Summary
The electrophysiological mechanisms underlying supraventricular dysrhythmias that accompany acute myocardial infarction were studied in rabbits subjected to ligation of right coronary artery. In vivo, sinus bradycardia, atrioventricular block and rapid atrial arrhythmias were observed 2 to 5 hours after coronary occlusion; evidence of ventricular arrhythmias was absent. The bradyarrhythmias were markedly improved after iv administration of atropine. The infarcted hearts were then removed and the isolated sinoatrial (SA) node, right atrium and atrioventricular (AV) node were studied with intracellular microelectrodes in vitro. Rapid, repetitive atrial depolarizations occurring spontaneously or initiated by premature atrial stimulation were observed only in preparations obtained from infarcted hearts. In disseminated areas localized within the SA node and the atrium, the subendocardial fibers had a reduced action potential amplitude but showed also normal potentials in other regions as compared with noninfarcted preparations. Sinus rate, poststimulatory sinus-node recovery time, intraatrial conduction and the parameters of AV nodal function including action potential amplitude and conduction were not significantly different in preparations isolated from infarcted and noninfarcted hearts. The results suggest that the observed bradyarrhythmias accompanying acute myocardial infarction may be partly due to a vagomimetic reflex whereas the supraventricular tachycardias seem to result from direct cellular damage.
Zusammenfassung
Die elektrophysiologischen Mechanismen von supraventrikulären Arrhythmien bei akutem Myokardinfarkt wurden an Kaninchen untersucht, bei denen die rechte Koronararterie unterbunden wurde. In vivo wurden 2 bis 3 Stunden nach Koronarverschluß eine Sinusbradykardie, atrioventrikuläre Blockierungen und atriale Tachykardien beobachtet. Atropin (i.v.) führte zu einer signifikanten Rückbildung der Bradykardien. Anschließend wurden die infarzierten Herzen freipräpariert und der rechte Vorhof einschließlich sinuatrialem (SA) und atrioventrikulärem (AV) Knoten mit intrazellulären Mikroelektroden in vitro untersucht. Im Vergleich zu Kontrollpräparaten von nichtinfarzierten Herzen wurden bei Vorhöfen von infarzierten Herzen folgende Befunde beobachtet:
1. Spontane atriale Tachykardien. 2. Abnahme der Amplitude des Aktionspotentials in disseminierten subendokardialen atrialen und SA nodalen Fasern, aber normale Aktionspotentiale bei der Mehrzahl der untersuchten Fasern. 3. Normale Sinusfrequenz, poststimulatorische Sinusknotenerholungszeit, intraatriale und AV nodale Leitungszeiten. Die Befunde deuten auf einen vagomimetischen Reflex als überwiegende Ursache der in vivo beobachteten Bradykardien hin, während die supraventrikulären Tachykardien möglicherweise durch eine direkte Schädigung der Zellmembran bedingt sind.
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References
Adgey, A. A. J., J. S. Geddes, S. W. Webb, J. D. Allen, R. G. G. James, S. A. Zaidi, J. F. Pantridge: Acute phase of myocardial infarction. Lancet1971, 501–504.
Allessie, M. A., F. I. M. Bonke, F. J. G. Schopman: Circus movement in rabbit atrial muscle as a mechanism of tachycardia. Circulation Res.33, 54–62 (1973).
Bigger, J. T. Jr., B. N. Goldreyer: Mechanism of supraventricular tachycardia. Circulation42, 673–683 (1970).
Bretag, A.: Synthetic interstitial fluid for isolated mammalian tissue. Life Sci.8, 319–329 (1969).
Corr, P. B., R. A. Gillis: Role of the vagus nerves in the cardiovascular changes included by coronary occlusion. Circulation49, 86–97 (1974).
Day, S. B., J. A. Johnson: Distribution of the coronary arteries of the rabbit. Anat. Record132, 633–641 (1958).
