MITRAL STENOSIS

ETIOLOGY AND PATHOLOGY

Two-thirds are female. generally rheumatic in origin;
very rarely, MS is congenital.
40% rheumatic heart disease MS
.
In rheumatic stenosis the valve leaflets are diffusely
thickened by
fibrous tissue and/or calcific deposits.
the valvular cusps become rigid,
(fish-mouth) valve.
Calcification of the stenotic mitral valve
. Thrombus formation and arterial embolization may arise
from the calcific valve itself, but more frequently arise
from the dilated left atrium (LA) in patients with atrial
fibrillation (AF)

PATHOPHYSIOLOGY
normal adults the mitral valve orifice is 4 to
6 cm2.
In the presence of significant obstruction, less than 2 cm2,
blood can flow from the LA to the left
ventricle (LV) only if propelled by an abnormally elevated
left atrioventricular pressure gradient
When the mitral valve opening is reduced to 1 cm2, often
referred to as critical MS, a LA pressure of
approximately 25 mmHg
is required to maintain a normal cardiac output (CO).
The elevated pulmonary venous and pulmonary arterial
(PA) wedge pressures reduce pulmonary compliance,
contributing to exertional dyspnea.
dyspnea are usually precipitated by clinical events that
increase the rate of blood flow across the mitral orifice,
tachycardia including that resulting from atrial fibrillation
augments
the transvalvular gradient and elevates further the LA

Cardiac Output
moderately severe MS
(mitral valve orifice 1.2 cm2 to 1.7
cm2),
the CO is normal or almost so at rest but
rises subnormally during exertion.
critical MS --- pulmonary vascular
resistance

Pulmonary Hypertension
The clinical and hemodynamic features of
MS
importantly -- level of the PAP.
Pulmonary hypertension results from :
(1) passive backward transmission of the elevated LA
pressure;
(2) pulmonary arteriolar constriction -- 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.
Severe pulmonary hypertension --- tricuspid
regurgitation (TR) & pulmonary incompetence ----right-sided heart failure.

SYMPTOMS
valvular obstruction is mild, --- physical signs of
MS may
be present without symptoms.
dyspnea and cough, fever, severe anemia,
paroxysmal atrial fibrillation and other
tachycardias, sexual intercourse, pregnancy, and
thyrotoxicosis.
dyspnea, -- orthopnea and paroxysmal
nocturnal dyspnea.
Pulmonary edema, atrial arrhythmias

Hemoptysis
results from rupture of pulmonary-bronchial
venous connections secondary to pulmonary
venous hypertension.
elevated pulmonary vascular resistances----never fatal.
Recurrent pulmonary emboli , sometimes
with infarction, --- important cause of morbidity
and mortality
Pulmonary infections, i.e., bronchitis,
bronchopneumonia, and lobar pneumonia,
commonly complicate untreated MS.
Infective endocarditis

Pulmonary Changes
pulmonary vascular bed : fibrous thickening of the walls
of the alveoli
and pulmonary capillaries occurs commonly in MS.
vital capacity, total lung capacity, maximal breathing
capacity, and oxygen uptake per unit of ventilation are
reduced
pulmonary capillary pressure rises during exercise.
airway resistance is abnormally increased
the diffusing capacity may be reduced.
transudation of fluid from the pulmonary capillaries into
the
interstitial and alveolar spaces.
the increased capacity of the pulmonary lymphatic system
to drain excess fluid ------- retards the development of
alveolar edema.

Thrombi and Emboli

Thrombi may form in the left atria, particularly in
the enlarged atrial appendages of patients with MS.
Embolization occurs much more frequently in patients
with AF,
in older patients, and in those with a reduced cardiac
output (CO). systemic embolization may be the presenting
complaint in otherwise asymptomatic patients with mild
MS.
thrombus may suddenly obstruct the stenotic mitral orifice
and cause
syncope, angina, and changing auscultatory signs with
alterations in
position.

PHYSICAL FINDINGS
Inspection and Palpation
blue facies
the jugular venous pulse reveals prominent a waves
due to vigorous right atrial systole.

Auscultation
The first heart sound (S1)
generally snapping, and slightly delayed.
The pulmonary component of the second
heart sound (P2) is often accentuated,
the second heart sound (S2) are closely split
or fixed.

Associated Lesions
pansystolic
this murmur is accentuated by inspiration
and diminishes during forced expiration (Carvallos sign)
pansystolic murmur of MR.
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
The Graham Steell murmur of pulmonary
regurgitation (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.

LABORATORY EXAMINATION
EKG In MS and sinus rhythm, the P
wave
usually suggests LA enlargement , tall
and peaked in lead II and upright in lead V1
RA enlargement
The QRS complex is usually normal.

