[Effect of the contractile function of the myocardium on the nature of hemodynamic reactions in patients with ischemic heart disease during Valsalva's test]. / Vliianie sostoianiia sokratitel'noi funktsii miokarda na kharakter gemodinamicheskikh reaktsii u bol'nykh ishemicheskoi bolezn'iu serdtsa pri provedenii testa Val'sal'vy.

Application of contrast cineventriculography and probe of the left ventricle indicated that there was a relationship between the status of myocardial contractility, its function, some hemodynamic parameters, the severity of regional left ventricular wall contractility impairments and the nature of a hemodynamic response to Valsalva's test. Normal left ventricular contractility determined sinusoidal responses. Decompensated impairments of myocardial contractility gave rise to a square wave. A response represented as a nil ++super-elevation was caused by a moderate impairment of left ventricular contractility and, probably, by the absence of adequate vasoconstriction in the fourth phase of Valsalva's test.

[The possible mechanisms for the development of myocardial ischemia during the performance of Valsalva's test by patients with ischemic heart disease]. / Vozmozhnye mekhanizmy razvitiia ishemii miokarda pri vypolnenii testa Val'sal'vy bol'nymi ishemicheskoi bolezn'iu serdtsa.

Changes in hemodynamics associated with Valsalva's test are responsible for a reduction in myocardial oxygen consumption and a decrease in diastolic coronary perfusion pressure in ischemic patients and subjects free of coronary heart disease. Due to stenosis and occlusion of coronary arteries lowering of perfusion coronary pressure in relevant patients becomes more profound and may induce ischemia in spite of diminished oxygen consumption. The main cause underlying onset of myocardial ischemia in patients with marked lesions of coronary arteries is initially low perfusion pressure and limited coronary reserve.

[Pathogenesis of homeometric and heterometric autoregulation of the heart in mitral valve defects]. / O patogeneze gomeometricheskoi i geterometricheskoi autoreguliatsii serdtsa pri mitral'nykh porokakh.

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).

[Diastolic coronary gradient during Valsalva's test in patients with ischemic heart disease]. / O dinamike diastolicheskogo koronarnogo gradienta pri probe Val'salvy u bol'nykh ishemicheskoi bolezn'iu serdtsa.

Thirty-five patients including 26 with coronary heart disease and 9 with a pain syndrome non-typical of angina were studied. All patients were subjected to Valsalva's standardized test during which the pressure was measured in the aorta and the heart left ventricle paralleled by simultaneous ECG registration at the three standard leads and at AVR lead. The test sensitivity equalled 50%, the test specificity was 88.9%. Both healthy subjects and coronary heart disease patients displayed a reduction of the diastolic coronary gradient during Valsalva's test, mostly due to the increased diastolic pressure in the left ventricle, which corresponded to the dissemination of coronary atherosclerosis (by coronographic findings). The mechanisms contributing to the development of ischemia associated with Valsalva's test include a fall in coronary perfusion, tachycardia and the reflectory influence of the pulmonary receptors.