The frequent association of pulmonary hypertension with symptomatic mitral stenosis has stimulated much investigation concerning its significance and the mechanism of its production. Two types are now recognized: passive hypertension, where the increased pressure in the left atrium and pulmonary veins and capillaries produced by the stenosed mitral valve is transmitted to the pulmonary artery; and active hypertensions, where much higher levels of pulmonary arterial pressure are due to an increased vascular resistance in the lungs (Bayliss et al., 1950a;Eliasch, 1952;Lewis et al., 1952). The causes of this increase in vascular resistance are not fully understood, but Parker and Weiss (1936), Larabee et al. (1949), Henry (1952), and Harrison (1953) have found thickening of the walls of the small pulmonary arteries, while Dexter et al. (1950), Holling (1952), and Ball et al. (1952 have suggested that reversible vasoconstriction may also occur. Angio-cardiography has demonstrated narrowing and irregularity of the smaller pulmonary arteries in patients with symptomatic mitral stenosis (Goodwin et al., 1952;Actis-Dato et al., 1952). The present investigation was undertaken to determine the significance of these changes, whether they could be detected on plain radiographs, and whether they were proportional to the pulmonary arterial pressure. The value of the symptoms, physical findings, and electrocardiographic signs, in estimating pulmonary arterial pressure was assessed by comparing them with the pressures measured by cardiac catheterization. An attempt was made to determine which of these methods provided the best estimate of the pressure.
METHODSFifty-one patients suffering from mitral stenosis of varying severity were studied. The series included patients with normal pulmonary arterial pressures and with all degrees of pulmonary hypertension. Thirty-five patients had aortic valve disease, but in all these mitral valve disease was the dominant lesion. Mitral incompetence, in association with stenosis, was diagnosed in 10 subjects, and in 4 of these was thought to be of greater hlmodynamic importance than stenosis. One patient had systemic hypertension in addition to mitral stenosis. Dyspncea was graded according to the classification of the New York Heart Association (1939).The clinical classification of pulmonary hypertension was as follows. Grade 0: normal left ventricular impulse, normal second sound in the pulmonary area. Grade I: tapping impulse, gentle sternal lift, narrow splitting of the second heart sound with slight accentuation of the pulmonary element. Grade II: tapping impulse, marked sternal heave, narrow splitting of the second heart sound with more accentuation of the pulmonary element. A systolic murmur over the pulmonary area and a triple rhythm were not found frequently enough to be of diagnostic value. 393 group.bmj.com on June 4, 2015 -Published by http://heart.bmj.com/ Downloaded from
