The role of the physical examination in the evaluation of patients with valvular heart disease is also considered in Chaps. 38 and 234; of electrocardiography (ECG) in Chap. 235; of echocardiography and other noninvasive imaging techniques in Chap. 236; and of cardiac catheterization and angiography in Chap. 237.
ETIOLOGY AND PATHOLOGY
Rheumatic fever is the leading cause of mitral stenosis (MS) (Table 258-1; see also Chap. 352). Other less common etiologies of obstruction to left ventricular inflow include congenital mitral valve stenosis, cor triatriatum, mitral annular calcification with extension onto the leaflets, systemic lupus erythematosus, rheumatoid arthritis, left atrial myxoma, and infective endocarditis with large vegetations. Pure or predominant MS occurs in ~40% of all patients with rheumatic heart disease and a history of rheumatic fever (Chap. 352). In other patients with rheumatic heart disease, lesser degrees of MS may accompany mitral regurgitation (MR) and aortic valve disease. With reductions in the incidence of acute rheumatic fever, particularly in temperate climates and developed countries, the incidence of MS has declined considerably over the past several decades. However, it remains a major problem in developing nations, especially in tropical and semitropical climates.
++ Table Graphic Jump Location TABLE 258-1Major Causes of Mitral Stenosis ||Download (.pdf) TABLE 258-1 Major Causes of Mitral Stenosis
|Rheumatic fever |
|Congenital (parachute valve, cor triatriatum) |
|Severe mitral annular calcification with leaflet involvement |
|SLE, RA |
|IE with large vegetations |
In rheumatic MS, chronic inflammation leads to diffuse thickening of the valve leaflets with formation of fibrous tissue often with calcific deposits. The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid, and the pathologic process eventually leads to narrowing at the apex of the funnel-shaped (“fish-mouth”) valve. Although the initial insult to the mitral valve is rheumatic, later changes may be exacerbated by a nonspecific process resulting from trauma to the valve due to altered flow patterns. Calcification of the stenotic mitral valve immobilizes the leaflets and narrows the orifice further. Thrombus formation and arterial embolization may arise from the calcific valve itself, but in patients with atrial fibrillation (AF), thrombi arise more frequently from the dilated left atrium (LA), particularly from within the LA appendage.
In normal adults, the area of the mitral valve orifice is 4–6 cm2. In the presence of significant obstruction, i.e., when the orifice area is reduced to <~2 cm2, blood can flow from the LA to the left ventricle (LV) only if propelled by an abnormally elevated left atrioventricular pressure gradient, the hemodynamic hallmark of MS. When the mitral valve opening is reduced to <1.5 cm2, referred ...