Echocardiogram
the most sensitive and
specific noninvasive method for diagnosing MS.
Transthoracic two dimensional color flow Doppler
echocardiographic imaging and Doppler ultrasound provide,
including an estimate of
the transvalvular gradient and of mitral orifice size,
the presence and severity of accompanying MR,
, echocardiography provides an assessment of the
size of the cardiac chambers, an estimation of the LV function,
an
estimation of the PAP, and an indication of the presence and
severity
of associated valvular lesions.
Transesophageal echocardiography provides
superior images and should be employed when transthoracic
imaging is inadequate for guiding therapy.

Roentgenogram
The earliest changes are straightening of the left
border
of the cardiac silhouette,
Prominence of the main pulmonary arteries,
Dilatation of the upper lobe pulmonary veins,
Backward displacement of the esophagus by an enlarged
LA.
In severe MS, however, all chambers and vessels upstream
to the narrowed valve are prominent.
Kerley B lines are fine, dense, opaque, horizontal lines that
are most
prominent in the lower and midlung fields and that result
from distention
of interlobular septa and lymphatics with edema when the
resting
mean LA pressure exceeds approximately 20 mmHg.

DIFFERENTIAL DIAGNOSIS
Atrial septal defect may be mistaken for MS; in both
conditions there is often clinical, EKG, and roentgenographic evidence
of RV enlargement and accentuation of the pulmonary vascularity. The
widely split S2 of atrial septal defect may be confused with the mitral
OS, and the diastolic flow murmur across the tricuspid valve may be
mistaken for the mitral diastolic murmur. However, the absence of LA
enlargement and of Kerley B lines and the demonstration of fixed
splitting of S2 all favor atrial septal defect over MS.
Left atrial myxoma may obstruct LA emptying, causing
dyspnea, a diastolic murmur, and hemodynamic changes resembling
those of MS. However, patients with an LA myxoma often have
features suggestive of a systemic disease, such as weight loss, fever,
anemia, systemic emboli, and elevated serum IgG concentrations. The
auscultatory findings may change markedly with body position. The
diagnosis can be established by the demonstration of a characteristic
echo-producing mass in the LA with two-dimensional echocardiography.

TABLE : Summary of Useful Medical Treatments in Valvular Heart

Disease
Source: NA Boon, P Bloomfield: The medical management of valvular heart
disease. Heart
87:395,Control
2002, with permission
Secondary
Symptom
Lesion
Prevention and
Natural History
Penicillin prophylaxis
Mitral stenosis
Diuretics for heart
against recurrent
failure; Digoxin, Beta
episodes of rheumatic
blockers, calcium
fever; Anticoagulants to
antagonists control
prevent systemic
atrial fibrillation
thromboembolism.
Mitral regurgitation

Aortic stenosis

Aortic regurgitation

Diuretics and
vasodilators (usually
ACE inhibitors) for heart
failure
Diuretics for heart
failure; nitrates and
blockers for angina
Diuretics and
vasodilators (usually
ACE inhibitors) for heart
failure

No proven treatment

No proven treatment
but lipid lowering
therapy may slow
progression of calcific
aortic stenosis
Vasodilators (nifedipine
or ACE inhibitors) to
protect the left
ventricular myocardium
and delay the need for
surgery

Penicillin prophylaxis of -hemolytic

streptococcal infections prevent rheumatic fever and prophylaxis
for infective endocarditis
restriction of sodium intake and maintenance doses of oral diuretics.
Digitalis glycosides usually do not benefit patients with MS and sinus
rhythm but are helpful in
slowing the ventricular rate of patients with AF.
Beta blockers or nondihydropyridine calcium antagonists
(e.g., verapamil or diltiazem) are useful in this regard.
Warfarin to an INR of 2-3:1 should be administered for at least 1 year
to patients with
MS who have suffered systemic and/or pulmonary embolization and
permanently to those with AF.
If AF is of relatively recent origin in a patient whose MS is not
severe enough to warrant balloon mitral valvotomy or surgical
valvotomy,
reversion to sinus rhythm pharmacologically or by means of
electrical countershock is indicated. Usually this reversion should be
undertaken after the patient has had 3 weeks of anticoagulant
treatment.

Mitral Valvotomy
effective if orifice is less than approximately 1.0 cm2/m2 body
surface area,
or 1.7 cm2 in normal-sized adults.
two techniques: percutaneous balloon mitral valvotomy
and surgical valvotomy.
balloon mitral valvotomy , a catheter is directed into the LA
after transseptal puncture and a
single or double balloon (Inoue balloon) is directed across the
valve
and inflated in the valvular orifice. Ideal patients have
relatively mobile, thin leaflets with no or little calcium,
without extensive subvalvular thickening and with no or mild
MR.
surgical valvotomy,.
In patients in whom percutaneous valvotomy is not possible,
unsuccessful,
or in those with restenosis,