Cardiac Aneurysm

CARDIAC ANEURYSM. Cardiac aneurysm, or aneurysm of the myocardium, is called a localized, circumscribed bulging of the heart wall, usually accompanied by thinning of the underlying myocardial area. Previously, total and partial aneurysms of the heart were distinguished. This division, still used by some, should be discarded, since total aneurysm falls entirely under the concept of cardiac dilatation. The basis of cardiac aneurysm is always an organic focal change in the muscular wall of the heart, which leads to a decrease or loss of elasticity and contractility of this area. Under the influence of intracardiac blood pressure, both systolic and diastolic (the latter acquiring particular significance at the end of diastole, at the moment of greatest relaxation of the heart muscle), the myocardial area that has lost its elasticity begins to stretch and bulge, forming an aneurysmatic sac. In some cases, a true rupture of the heart may occur with bleeding into the pericardial region and with the phenomena of so-called cardiac tamponade. Such ruptures occur less frequently than one might expect; on the one hand, this is prevented by local adhesive (supra-aneurysmatic) pericarditis, and on the other hand, by the same parietal peri-aneurysmatic endocarditis on the inner surface, with a callous thickening of the endocardium, with thrombotic masses superimposed on it from the inside. These latter may organize and ossify. As a result, a thick layer of scar tissue can form in such an area, dense enough to withstand the intracardiac blood pressure. Patients with such aneurysms often live for years without rupture. Cardiac aneurysms are acute and chronic. - Acute cardiac aneurysms develop on the basis of embolic, focal, purulent myocarditis, heart abscesses, or, most often, in the case of ulcerative septic endocarditis near the heart valves, when the inflammatory process spreads in the form of parietal endocarditis and, then passing to the myocardium, ulcerates the wall. Aneurysms of the membranous part of the septum usually end with a rupture toward the area of least pressure, i.e., into the right ventricle. In this way, the majority of so-called acquired perforations of the septum are formed. - Chronic cardiac aneurysms develop, mainly, on the basis of arteriosclerosis of the coronary arteries of the heart and their branches, accompanied by narrowing, obliteration, or thrombosis of their lumen and subsequent disturbance of the nutrition of the myocardium. In the myocardium, a necrotic infarct may form, which is replaced by granulation, and then by scar connective tissue - cardiac callus. Much less often, chronic cardiac aneurysms develop on the basis of coronary artery embolism, nodular periarteritis (periarteritis nodosa), myocardial injuries, and chronic focal cardiomyosclerosis, in which bulging is given by several small foci located close to each other. Syphilis, with significant damage to the coronary vessels, does not lead to the formation of cardiac aneurysm. Chronic cardiac aneurysms are most often found in the left ventricle, in the lower part of its anterior wall, at the apex of the heart - so-called apical aneurysms. Aneurysms in the interventricular septum, consisting almost entirely of the muscle of the left ventricle, occur somewhat less frequently. The third most frequent location is on the posterior wall of the left ventricle, immediately below the base of the heart. These so-called basal aneurysms are anatomically distinguished from apical aneurysms by their narrower opening into the aneurysmatic sac. Chronic aneurysms on other parts of the left ventricle occur much less frequently, and in the right ventricle and atria even less frequently. Sometimes several aneurysms are found at different places and in different stages of formation (for example, up to four at once have been described). Aneurysms usually form a very slightly convex surface in relation to the surface of the rest of the heart; therefore, their recognition in life on the basis of X-ray has not yet been achieved. Data on roentgen-kinematographic analysis have not yet been published. Cardiac aneurysm, as such, often gives no characteristic clinical symptoms. The clinical picture corresponds to the basic pathological process on the basis of which the cardiac aneurysm arises. In acute cardiac aneurysms, this will, for the most part, be a septic infection (septic endocarditis). In chronic cases - the picture of cardiomyosclerosis and sclerosis of the coronary arteries with attacks of angina pectoris. Therefore, the in vivo diagnosis of cardiac aneurysm is very difficult, and most authors consider it generally impossible. However, in recent years, more than 10 cases have been published in which the diagnosis of cardiac aneurysm was made in life and confirmed at autopsy. Almost all of these cases refer to chronic cardiac aneurysm on the basis of arteriosclerosis. The main point of support for the in vivo diagnosis of cardiac aneurysm is, first of all, the possibility to establish, mainly from the anamnesis, the formation of a myocardial infarct. The syndrome of myocardial infarct is now developed in detail and does not present difficulties for diagnosis. It is, in general terms, reduced to an unusually prolonged and severe attack of angina pectoris, lasting for hours or days and accompanied in the future by signs of cardiac weakness. The latter should not necessarily be expressed, as some think, in severe suffocation, dyspnea, collapse, and other violent phenomena, since much will depend on the location and extent of the infarct. On the contrary, cardiac insufficiency, characterized by the formation of an infarct, very often reduces only to a moderate decrease in blood pressure, tachycardia, general muscle weakness, and in some cases exclusively to a slight subfebrile rise in temperature. Ordinary attacks of angina pectoris are not accompanied by a rise in temperature. Its appearance always indicates the formation of myocardial necroses, myxomatous degeneration (see), often with epicardial endocarditis or pericarditis, and serves as one of the most important objective signs for the in vivo recognition of myocardial infarcts. Over time, the infarct is replaced by cardiac callus. The initial cardiac dilatation, if it existed, decreases, and the patient gradually improves. But, if - or directly after the formation of the infarct or after months, even after apparent recovery (Sternberg, Pletnev) - the patient begins to dilate the heart without visible reason and slowly and irresistibly increases, despite treatment, and progressive cardiac insufficiency with suffocation, dyspnea, edema, etc., sets in - then almost always in the basis of such late post-infarct decompensation lies myocardial aneurysm.