[Pathogenesis of homeometric and heterometric autoregulation of the heart in mitral valve defects]

Right ventricular (RV) function was investigated using rheopulmonography at Valsalva's manoeuvre and echocardiography in 36 patients with rheumatic heart disease which were divided into three groups: with RV normal-size chamber and normal thickness of the wall (I), with normal-size RV chamber and myocardial hypertrophy (II), with RV dilatation and hypertrophy. In patients of group I there appeared mitral stenosis of degree I (Gorlin) and insignificant elevation of pressure in the pulmonary artery. Mitral defect was compensated through the mechanism "stress-mobilization" underlying homeometric autoregulation of the heart. As a result, muscular thickness grows without hypertrophy and becomes stronger. In more pronounced narrowing of mitral opening (group II) the second stage of the compensation comes: in latent pulmonary hypertension hypertrophy develops as a prolonged adaptation to greater load. Hypertrophic myocardium is the most resistant to overloading with external pressure. In group III patients with mitral narrowing degree 2 and more distinct pulmonary hypertension one can observe an addition of Frank--Starling mechanism--heterometric type of autoregulation. In spite of its triggering compensation of the defect remains insufficient (circulation deficiency becomes clear-cut in patients of group III).