- Exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea,
or fatigue (later stages).
- Opening snap, loud S1 (closing snap), diastolic rumbling murmur;
with pulmonary hypertension, a parasternal lift with a loud P2.
- ECG evidence of left atrial enlargement or atrial fibrillation;
right ventricular hypertrophy in later stages.
- Chest radiographic signs of left atrial enlargement and normal
left ventricular size.
- Thickened mitral valve leaflets with restricted valve motion
and reduced orifice area demonstrated on two-dimensional echocardiography.
- An elevated transmitral pressure gradient and prolonged pressure
half-time by Doppler echocardiography.
The normal mitral apparatus is a complex structure whose components must permit a large volume of blood to pass from the left atrium
to the left ventricle. The cross-sectional area of a normal mitral
valve ranges from 4 cm2 to 6 cm2 in an adult and
a transmitral pressure gradient develops when the valve is narrowed
to < 2.5 cm2. Left atrial pressures begin to rise and
are transmitted to the pulmonary vasculature and right side of the
heart. Several congenital and acquired conditions result in impaired
filling of the left ventricle and may be confused with mitral stenosis
Table 9–1. Conditions Causing Left Ventricular Inflow Obstruction. |Favorite Table|Download (.pdf)
Table 9–1. Conditions Causing Left Ventricular Inflow Obstruction.
Valvular mitral stenosis
Pulmonary vein stenosis
The predominant cause of mitral stenosis in adults is rheumatic involvement of the mitral valve and approximately two-thirds of
all patients with rheumatic mitral stenosis are female. However,
a large proportion of patients with rheumatic valve disease—nearly
50%—have no history of rheumatic fever. Other
causes of mitral stenosis are extremely rare. These figures will
most likely change due to the impressive reduction of rheumatic
fever in developed countries, although rheumatic fever remains a
problem in developing countries and most likely reflects the reduced availability
of antibiotics and the virulence of the strains of Streptococcus.
Acute rheumatic fever may produce a pancarditis involving the endocardium, myocardium, and pericardium. Aschoff bodies in the
myocardium are very specific for a history of rheumatic carditis.
Involvement of the mitral valve apparatus is the rule and may produce
fusion and thickening of the commissures, cusps, and chordae tendineae.
In addition, the fibrosis and calcification of the leaflets may
extend to the valve ring. It is still debatable if the progression
of mitral stenosis is due to a smoldering rheumatic process and recurrent
infections or the constant trauma of turbulent flow produced by
a deformed valve.
As the stenosis progresses, a transmitral pressure gradient develops to facilitate flow across the stenotic valve in diastole. Furthermore,
the atrial contraction may augment this diastolic pressure gradient
(assuming the heart is in normal sinus rhythm). Both the mitral
valvular gradient (MVG) and mitral valvular flow (MVF) ...