STRESS-INDUCED ARRHYTHMIC DISEASE OF THE HEART .1.

Authors
Citation
Fz. Meerson, STRESS-INDUCED ARRHYTHMIC DISEASE OF THE HEART .1., Clinical cardiology, 17(7), 1994, pp. 362-371
Citations number
62
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
01609289
Volume
17
Issue
7
Year of publication
1994
Pages
362 - 371
Database
ISI
SICI code
0160-9289(1994)17:7<362:SADOTH>2.0.ZU;2-F
Abstract
This review deals with the following principal concepts: (1) Heart inj uries in single severe stress episodes manifested primarily in disturb ances of membrane lipid bilayer, sarcolemmal Na, K-pump, and sarcoplas mic Ca-pump with concurrent limited disturbances of the heart energy s upply, namely, of the creatine kinase and glycolysis systems. These di sturbances cause small focal myocardial lesions and reduce cardiac ele ctrical stability: the fibrillation threshold falls and ectopic activi ty increases. In repeated stress, this damage, localized mainly in the richly innervated conduction system, accumulates to cause even more p ronounced 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. How ever, the entire primary complex of stress-induced injuries and distur bances of the heart's electrical stability occurs despite the increase d coronary blood flow. Thus, beta-adrenergic stress-induced injuries m ay indeed develop as primary stress damage to cardiomyocytes without a ny relation to ischemia. (3) The main factor determining high vulnerab ility or, on the contrary, resistance of the heart to stress is the st ate of stress-limiting systems, namely, the opioidergic, GABAergic, ch olinergic, adenosinergic, and other systems. Activation of these syste ms by adaptation to repeated stress or other factors prevents serious injuries to the heart in severe stress. Conversely, genetically determ ined or acquired dysfunction of these systems predisposes to severe ar rhythmias and sudden death. Thus, in stress-induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic are outsi de the heart, but they differ from those observed in ischemia. (4) The clinical picture of stress-induced arrhythmic disease, that is, alter ations in electrocardiogram, coronarogram, and patient responses to st ress, physical loads, and tranquilizers differ, as do pathologic alter ations in the heart. These differences are summarized at the end of th is review.