[The possibility of determining the functional status of the hypertrophied myocardium in multiple valvular defects of the heart].

A comprehensive angiocardiographic study with computer-aided data processing were performed in 46 patients (mean age 34.2 years) with multivalvular diseases. Thirty two patients were diagnosed as having mitral and aortic defect, 14 had mitral, aortic and tricuspid defect.

[Intracardiac mechanisms of compensation of isolated aortic insufficiency].

A complex angiographic examination was performed in 28 patients with rheumatic aortic valvular disease. The major mechanism of compensation in aortic failure was found to be an increase in left ventricular end-diastolic volume at the expense of added regurgitating blood volume. It was shown that isolated aortic failure was a good compensated defect with high functional myocardial reserves and coronary circulation along with adequate left ventricular dilatation and normal-stress nature of left ventricular hypertrophy.

[Late thrombo-embolic complications after heart valve prosthesis].

A follow-up study of 444 patients with artificial heart valves of different makes demonstrated increased wear and thrombogenic properties of the hemispheric MKC-27 prosthesis, used in mitral position, over 5 years of follow-up. High risk of thrombo-embolic complications is related to interrupted anticoagulant treatment. Their rate could be reduced through improving the quality of anticoagulant treatment, i.

[Isolated mitral valve insufficiency in comparison with mitral-tricuspid insufficiency: various mechanisms of compensating for the defect and functional status of the myocardium].

A combined analysis of ventricular contractility and intracardiac hemodynamic compensatory mechanisms was carried out, on the basis of angiocardiographic findings, in 37 patients with rheumatic mitral incompetence. Atrial fibrillation aggravates essentially the defect's hemodynamics, while added tricuspid incompetence is accompanied by a certain off-loading in the lesser circulation network. A grossly perversed phasic structure of intramyocardial stress was noted, apparently being a compensatory mechanism.