the
course of AS when left ventricular failure occurs
Some patients have a palpable fourth heart sound (S4) due to
vigorous left atrial contraction into the noncompliant ventricle
A systolic thrill may be felt at the base of the heart (second
intercostal space) or at the sternal notch, especially during full
expiration with the patient leaning forward
 PHYSICAL FINDINGS IN AS
Soft S2,Paradoxical S2 split,Ejection click,S4 gallop
S3 generally occurs late in the course, when the LV dilates
The murmur of AS is characteristically an ejection (mid) systolic murmur that commences
shortly after the S1, increases in intensity to reach a peak toward the middle of ejection, and
ends just before aortic valve closure. It is characteristically low-pitched, rough and rasping in
character, and loudest at the base of the heart, most commonly in the second right intercostal
space. It is transmitted upward along the carotid arteries (the murmur is transmitted well
and equally to the carotid arteries. Diminished intensity in one carotid artery may indicate
the presence of a stenosis in that vessel)
The murmur may also radiate to the apex of the heart where it may have a different quality
(musical due to high frequency vibrations) and may be louder, suggesting that the patient
also has mitral regurgitation. This is known as the Gallavardin phenomenon. Another finding
that has led to the misperception of two murmurs with different etiologies is that the
murmur is often softer or even inaudible in the chest area between the apex and base
In almost all patients, AS is associated with a small degree of aortic regurgitation since the
stiff, calcified, and rigid aortic valve leaflets may not coapt normally
The duration and intensity of AS murmur has correlation with severity of AS
 INVESTIGATIONS
ECG: LV hypertrophy and in advanced cases, ST-segment depression and T-wave
inversion (LV "strain")
ECHO: LVH,nature of the valve,severity grading,LV function,etiology of the
AS,complications of AS,concomitant other valvular lesions
CXR
 The chest x-ray may show no or little overall cardiac enlargement for many years
 Hypertrophy without dilatation may produce some rounding of the cardiac apex in
the frontal projection and slight backward displacement in the lateral view
 Aortic calcification is usually readily apparent on fluoroscopic examination or by
echocardiography; the absence of valvular calcification in an adult suggests that
severe valvular AS is not present
 In later stages of the disease, as the LV dilates there is increasing roentgenographic
evidence of LV enlargement, pulmonary congestion, and enlargement of the LA, PA,
and right side of the heart
CT/MRI scan
Cardiac catheterization
SEVERITY OF AS IN ADULTS (BASED ON ECHO)
New approach: Severity Assessment
Natural history of asymptomatic AS
 MEDICAL TREATMENT OF AS
In patients with severe AS (<1.0 cm2), strenuous physical activity should be avoided, even in the
asymptomatic stage
Care must be taken to avoid dehydration and hypovolemia to protect against a significant
reduction in CO
Medications used for the treatment of hypertension or CAD, including beta blockers and ACE
inhibitors, are generally safe for asymptomatic patients with preserved left ventricular systolic
function
 Most medical interventions carry the risk of destabilizing patients with severe or symptomatic
AS:
 Diuretics reduce preload, on which the patient may depend for maintenance of cardiac output.
Vasodilators in the presence of a fixed valvar stenosis may reduce systemic blood pressure and
reduce coronary artery perfusion pressure. Positive inotropic agents such as dobutamine must
be used with caution; tachycardia (with reduced cardiac output) and myocardial ischemia (due
to increased oxygen demand) may occur
Nitroglycerin is helpful in relieving angina pectoris
Retrospective studies have shown that patients with degenerative calcific AS who receive HMG-
CoA reductase inhibitors ("statins") exhibit slower progression of leaflet calcification and aortic
valve area reduction than those who do not
 SURGICAL MANAGEMENT OF AS

AVR is carried out in asymptomatic patients with severe or moderately severe stenosis who
undergo coronary artery bypass grafting, surgery of ascending aorta or another valve as
well.
 Long-term outcome after aortic valve replacement in aortic stenosis.

Relative survival after aortic valve replacement in operative survivors by age.

