++

  • 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.

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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).

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Table Graphic Jump Location
Table 9–1. Conditions Causing Left Ventricular Inflow Obstruction. 
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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.

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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.

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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) are required ...

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