Friedman, P. L., J. R. Stewart, A. L. Wit: Spontaneous and induced cardiac arrhythmias in subendocardial Purkinje fibers surviving extensive myocardial infarction in dogs. Circ. Res.33, 612–626 (1973).
Friedman, P. L., J. R. Stewart, J. J. Fenoglio, A. L. Wit: Survival of subendocardial Purkinje fibers after extensive myocardial infarction in dogs. In vitro and in vivo correlation. Circ. Res.33, 597–611 (1973).
Goldreyer, B. N., J. T. Bigger: Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation43, 15–26 (1971).
James, T. N.: Myocardial infarction and atrial arrhythmias. Circulation24, 761–776 (1961).
James, T. N.: Anatomy of the cardiac conduction system in the rabbit. Circ. Res.20, 638–648 (1967).
Janse, M. J., F. J. L. van Capelle, G. E. Freud, D. Durrer: Circus movement within the AV node as a basis for supraventricular tachycardia as shown by multiple microelectrode recording in the isolated rabbit heart. Circ. Res.28, 403–414 (1971).
Jewitt, D. E., R. Balcon, E. B. Raftery, S. Oram: Incidence and management of supraventricular arrhythmias after acute myocardial infarction. Amer. Heart J.77, 290–293 (1969).
Killip, T., J. Gault: Mode of onset of atrial fibrillation in man. Amer. Heart J.70, 172–179 (1965).
Klass, M., L. J. Haywood: Myocardial fibrillation associated with acute myocardial infarction: A study of 34 cases. Amer. Heart J.79, 752–760 (1970).
Lippestad, C. T., P. F. Marton: Sinus arrest in proximal right coronary artery occlusion. Amer. Heart J.74, 551–556 (1967).
El-Sherif, N., B. J. Scherlag, R. Lazzara, R. R. Hope: Re-entrant ventricular arrhythmias in the late myocardial period. 1. Conduction characteristics in the infarction zone. Circulation55, 686–702 (1977).
Myers, R. W., A. S. Pearlman, R. M. Hyman, R. A. Goldstein, K. M. Kent, R. E. Goldstein, S. E. Epstein: Beneficial effects of vagal stimulation and bradycardia during experimental acute myocardial ischemia. Circulation49, 943–947 (1974).
Narula, O. S., P. Samet, R. P. Javier: Significance of the sinus-node recovery time. Circulation45, 140–158 (1972).
Paes de Carvalho, A., W. C. De Mello, B. F. Hoffman: Electrophysiological evidence for specialized fiber types in rabbit atrium. Am. J. Physiol.196, 483–488 (1959).
Senges, J., T. Mizutani, D. Pelzer, J. Brachmann, U. Sonnhof, W. Kübler: Effect of hypoxia on the sinoatrial node, atrium and atrioventricular node in the rabbit heart. Accepted for publication to Circ. Res. (1978).
Senges, J., J. Brachmann, D. Pelzer, T. Mizutani, W. Kübler: Effects of components of ischemia on electrical activity and reentry in the ventricular conducting system. Accepted for publication to Circ. Res. (1978).
Wit, A. L., P. F. Cranefield: Triggered activity in cardiac muscle fibers of the simian mitral valve. Circ. Res.38, 85–98 (1976).
Wit, A. L., B. N. Goldreyer, A. N. Damato: An in vitro model of paroxysmal supraventricular tachycardia. Circulation43, 862–875 (1971).
Wit, A. L., J. T. Bigger: Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation51 and52 (suppl III), III 96-III 115 (1975).
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With 8 figures and 2 tables
The studies were supported by the German Research Foundation within the SFB 90 “Cardiovaskuläres System”. Dr.Mizutani is a Research Fellow of the Alexander von Humboldt Stiftung.
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Mizutani, T., Senges, J., Brachmann, J. et al. Supraventricular arrhythmias in experimental myocardial infarction. Basic Res Cardiol 74, 83–94 (1979). https://doi.org/10.1007/BF01907687
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DOI: https://doi.org/10.1007/BF01907687