[Noninvasive method of studying intracardiac and systemic hemodynamics in a mitral valve lesion by calculating the mitral regurgitation volume and mean dynamic pressure in the left atrium]. / Neinvazivnyi sposob issledovaniia vnutriserdechnoi i sistemnoi gemodinamiki pri porazhenii mitral'nogo klapana putem rascheta ob''ema mitral'noi regurgitatsii i srednedinamicheskogo davleniia v levom predserdii.

Comparative hemodynamic studies, making use of different techniques, have demonstrated that tetrapolar transthoracic rheoplethysmography is a very accurate instrument of determining effective stroke volume in cases of mitral regurgitation, and that the latter can be detected by echocardiography and rheoplethysmography. Intracardiac hemodynamic disorders can be assessed on the basis of echographic estimates of left-atrial mean dynamic pressure.

[Shock lung syndrome in myocardial infarct (electron microscopic and biochemical study)]. / Sindrom shokovogo legkogo pri infarkte miokarda (élektronno-mikroskopicheskoe i biokhimicheskoe issledovanie).

A comprehensive clinical sample (375 cases of myocardial infarction, with uncomplicated course in 115, pulmonary edema in 80, cardiac asthma in 37, pulmonary edema combined with cardiogenic shock in 55, and other complications in 88; 89 fatal cases altogether) was used to demonstrate that the shock lung associated with myocardial infarction was rooted in strained operation of various pulmonary functions other than gaseous exchange and inadequate inactivation of vasoactive substances (histamine, serotonin, kinins). The ultrastructural pattern of the shock lung is characterized by damaged aerohematic barrier edema, hypercoagulation, atelectases and the sludging of aggregated erythrocytes. Acute respiratory insufficiency is not always associated with cardiogenic shock and may develop spontaneously in myocardial infarction.

[Ultrastructural bases of pulmonary edema in myocardial infarct]. / Ul'trastrukturnye osnovy oteka legkikh u bol'nykh infarktom miokarda.

A total of 347 patients with myocardial infarction were investigated. Of those, 115 had uncomplicated course of the disease, while pulmonary edema developed in 80, cardiac asthma in 37, pulmonary edema and cardiogenic shock in 35, and various other complications in 80; the outcome was lethal in 80 cases. The pathogenetic contribution of increased permeability to the development of myocardial infarction and its complications is demonstrated. Transendothelial pinocytosis is a trigger mechanism of pulmonary edema. Its pathomorphism is achieved in five steps, each corresponding to a certain degree of ultrastructural transformation of endothelial and alveolar cells. Pulmonary surfactant damage adds to the effect of tissue factors of increased aerohematic barrier permeability.

[Effect of drugs on the permeability of the histohematic barriers in a complicated course of myocardial infarct]. / Medikamentoznoe vozdeistvie na pronitsaemost' gistogematicheskikh bar'erov pri oslozhnennom techenii infarkta miokarda.

The investigations have shown the pathogenetic role of enhanced capillary permeability on the development of myocardial infarction and its complications. To a definite degree the above disorders are conditioned by the activation of the kallikrein-kinin system. This made us try contrykal with heparin in the comprehensive system of treatment of these patients. A clear-cut clinical and laboratory effect has been obtained which justifies recommending the use of protease inhibitors in complicated myocardial infarction.