The aim. To study the morphological manifestations of the response of the myocardial capillaries to cardioplegia in patients with valvular defects and coronary heart disease. Materials and methods. Morphological research of operative and sectional material was carried out. Myocardium fragments for microscopical study were obtained from patients at different stages of an open-heart surgery and patients who died at the stage of conservative treatment without surgical intervention. Similar samples of the myocardium of a healthy young man who died from injuries incompatible with life were studied as a control. For electron microscopy study, samples of myocardium were taken from patients at the 185th minute of perfusion. Results. Histological preparations of the myocardium showed pronounced diffuse hypertrophy of cardiomyocytes (CMCs), sometimes at the stage of decompensation (perinuclear edema, loss of myofibrils, apoptosis). This transformation of CMCs was obviously related to their functional overload caused by combined defects of the mitral and aortic valves. Changes in muscle fibers were accompanied by interstitial and perinuclear fibrosis. In the pool of coronary arteries affected by atherosclerosis, signs of small focal coronary fibrosis were visible, as well as rough post-infarction scars in 3 patients. All the patients had signs of acute hypoxic damage to the myocardium in the form of CMCs shortening and interstitial edema. Conclusions. In patients with combined defects of the aortic and mitral valves of the heart with coronary artery disease, the phenomena of myocardial fibrosis prevail. Heart valve disease combined with coronary heart disease lead to the development of both alterative and compensatory-adaptiveprocesses in the vessels of the microcirculatory bed. The greatest loss of vital organelles in small vessels is observed at 185 min after administration of cardioplegic solution, irreversible changes develop 3 h after perfusion.

Aim of the study. To determine the effect of surgical tactics on the duration of ischemic period with simultaneous combined correction of two or three valves of the heart and myocardial revascularization Materials and methods. The work is based on the analysis of the results of single-stage multivalve correction in conjunction with coronary artery bypass grafting in 93 patients, which was performed at the National Amosov Institute of Cardiovascular Surgery for the period from 2014 to 2016. Depending on the tactical approach and the sequence of surgical procedures, patients were divided into groups. 1 – “CABG off pump and subsequent correction of heart valves” (n = 15); 2 – “Correction of heart valves and bypass grafting in conditions of cardioplegia” (n = 78). Results. Using different approaches to achieve high-quality protection of the myocardium at the time of its ischemia, minimizing the impact of artificial circulation on the body by improving the conditions and reducing the ischemic heart time showed significant advantages of the method of pre-shunting CA in the working heart. Conclusions.1. Correction of combined multiple valve pathology with coronary heart disease requires prolonged cardiopulmonary bypass time and ischemic heart time, which requires reliable protection of the myocardium, which is difficult to carry out in the presence of stenoses in the lumen of the CA. 2. The use of the method of preventive restoration of coronary blood flow by bypassing the spacecraft on the working heart before clamping of the aorta, has significant advantages in the duration of the cardiopulmonary bypass time and ischemic time of the heart.

The case of differential diagnosis and treatment of a patient with pulmonary embolism (PE), the source of which was the thrombus formed in the right ventricle of the heart, is presented. The peculiarity of this case was the untimely diagnosis of the disease, which simulated pneumonia, the treatment of which did not improve the clinical condition of the patient. Tomography allowed to determine the thrombosis of the right branch of the pulmonary artery and to send the patient to the cardiac surgery center for further treatment. Diagnosis of a probable source of embolism occurred after echocardiography, which revealed a tumor-like lesion of the right ventricle of large size and dense consistency. The results of surgical treatment of the patient, during which extensive formation of the right ventricle was removed, a dense elastic consistency with signs of fragmentation confirmed the prediction of this particular source of pulmonary embolism. Removal of blood clots from the right branch of the pulmonary embolism showed their similar macrostructure with right ventricular formation. The appearance and macrostructure of the formation did not allow to determine with certainty its character. Only histological examination was able to determine the thrombogenicity of the origin of this formation. The recurrent nature of pneumonia, without the presence of risk factors, in young patients may be the basis for more thorough examination to identify atypical clinical conditions. The restoration of the source of the body is of great importancefor the prevention of its relapse. Finding the source of pulmonary embolism should necessarily include echocardiography to carefully examine possible lesions of intracardiac structures with the formation of blood clots that may be responsible for its occurrence.

Relevance. Adaptation of the heart chambers to their volume overload, which increases with diastolic filling of the left ventricle (LV) or systolic regurgitation in the left atrium (LA) in case of mitral valve insufficiency leads to remodeling of the myocardium of these chambers. Longitudinal hypertrophy of cardiomyocytes (CMCs), realized by building up new sarcomeres at the end of existing myofibrils, is an adaptation mechanism in the early stages, but eventually turns into maladjustment, which leads to heart failure. Hypertrophied CMCs, damaged during decompensation, are replaced by connective tissue due to excessive activation of fibroblasts with deposition of the extracellular matrix, which is also an element of the myocardial remodeling. The progression of heart failure is also associated with a mismatch between blood supply and myocardial oxygen demand, since an increase in the size of the CMCs is accompanied by a rarefaction of the intramural network of microvessels. It is believed that the violation of the ratio of the size of the heart, angiogenesis and cardiac function are the basis for the transition of adaptive compensation of the heart to decompensation with the progression of heart failure. Objective: to study morphological changes in the myocardium of the LV and LA in patients with mitral valve insufficiency. Materials and methods. Macroscopically, the condition of the myocardium was studied on the material of 14 autopsies of patients who died of NdMK insufficiency. History of NdMK – from 3 months. up to 2.4±1.1 years. As a control, the hearts of 3 deaths without cardiopathology were studied. The material for light microscopy was pieces of myocardium from different segments of the left ventricle, as well as from the walls of the left ventricle, obtained during autopsy.Morphological (macroscopic, histological and electron microscopic), morphometric and statistical research methods were used. Results. With LV dilatation associated with chronic mitral valve insufficiency, lengthening of each CMCs provides an increase in the area of ​​the myocardial walls, and, accordingly, the size of the cavity of the corresponding chamber of the heart, which compensates to some extent for the increase in diastolic blood volume in the LV and systolic blood volume in the LA. However, the factor limiting this compensation mechanism is the deficiency of the myocardial microvasculature associated with limited capillary growth. The contradiction between the need for the myocardium to lengthen the CMCs and the inability of capillaries to provide them with oxygen leads to a breakdown in compensation with an increase in fibrotic changes. This is a factor limiting the further increase in the volume of the cavity. Conclusions. Overloading of the myocardium with volume leads to an increase in the length of the CMCs, on average, from 57.3±9.1 µm to 93.7±12.4 µm. The increase in the length of the CMCs is due to the increase in the number of sarcomeres from 43.7±8.4 to 62.5±14.5. The diameter of the CMCs in this case does not increase reliably. Overloading of the heart cavities with volume is often accompanied by desynchronization of the CMCs contraction, which leads to disruption of the integrity of the myocytic "working syncytium" and pronounced interstitial fibrosis.