The role of the physical examination in the evaluation of patients with valvular heart disease is also considered in Chaps. 51e and 267; of electrocardiography (ECG) in Chap. 268; of echocardiography and other noninvasive imaging techniques in Chap. 270e; and of cardiac catheterization and angiography in Chap. 272.
Rheumatic fever is the leading cause of mitral stenosis (MS) (Table 284-1). 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 approximately 40% of all patients with rheumatic heart disease and a history of rheumatic fever (Chap. 381). 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 284-1Major Causes of Mitral Valve Disease |Favorite Table|Download (.pdf) TABLE 284-1Major Causes of Mitral Valve Disease
|Valve Lesion ||Etiologies |
|Mitral stenosis ||Rheumatic fever |
| ||Congenital |
| ||Severe mitral annular calcification |
| ||SLE, RA |
|Mitral regurgitation ||Acute |
| || Endocarditis |
| || Papillary muscle rupture (post-MI) |
| || Trauma |
| || Chordal rupture/leaflet flail (MVP, IE) |
| ||Chronic |
| || Myxomatous (MVP) |
| || Rheumatic fever |
| || Endocarditis (healed) |
| || Mitral annular calcification |
| || Congenital (cleft, AV canal) |
| || HOCM with SAM |
| || Ischemic (LV remodeling) |
| || Dilated cardiomyopathy |
| || Radiation |
In rheumatic MS, chronic inflammation leads to diffuse thickening of the valve leaflets with formation of fibrous tissue and/or calcific deposits. The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid, and these changes, in turn, lead 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 ...