The spectrum of pure mitral stenosis: Hemodynamic studies in relation to clinical disability

Abstract

The pathophysiology of mitral stenosis is reassessed, with special emphasis upon relation of physiologic variables to severity of symptoms and degree of disability. Data from 44 patients with pure mitral stenosis are presented. Cathetcrization of the left side of the heart was performed in all and catheterization of the right side of the heart in 25 patients. Twenty-six patients were in Class I or II (American Heart Association Functional Classification) with mild symptoms or none at all, while 18 patients were in Class III with severe symptoms. As expected, inverse relationships existed between left atrial pressure and mitral valve area ( r = − 0.618), pulmonary arterial pressure and mitral valve area ( r = − 0.575), and between mean mitral diastolic pressure gradient and mitral valve area ( r = − 0.708). There was a positive relationship between cardiac index and mitral valve area ( r = + 0.407). All correlation coefficients were significant to the 1 per cent level. Seventeen of the 26 patients in Classes I and II had mitral valve areas of 1.5 cm 2, or less. This indicates that severe mitral stenosis can be found in a nearly asymptomatic state. All of the 18 Class III patients had valve areas of less than 1.5 cm 2. These two groups of patients with similar degree of valve narrowing were compared. Cardiac output was significantly ( p < 0.01) reduced in both categories (2.81 L. min. M 2. for Classes I and II, and 2.82 L. min. M 2. for Class in patients). Left atrial pressure in the two groups, 18 and 19 mm. Hg, respectively, and mean diastolic pressure gradient, 11 and 13 mm. Hg, respectively, did not show significant differences. However, pulmonary arterial pressure, 22 mm. Hg in Classes I and II and 36 mm. Hg in Class II, as well as pulmonary arteriolar resistance, 105 compared to 425 dynes sec. cm. −5, did allow a hemodynamic distinction between the two clinically different groups. These data suggest that the degree of pulmonary vascular disease is an important determinant of the symptoms of mitral stenosis. For Class I and II patients, history, physical examination and radiographic studies did not allow an accurate prediction of the mitral valve size. It is suggested that one of the earliest adaptive mechanisms to mitral blockade is a decrease in cardiac output and that this is not mediated, initially, through an elevated pulmonary vascular resistance, myocardial failure or atrial fibrillation. It is one of the means by which a patient with severe stenosis of the mitral valve may remain asymptomatic for prolonged periods of time.