MITRAL VALVE

DISEASE
By

Magdi A. Ghareeb
MD, FECC
Professor of cardiology
 Mitral Stenosis
 Definition
 Mitral stenosis leads to an obstruction of
blood between the left atrium (LA) and the
left ventricle (LV), caused by abnormal
mitral valve function
 The mitral valve area in a healthy
individual measures 4 -6 cm2
 Etiology

 1 -Rheumatic carditis.
 2- Non rheumatic stenosis is rare in adult. In
infants and children resulting from Dysplasia of
the valve or from the parachute deformity or
supra valvular ring in the left atrium.
In adults:
 -Atrial myxomobacterial vegetations.
 -Calcification of the valvular ring in the elderly.
 Pathophysiology:
 Obstruction of flow during the diastolic filling period of
the left ventricle creates a pressure gradient between the
left atrium and the left ventricle.
 This pressure gradient is related to orifice size and
diastolic flow though the mitral valve
 Obstruction to flow increases left atrial pressure and
volume which is reflected to the pulmonary veins,
capillaries and eventually to the pulmonary arteries and
right ventricle and atrium.
 Chronic elevation of left atrial pressure will cause
hyperplasia and hypertrophy of the pulmonary vessels,
veins, capillaries and arteries.
 RV hypertrophy results from chronic pulmonary
hypertension.
 Clinical manifestations:
History:
 50% of patients with recognized mitral stenosis have
a history of acute rheumatic fever. Symptomatic
patients complain from:
 Dyspnea
 Fatigue
 Palpitation
 Hemoptysis
 Hoarseness of voice
 Chest pain
 Cerebrovascular accident from an embolus may be
the initial symptom.
 Clinical manifestations:
Physical examination:
General signs:
 Resting tachycardia or atrial fibrillation.
 Mitral facies with malar flush and peripheral
cyanosis.
 The neck veins may be distended if right
ventricular failure is present.
 Systolic pulsation of the deep jugular veins
indicates tricuspid regurgitation and a prominent
wave suggests concomitant tricuspid stenosis.
 Cardiac signs:
The typical auscultatory findings are:
 Accentuated first heart sound (S 1).
 Opening snap.
 Diastolic rumbling murmur at the apex.
 If pulmonary hypertension and right ventricular
hypertrophy have developed, a right ventricular
lift can be palpated along the left sternal border.
 With severe mitral stenosis, it is often possible to
palpate an accentuated first heart sound (S1)
and the vibrations of the diastolic rumble at the
cardiac apex.
Accentuated first heart sound:
=> Is due to sudden cessation of the upward motion of
the valve that has been depressed in the left ventricular
chamber during the diastolic filling period.
=> The mobility of valve leaflets, the diastolic gradient
across the valve and PR interval of the ECG all
contribute to the intensity of the first heart sound.
=> When the mobility of the mitral valve is diminished due
to calcification as well as associated mitral
regurgitation, the S1 diminishes in intensity.
=> Shortening of PR interval by tachycardia, fever or
thyrotoxicosis can all accentuate S1
 The opening Snap (OS):
=> It is produced during maximum excursion of the
anterior leaflet of the mitral valve.
=> The OS can occur 0.03 to 0.14 sec after the
second heart sound (S2).
=> The higher the left atrial pressure, the shorter the
interval between the aortic valve closure (S2) and
the opening snap (S2-OS time).
=> Critical mitral stenosis produces a S2 -OS time of
less than 0.08 sec.
 Diastolic rumbling murmur:
=> The murmur is low -pitched; best heard
with the bell of the stethoscope and
becomes accentuated in the latter phase of
diastole with atrial contraction.
=> Although the presystolic component of the
rumble is augmented by atrial contraction,
rarely this phase of the murmur will
increase with atrial fibrillation
 Diastolic rumbling murmur:
 The diastolic murmur may be localized to a small
area of the apex and become audible only after
the patient turns to the left lateral decubitus
position.
 The intensity of the murmur does not necessarily
relate to the severity of mitral stenosis.
 A rumble starting with the opening snap and
continuing to the first sound suggest more
severe impairment.
 The rumble may distinguish or disappear in the
late stages of the disease when the cardiac
output declines.
 Diastolic rumbling murmur:
Other conditions associated with a mitral diastolic
rumble include:
 Left atrial myxoma
 Atrial septal defect
 Patent ductus arteriosus.
 Calcification of the mitral annulus.
 Carey coomb 's murmur in acute rheumatic fever.
 Austin flint murmur due to aortic regurgitation.
 Electrocardiogram:
The characteristic ECG finding in MS is the
broad, notched P wave most prominent in
lead II with a negative terminal deflection
in lead V1.
Atrial fibrillation is common. It develops in
any condition associated with left atrial
enlargement.
When pulmonary hypertension develops
right ventricular hypertrophy may manifest.
 Chest Roentgenogram:
 Left atrial hypertension, which results in left atrial
enlargement, prominence of pulmonary arteries.
 Right ventricular enlargement.
 Left atrial enlargement appears as a
straightening of the left cardiac border on the
standard post-ant chest film.
 Large left atrium may elevate the left main
branches and produce posterior elevation of the
barium filled oesophagus.
 Chest Roentgenogram:
 When the pulmonary capillary pressure exceeds the
oncotic pressure of plasma proteins (normal = 20 -25
mmHg) fluid accumulates in the interstitial space of
the lungs.
 The interlobular septal changes and the linear
shadows are perpendicular to the pleura at the
bases of lungs and known as Kerley's B lines
 Acute elevation of pulmonary venous pressure will
cause pulmonary edema with alveolar extravasation
of fluid.
 Right ventricular dilatation and hypertrophy is
recognized on the lateral chest roentgenogram.
 Echocardiography
 Two-dimensional echocardiography can
display the orifice size and area.
 Doppler readings can provide accurate
estimates of diastolic gradient and serve a
basis for evaluation of mitral valve area.
 Information on left atrial dimensions, right
ventricular enlargement and left ventricular
size can be obtained from the
echocardiogram.
 Cardiac Catheterization
Cardiac catheterization can be used to:
 Determine the gradient across the mitral valve.
 Provide data for calculation of the mitral valve
area.
 Identify other valve lesions.
 Assess ventricular function.
 Determine the status of the coronary arteries.
 The normal mitral valve area is 4 to 6 cm2.
 The hemodynamic abnormalities develop when
the valve is <2 cm2 and with a mitral valve area <
I cm2, dyspnea, fatigue, pulmonary hypertension,
right ventricular failure and reduced cardiac
output are generally present.
 Natural history and prognosis of MS
 The average age of onset of rheumatic fever is 12 years
with latent period of about 19 years from the acute
episode to the detection of murmur of MS.
 Dyspnea and fatigue are the most common symptoms
and can be due to pulmonary hypertension and right
ventricular failure.
 Atrial fibrillation, fever, emotional stress or pregnancy
can increase the COP and abruptly elevate the
pulmonary capillary pressure with the development of
pulmonary edema.
 Severe pulmonary hypertension will reduce the COP and
the pressure load will lead to dilatation of the right
ventricle.
 Natural history and prognosis of MS