 VALVULAR HEART DISEASE
AORTIC REGURGITATION
MAJOR CAUSES OF AR
 PATHOPHYSIOLOGY OF AR
All forms of AR produce a similar hemodynamic abnormality
The inability of the aortic valve leaflets to remain closed or coapted during diastole
results in a portion of the left ventricular stroke volume leaking back from the aorta
into the left ventricle
The added volume of regurgitant blood produces an increase in left ventricular end-
diastolic volume; according to Laplace's law, the increase in left ventricular end-diastolic
volume causes an elevation in wall stress. Chronic AR is thus a state in which LV
preload and afterload are both increased
The heart responds with compensatory myocardial hypertrophy, which returns wall
stress toward normal
At autopsy the hearts of these patients may be among the largest encountered,
sometimes weighing >1000 g
In patients with acute severe AR, the LV is unprepared for the regurgitant volume load.
LV compliance is normal or reduced, and LV diastolic pressures rise rapidly, occasionally
to levels >40 mmHg. The LV pressure may exceed the LA pressure toward the end of
diastole, and this reversed pressure gradient closes the mitral valve prematurely
 SYMPTOMS OF AR
Patients with AR may remain asymptomatic for decades (as long as 10–15 years), even if there is
progressive ventricular dilatation. If, however, there is a large regurgitant volume, the patient
may complain of symptoms related to the increased mass of the enlarged left ventricle. These
include:
o A sense of pounding and an uncomfortable awareness of the heartbeat. These symptoms are
especially pronounced when lying down or lying on the left side which brings the left
ventricular apex closer to the chest wall, augmenting the sensation during systolic contraction
o Atypical chest pain induced by a mechanical interaction between the heart and the chest wall
o Palpitations due to tachycardia or premature beats
o Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal
dyspnea, and eventual pulmonary edema) occur in the presence of left ventricular dysfunction
o Angina pectoris is uncommon with isolated AR, since the coronary arteries are typically dilated
o In patients with acute severe AR, as may occur in infective endocarditis, aortic dissection, or
trauma, the LV cannot dilate sufficiently to maintain stroke volume, and LV diastolic pressure
rises rapidly with associated marked elevations of LA and PA wedge pressures. Pulmonary
edema and/or cardiogenic shock may develop rapidly
 PHYSICAL FINDINGS OF AR (ARTERIAL PULSE)
The arterial pulse pressure is widened, and there is an elevation of the systolic pressure,
sometimes to as high as 300 mmHg, and a depression of the diastolic pressure
The level of cuff pressure at the time of muffling of the Korotkoff sounds (Phase IV)
generally corresponds fairly closely to the true intraarterial diastolic pressure
“Water-hammer" or Corrigan's pulse
deMusset's sign — A head bob occurring with each heart beat
Traube's sign — A pistol shot pulse (systolic and diastolic sounds) heard over the femoral
arteries
Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially
compressed
Quincke's pulses — Capillary pulsations in the fingertips or lips
Mueller's sign — Systolic pulsations of the uvula
Becker's sign — Visible pulsations of the retinal arteries and pupils
Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60
mmHg
Mayne's sign — More than a 15 mmHg decrease in diastolic blood pressure with arm
elevation from the value obtained with the arm in the standard position
Rosenbach's sign — Systolic pulsations of the liver
Gerhard's sign — Systolic pulsations of the spleen
 PHYSICAL FINDINGS OF AR (PALPATION)
The LV impulse is heaving and displaced laterally and inferiorly
The systolic expansion and diastolic retraction of the apex are
prominent
A diastolic thrill is often palpable along the left sternal border,
and a prominent systolic thrill may be palpable in the
suprasternal notch and transmitted upward along the carotid
arteries. This systolic thrill and the accompanying murmur do
not necessarily signify the coexistence of AS
In many patients with pure AR or with combined AS and AR,
the carotid arterial pulse is bisferiens, i.e., with two systolic
waves separated by a trough
 PHYSICAL FINDINGS OF AR (AUSCULTATION)
The aortic valve closure sound (A2) is usually absent
An S3 and systolic ejection sound are frequently audible, and occasionally an S 4 also may be heard
The murmur of chronic AR is typically a high-pitched, blowing, decrescendo diastolic murmur, heard best
in the third intercostal space along the left sternal border
In patients with mild AR, this murmur is brief but, as the severity increases, generally becomes louder and
longer, indeed holodiastolic
When the murmur is soft, it can be heard best with the diaphragm of the stethoscope and with the patient
sitting up, leaning forward, and with the breath held in forced expiration
"Cooing" or musical diastolic murmurs suggest eversion of an aortic cusp vibrating in the regurgitant
stream
A mid-systolic ejection murmur is frequently audible in isolated AR. It is generally heard best at the base of
the heart and is transmitted along the carotid vessels. This murmur may be quite loud without signifying
aortic obstruction
A third murmur frequently heard in patients with severe AR is the Austin Flint murmur, a soft, low-pitched,
rumbling mid-diastolic murmur. It is probably produced by the diastolic displacement of the anterior leaflet
of the mitral valve by the AR stream but does not appear to be associated with hemodynamically significant
mitral obstruction
In acute severe AR, the elevation of LV end-diastolic pressure may lead to early closure of the mitral valve,
an associated mid-diastolic sound, a soft or absent S 1, a pulse pressure that is not particularly wide, and a
soft, short diastolic murmur of AR
 INVESTIGATIONS
ECG: LVH,strain pattern and left axis deviation and/or QRS
prolongation denote diffuse myocardial disease, generally associated
with patchy fibrosis, and usually signify a poor prognosis
CXR:
 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
 When AR is caused by primary disease of the aortic root,
aneurysmal dilatation of the aorta may be noted, and the aorta may
fill the retrosternal space in the lateral view
• ECHO (see severity assessment on next slide)
• Cardiac catheterization and angiography
 MEDICAL MANAGEMENT OF ACUTE AR
Patients with acute severe AR may respond to intravenous
diuretics and vasodilators (such as sodium nitroprusside), but
stabilization is usually short-lived and operation is indicated
urgently
 Intraaortic balloon counterpulsation is contraindicated
Beta-blockers are also best avoided so as not to reduce the CO
further or slow the heart rate, which might allow
proportionately more time in diastole for regurgitation to occur
Surgery is the treatment of choice
 MEDICAL MANAGEMENT OF CHRONIC AR
Early symptoms of dyspnea and effort intolerance respond to treatment with diuretics
and vasodilators (ACE inhibitors, dihydropyridine calcium channel blockers, or
hydralazine) may be useful as well
The use of vasodilators to extend the compensated phase of chronic severe AR before
the onset of symptoms or the development of LV dysfunction is more controversial
Expert consensus is strong regarding the need to control systolic blood pressure (goal
<140 mmHg) in patients with chronic AR, and vasodilators are an excellent first choice
as antihypertensive agents
Cardiac arrhythmias and systemic infections are poorly tolerated in patients with
severe AR and must be treated promptly and vigorously
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
Patients with syphilitic aortitis should receive a full course of penicillin therapy
Beta blockers may be useful to retard the rate of aortic root enlargement in young
patients with Marfan syndrome and aortic root dilatation with no or only mild AR
Patients with severe AR should avoid isometric exercises
SURGICAL MANAGEMENT OF CHRONIC AR
Self Study: Assignment
Priority:
Tricuspid Stenosis
Pulmonary Stenosis

Functional : Less clinical importance

Tricuspid regurgitation
Pulmonary Regurgitation