Dilatational, hypertrophic, aneurysmal, and endocardial variants of remodeling were revealed in the postinfarction heart. The most prevalent dilatational remodeling is characterized by uniform or nonuniform elongation of ventricular cavities and increase in ventricular volume. Characteristic features of the hypertrophic type are hypertrophied interventricular septa and left ventricular wall and reduced or unchanged left ventricular volume. Pronounced changes in the configuration of the left ventricle due to the formation of single or multiple aneurysms were typical of aneurysmal remodeling. Endocardial remodeling was characterized by cicatricial changes and smoothed relief of the parietal endocardium. These variants and forms of remodeling determine disturbances in intracardial hemodynamic and thanatogenesis in the postinfarction period.
We performed a pathomorphological study of 200 hearts with cicatricial changes from patients died from hypertensive disease. Most postinfarction scars in men were transmural and localized in the anterior and posterior wall of the left ventricle and in the interventricular septum. Non-transmural scars were revealed in the lateral wall (primarily in women). Pathognomonic changes in the architectonics of the heart included reduction of regional blood flow and segmentary, discontinuously extended, and diffusely extended atherosclerotic obstruction. Changes in the index of blood supply to the myocardium corresponded to pronounced decrease in vascularization of the hypertrophic left ventricle. A correlation was found between the index of blood supply to the myocardium and mean systolic and diastolic blood pressure. Therefore, the coronary bed did not satisfy the demands of hypertensive heart with cicatricial changes.
Pathomorphological criteria of arrhythmogenic heart include structural compartmentalization with primary changes in the right ventricle and interventricular septum, fibro- and lipomatosis of the myocardium, and disseminated coronary obstruction. Ischemic focuses in the conducting system are the site of formation of arrhythmogenic substance promoting the development and progression of cardiac arrhythmias. Cardioneuropathy and pathological motility of the interventricular septum lead to systolic dysfunction and contribute to asynchronous excitation and contraction of ventricles in arrhythmogenic heart.
A total of 112 hearts with limited local dilatation zones in coronary arteries (antiocclusion factor) selected from 500 patients dead from chronic forms of coronary heart disease were studied by postmortem contrast polypositional coronarography and cardiometry. A relationship between antiocclusion factor, on the one hand, and coronary artery stenosis and degree of vascularization of the left ventricular wall, on the other, was shown. The adaptation role of antiocclusion factor in coronary blood flow disorders caused by atherosclerotic obstruction (stenosis, occlusion, thrombosis) of the major coronary arteries was demonstrated. The incidence of antiocclusion factor in individual segments of coronary arteries depending on the type of atherosclerotic involvement and index of myocardial blood supply was determined.
Postmortem contrast cardiac ventriculography, coronarography, volume-mass and planimetric cardiometry, as well as echocardiography and pathomorphological data correlation technique were employed for examination of the hearts from patients died from hypertrophy cardiomyopathy (n=100). The following variants of midventricular hypertrophy of the interventricular septum (midventricular obstruction) were established: midleft ventricular, midright ventricular, midproximal, midmaximal. Isolated distal apex hypertrophy and apical hypertrophy were also documented. These variants and forms of cardiac pathology are determined by peculiar changes in geometrical structure of the septum and left ventricle. Multiplanar variability and mobility of interventricular septum combined with peculiar catenary shape promote specific abnormalities of intracardiac hemodynamics determining dissociation between the echocardiographic and pathomorphological diagnostic data and underlying the leading elements of patho- and thanatogenesis of hypertrophic cardiomyopathy.
Pathognomonic incidence of myocardial bridges during obstructive hypertrophic cardiomyopathy, hypertension, and ischemic heart disease was established. Myocardial bridges were predominantly found in the median segments of major coronary arteries with prevailence of bridge-like obstructions in the anterior interventricular branch of the left coronary artery. Typical changes in cardiac angioarchitectonics indicating pronounced inadequacy of coronary blood flow were determined depending on the segmentary directionality of bridge obstruction. The data attest to pronounced pathogenetic role of myocardial bridges in sudden cardiac death.
The hearts of patients who died of coronary disease and had myocardial bridges were studied by postmortem coronary angiography, cardioventriculography, and complex pathomorphological analysis. The relationship between the incidence and pathomorphology of myocardial bridges, on the one hand, and the type of blood supply, segmentary topography of the major coronary arteries, geometry of the left ventricle, and coronary changes in different forms of coronary disease, on the other, was analyzed. Diagnostic criteria were developed and the main components of the etiology, patho- and thanatogenesis in coronary patients with coronary arteries not affected by atherosclerosis are presented.
New geometric characteristics of the right ventricle depended on the localization of macrofocal transmural scars in the left ventricle of postinfarction heart. Most pronounced changes in the right ventricle were observed during dilatational and hypertrophic remodeling of the heart. The increase and decrease in the volume were most frequently occurring and pathognomonic forms of pathomorphological changes in the right ventricle. Dilatational remodeling was accompanied by a decrease in the volume of the right ventricle. The increase in the volume of this ventricle was typical of hypertrophic remodeling. Pathological variability in the right ventricle underlies the development of severe disturbances in intracardiac hemodynamics, i.e., patho- and thanatogenesis of postinfarction heart.
The author presents a retrospective and complex pathomorphological analysis in 152 autopsy cases. Death was caused by different forms of cardiomyopathies. Aim of the study to reveal the frequency of pathology, causes and mechanisms of death. The prevailing frequency of dilated cardiomyopathy was established--106 cases, 0.88%. Hypertrophic and restrictive forms--32 (0.27%) and 14 (0.12%) of cases. the dominating cause of death (42.7%) was chronic cardiac failure. Other death causes were as follows: thrombosis and embolism--17.8%; arrhythmic collapse--13.2%; ventricular fibrillation--9.9%; acute left-ventricular failure--8.6%; real cardiogenic shock--7.8% of all cases of cardiomyopathies.