title: Stress-induced arrhythmic disease of the heart--Part I.
abstract: This review deals with the following principal concepts: (1) Heart injuries in single severe stress episodes manifested primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K-pump, and sarcoplasmic Ca-pump with concurrent limited disturbances of the heart energy supply, namely, of the creatine kinase and glycolysis systems. These disturbances cause small focal myocardial lesions and reduce cardiac electrical stability: the fibrillation threshold falls and ectopic activity increases. In repeated stress, this damage, localized mainly in the richly innervated conduction system, accumulates to cause even more pronounced disturbances of electrical stability and severe arrhythmias. (2) Severe stress and beta-adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress-induced injuries and disturbances of the heart's electrical stability occurs despite the increased coronary blood flow. Thus, beta-adrenergic stress-induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. (3) The main factor determining high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress-limiting systems, namely, the opioidergic, GABAergic, cholinergic, adenosinergic, and other systems. Activation of these systems by adaptation to repeated stress or other factors prevents serious injuries to the heart in severe stress. Conversely, genetically determined or acquired dysfunction of these systems predisposes to severe arrhythmias and sudden death. Thus, in stress-induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic links are outside the heart, but they differ from those observed in ischemia. (4) The clinical picture of stress-induced arrhythmic disease, that is, alterations in electrocardiogram, coronarogram, and patient responses to stress, physical loads, and tranquilizers differ, as do pathologic alterations in the heart. These differences are summarized at the end of this review.
authors.affiliation: Laboratory of Heart Pathophysiology, Institute of General Pathology and Pathophysiology, Moscow, Russia.
authors.forename: F Z
authors.initials: FZ
authors.lastname: Meerson
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D005790:General Adaptation Syndrome / Q000378:metabolism / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology; D006801:Humans; D017202:Myocardial Ischemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D013312:Stress, Physiological / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology