PRIMARY STRESS-INDUCED MYOCARDIAL DAMAGE AND ARRHYTHMIC HEART

The review deals with the following principal concepts: 1. Heart injur ies in single severe stress manifesting themselves primarily in distur bances of membrane lipid bilayer, sarcolemmal Na, K-pump and sarcoplas mic Ca-pump. At the same time there appear limited disturbances of the heart energy supply, namely, of creatine kinase system and glycolysis system. These disturbances cause small-focal myocardial lesions, lead to disorders of myocardium stretchability (poststress rigidity) and r educe the cardiac electrical stability: fibrillation threshold falls a nd ectopic activity increases. This complex of injuries is reversible to a considerable extent, but in repeated stress, the above mentioned damages localized mainly in richly innervated conduction system accumu late to cause even more pronounced disturbances of electric stability and severe arrhythmias. 2. Severe stress and beta-adrenergic effects o n the heart regularly result in coronary vasodilation and increased co ronary blood flow. However, the entire primary complex of stress-induc ed injuries and disturbances of the heart electric stability occur in this process despite the increased coronary blood flow. This correspon ds to a well-known fact that isoproterenol, a selective beta-agonist, dilates blood vessels and simultaneously provokes a complex of injurie s in the heart similar to the stress-induced one. Thus beta-adrenergic stress-induced injuries may indeed develop as primary stress damage t o cardiomyocytes without any relation to ischemia. 3. The main factor determining a high vulnerability or, on the contrary, resistance of th e heart to stress is the state of stress-limiting systems, namely, opi oidergic, GABAergic, cholinergic, adenosinergic and other ones. Activa tion of these systems by adaptation to repeated stress or some other f actors prevents serious injuries of the heart in severe stress. On the contrary, genetically determined or acquired invalidity of these syst ems predisposes one to severe arrhythmias and sudden death. Thus, in s tress-induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic links are outside the heart, but they differ fr om those observed in ischemia. 4. The clinical picture of stress-induc ed arrhythmic disease, i. e. alterations in ECG, coronarogram and pati ent responses to stress, physical loads, tranguilizers, as well as pat hological alterations in the heart are different. These differences ar e summarized at the end of the review.