 Right sided heart failure followed with

neck vein distension, hepatic enlargement
ascitis, and peripheral edema.
 Atrial fibrillation develops in 40 to 50 % of
patients with mitral stenosis particularly in
those over the age of 40 years.
 The onset of atrial fibrillation may lead to
further dilatation of the left atrium.
 Natural history and prognosis of MS
 Atrial fibrillation may be paroxysmal or respond to
pharmacological agents or cardioversion.
 As the atrial fibrillation becomes more chronic,
resistance to cardioversion develops.
 A serious complication of mitral stenosis is systemic
embolization.
 A history of atrial fibrillation as well as the age of the
patient appears associated with a higher incidence of
systemic embolization.
 Bacterial endocarditis is infrequent in isolated mitral
stenosis, but prolonged fever should always raise this
possibility.
 Treatment
Medical:
 In mitral stenosis efforts are directed at prevention of
recurrent rheumatic fever and bacterial endocarditis.
 Rheumatic fever prophylaxis should continue until the
age of 35 years.
For endocarditis prophylaxis:
 In dental and bronchoscopy:
 2 gm of penicillin orally 1 hour before the dental and
then 1 and 6 hours after the procedure.
 Treatment
 For genitourinary, gastrointestinal
procedures:
2 gm ampicillin should be given IM or IV +
gentamycin 1.5 mg/Kg IM or IV 1 hour
before the procedure then 8 hours later.
 For minor procedures:

 3 gm amoxicillin orally 1 hour before the

procedure and 11/2 gm 6 hours later.
 Treatment
 Digitalis should be used in patients with atrial
fibrillation to slow the ventricular rate. Digitalis
may be useful in preventing paroxysmal atrial
fibrillation.
 Anticoagulation should be used in patients with
mitral stenosis who have chronic atrial fibrillation
or paroxysmal atrial fibrillation unless there is a
contraindication to the use of the drug.
 Systemic embolization requires anticoagulation
for an indefinite period.
 If the embolus is to an extremity or in the
mesenteric system, surgery should be planned.
Percutaneous balloon mitral valvuloplasty was
proved to be successful in patients with
symptomatic mitral stenosis.
 This procedure is carried out when the patient's
valve area is < 1.5 cm2
 Transesophgeal echocardiography is mandatory
prior to the procedure for screening of the left
atrium and more importantly the left atrial
appendage which is not visualized by
transthoracic echocardiography.
 In patients with left atrium or left atrial
appendage thrombus PBMV is contraindicated.
Those patients are referred to surgery.
 Surgery
 PBMV now replaced closed mitral
commissurotomy which was used to be
performed in the past.
 Open mitral commissurotomy is used in selected
patients e.g. patients with left atrial thrombus.
 Mitral valve replacement is used in patients with
heavily calcific and severely deformed valves.
 The artificial valve used in Egypt is the
mechanical tilting disc bileaflet valve.
 Mitral Regurgitation
Definition:
Mitral regurgitation occurs when contraction
of the left ventricle ejects blood into the left
atrium as a result of abnormalities in the
mitral valve apparatus
 Etiology:

A- Chronic Regurgitation:
1 -Rheumatic fever.
2- Prolapse of the mitral valve.
3- Coronary artery disease.
4- Left ventricular dilatation.
5- Calcific mitral annulus.
6- Papillary muscle dysfunction (infarction).
7 -Congenital heart disease.
8- Systemic lupus erythematosus.
B- Acute Regurgitation:
1 -Rupture of chordae tendinae (myxomatous,
endocarditis, trauma)
2- Rupture of papillary muscle (infarction, trauma)
3 -Perforation of leaflets ( endocarditis).
The abrupt hemodynamic alterations produce
marked elevation of the left ventricular end-
diastolic pressure, left atrial pressure and
pulmonary capillary pressure.
 Clinical manifestations
Symptoms:
 Chronic mitral regurgitation can be tolerated for
many years without clinical evidence of a
reduction in cardiac reserve.
 Fatigue and dyspnea are initial symptoms which
can gradually progress to orthopnea,
paroxysmal nocturnal dyspnea and peripheral
edema.
 In acute mitral regurgitation from sudden
disruption of mitral valve apparatus, the
symptoms are those of congestive heart failure
or acute pulmonary edema.
 Physical examination:

In chronic mitral regurgitation:

 Displacement of the cardiac apex impulse with a
hyperdynamic motion over a diffuse area.
 By auscultation, there is high pitched
holosystolic murmur beginning with the 1st heart
sound and extending to the 2nd heart sound. It
is heard at the cardiac apex and radiates to the
left.
 The 1st heart sound is diminished and the
duration of systolic is shortened.
 A ventricular gallop sound is fre audible at the
apex.
In acute mitral regurgitation:
 The physical findings are often those of
acute pulmonary edema and left
ventricular failure.
 The heart size may be normal with
hyperactive apical motion.
 In acute regurgitation which is often due to
rupture of the chordae tendineae, the
holosystolic murmur is harsh and can be
heard over the back of the neck, vertebrae
and sacrum.
 Electrocardiogram
 Left atrium or left ventricular enlargement.
 Atrial fibrillation can develop.
 When coronary artery disease is the
mechanism for mitral regurgitation, Q
wave abnormalities of a previous infarction
are frequently present.
 Chest Roentgenogram
 Left ventricular and left atrial enlargement
develop in long standing mitral
regurgitation.
 In coronary artery disease, heart size can
range from normal to significant dilatation
of both the left ventricle and left atrium.
 Acute mitral regurgitation can manifest
with acute mitral regurgitation on a normal
cardiac size.
 Echocardiogram
In rheumatic disease echocardiogram can be
used to evaluate:
 Valve motion
 Thickness
 Calcification of the mitral valve apparatus.
In acute mitral regurgitation echocardiogram
can detect:
 Ruptured chordae.
 Ruptured papillary muscle.
 Perforated valve leaflet.
 Cardiac catheterization
 Cardiac catheterization can confirm the
diagnosis of mitral regurgitation, assess
ventricular function.
 Recognize other underlying cardiac
lesions.
 Can delineate the anatomy of coronary
arteries.
 Pathophysiology
 Chronic mitral regurgitation causes a volume
overload on the left ventricle and left atrium.
 The compensatory mechanism of the left
ventricle to chronic mitral regurgitation is
dilatation of the chamber.
 Dilatation of the left ventricle is accompanied by
an increase in wall thickness and hypertrophy to
maintain mechanical function.
 In acute mitral regurgitation hemodynamics differ
from chronic form because the valvular
regurgitation is often abruptly imposed on a
normal ventricle
 Natural history and prognosis
The prognosis will depend on the underlying
etiology and the state of the left ventricular
function
 In chronic mitral regurgitation volume overload may be
tolerated for many years before symptoms of heart
failure develop
 Left atrial enlargement predisposes to left atrial
fibrillation which Can be complicated by embolization.
 Infective endocarditis can develop
 In acute mitral regurgitation the clinical course is often
complicated by acute pulmonary edema and sometimes
cardiogenic shock.