The nature of pulmonary hypertension in mitral stenosis.

It is known that both functional reversible, and organic, narrowing of the pulmonary arterioles play a part in the increased pulmonary arteriolar resistance found in many cases of mitral stenosis. Parker and Weiss (1936), Larrabee et al. (1949), Henry (1952), and Harrison (1953) have demonstrated occlusive changes in the small arteries. The observations of Hickam and Cargill (1948), Bayliss et al. (1950a), and Holling (1952) that a rise in pulmonary artery pressure without a rise in cardiac output can occur in severe mitral stenosis on exercise, suggests a functional vasoconstriction, and this view has received support from Dexter et al. (1950) and Gorlin et al. (1951). Moreover, the narrowing of the small pulmonary arteries in patients with mitral stenosis and pulmonary hypertension which has been demonstrated by angiocardiography in life (Goodwin et al., 1952; Actis-Dato et al., 1952; Davies et al., 1953) has often been absent in post-mortem injection studies of lungs from such patients (Steiner and Goodwin, 1954). In addition, the frequent fall in arteriolar resistance following successful valvotomy, argues a reversible process (Werk6 et al., 1953; Baker et al., 1952). The cause of the arteriolar constriction is not known, but it has been regarded teleologically as a protective phenomenon, shielding the pulmonary capillaries from the right ventricle (Lewis et al., 1952; Wood, 1952). Taquini et al. (1953) have suggested that since the increased arteriolar resistance imposes a severe load on the right ventricle, such patients follow a rapidly downhill course (" mitral stenosis with cor pulmonale "). Araujo and Lukas (1952) found that increased arteriolar resistance on exercise did not prevent large increases in pulmonary venous pressure in patients with mitral stenosis, and rejected the concept of a compensatory increase in pulmonary arteriolar resistance, believing this to be due primarily to anatomical narrowing of the arterioles.