Abstract
Myocardial infarction represents a highly likely source of reentrant ventricular arrhythmias, Although most studies of the early phase of ventricular arrhythmias that follow acute ligation of a major coronary artery in the dog have shown some of the basic prerequisites for reentry in the form of desynchronized slow conduction in ischemic myocardium (1–8), they all fall short of actually documenting the presence of reentry. This was due, we believe, to the highly dynamic situation following acute ligation of a major coronary artery with constantly changing electrophysiological properties in the ischemic zone. Thus, it is difficult to conduct systematic electrophysiological studies of the possible reentrant mechanism under such dynamic conditions. In addition, the recording techniques usually failed to demonstrate the one unequivocal evidence for reentry, viz: the presence of continuous electrical activity originating from the infarction zone that regularly and predictably bridge the diastolic interval between the reentrant beat and the preceding impulse, as well as between consecutive reentrant beats (9).
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References
Gambetta M, Childers RW: The initial electrophysiologic disturbance in experimental myocardial infarction. Ann Intern Med 70: 1076, (abstr) 1969.
Han J: Mechanisms of ventricular arrhythmias associated with myocardial infarction. Am J Cardiol 24: 800–813, 1969.
Durrer D, Van Dam RTH, Freud GE, Janse MJ: Reentry and ventricular arrhythmias in local ischemia and infarction of the intact dog heart. Proc Kon Ned Akad Van Wetensch Amsterdam C73: no 4, 1971.
Waldo AL, Kaiser GA: A study of ventricular arrhythmias associated with acute myocardial infarction in the canine heart. Circulation 47: 1222–1288, 1973.
Boineau JP, Cox JL: Slow ventricular activation in acute myocardial infarction. A source of re-entrant premature ventricular contractions. Circulation 48: 702–713, 1973.
Scherlag BJ, El-Sherif N, Hope R. Lazzara R: Characterization and localization of ventricular arrhythmias due to myocardial ischemia and infarction. Circ Res 35: 372–383, 1974.
Williams DO, Scherlag BJ, Hope R, El-Sherif N. Lazzara R: The pathophysiology of malignant ventricular arrhythmias during acute myocardial ischemia. Circulation 50: 1163–1172, 1974.
El-Sherif N, Scherlag BJ, Lazzara R: Electrode catheter recordings during malignant ventricular arrhythmias following experimental acute myocardial ischemia. Circulation 51: 1003–1014, 1975.
El-Sherif N, Scherlag BJ, Lazzara R, Hope RR: Reentrant ventricular arrhythmias in the late myocardial period. 1. Conduction characteristics in the infarction zone. Circulation 55: 686–702, 1977.
El-Sherif N, Hope RR, Scherlag BJ, Lazzara R: Reentrant ventricular arrhythmias in the late myocardial infarction period. 2. Pattern of initiation and termination of reentry. Circulation 55: 702–719, 1977.
El-Sherif N, Lazzara R, Hope RR, Scherlag BJ: Reentrant ventricular arrhythmias in the late myocardial infarction period. 3. Manifest and concealed extrasystolic grouping. Circulation 56: 225–234, 1977.
El-Sherif N, Scherlag BJ, Lazzara R, Hope RR: Reentrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine. Circulation 56: 395–402, 1977.
El-Sherif N, Lazzara R: Reentrant ventricular arrhythmias in the late myocardial infarction period. 5. Mechanism of action of diphenylhydantoin. Circulation 57: 465–472, 1978.
El-Sherif N: Reentrant ventricular arrhythmias in the late myocardial infarction period. 6. Effect of the autonomic system. Circulation 58: 103–110, 1978.
El-Sherif N, Lazzara R: Reentrant ventricular arrhythmias in the late myocardial infarction period. 7. Effect of verapamil and D-600 and role of the “slow channel”. Circulation 60: 605–615, 1979.
Lazzara R, Hope RR, El-Sherif N, Scherlag BJ: Effects of lidocaine on hypoxic and ischemic cardiac cells. Am J Cardiology 41: 872–879, 1978.
Smith RA, EI-Sherif N, Evans AK: Epicardial mapping of ventricular reentrant pathways in the late myocardial infarction period. (abstr) Am J Cardiol 41: 427, 1978.
Edwards JE: What is myocardial infarction? Circulation 39, 40 (suppl IV): IV-5–12, 1969.
Schmitt FO, Erlanger J: Directional differences in the conduction of the impulse through heart muscle and their possible relation to extrasystolic and fibrillary contractions. Am J Physiol 87: 326, 1928.
Schamroth L, Marriott HJL: Concealed ventricular extrasystoles. Circulation 27: 1043–1049, 1963.
Schamroth L: The physiological basis of ectopic ventricular rhythm: A unifying concept. So Afr Med J (suppl) 3–26: 1971.
El-Sherif N, Scherlag BJ, Lazzara R, Samet P: Pathophysiology of tachycardia and bradycardia-dependent block in the canine proximal His-Purkinje system after acute ischemia. Am J Cardiol 33: 529–540, 1974.
Lazzara R, El-Sherif N, Scherlag BJ: Disorders of cellular electrophysiology produced by ischemia of the canine His bundle. Circ Res 36: 444–454, 1975.
Lazzara R, El-Sherif N, Hope RR, Scherlag BJ: Ventricular arrhythmias and electrophysiologic consequences of ischemia and infarction. Cir Res 42: 740–749, 1978.
Cranefield PF, Klein HO, Hoffman BF: Conduction of the cardiac impulse: 1. Delay, blocks and one-way block in depressed Purkinje fibers. Circ Res 28: 199–219, 1971.
Cranefield PF, Wit AL, Hoffman BF: Conduction of the cardiac impulse. II. Characteristics of very slow conduction. J Gen Physiol 59: 227–246, 1972.
Cranefield PF: The conduction of the cardiac impulse. Mount Kisco, New York, Futura Pub Co, 1975.
Carmeliet E, Vereeke S: Adrenaline and the plateau phase of the cardiac action potential: Importance of Ca+ + Na+, and K+ conductance. Pflueger Arch 313: 300–315, 1969.
Pappano AJ: Calcium-dependent action potentials produced by catecholamines in guinea pig atrial muscle fibers depolarized by potassium. Circ Res 27: 379–390, 1970.
Shigenobu K, Sperelakis N: Calcium current channels induced by catecholamines in chick embryonic hearts whose fast sodium channels are blocked by tetrodotoxin or elevated potassium. Circ Res 31: 932–952, 1972.
Wit AL, Hoffman BF, Cranefield PF: Slow conduction and reentry in the ventricular conducting system. Return extrasystole in canine Purkinje fibers. Circ Res 30: 11–22, 1972.
Shigenobu K, Schneider JA, Sperelakis N: Verapamil blockade of slow Na+ and Ca++ responses in myocardial cells. J Pharmacol Exp Ther 190: 280–288, 1974.
Wit AL, Bigger JT Jr: Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 51 (suppl 3): 96–115, 1975.
Thomas M, Shulman G, Opie L: Arteriovenous potassium changes and ventricular arrhythmias after coronary artery occlusion. Cardiovasc Res 4: 327–333, 1970.
Cherry G, Myers MB: The relationship to ventricular fibrillation of early tissue sodium and potassium shifts and coronary vein potassium levels in experimental myocardial infarction. J Thorac Cardiovasc Surg 61: 587–598, 1971.
Griffith J, Leung F: The sequential estimation of plasma catecholamines and whole blood histamine in myocardial infarction. Am Heart J 82: 171–179, 1971.
Downar E, Janse MJ, Durrer D: The effect of “ischemic” blood on transmembrane potentials of normal porcine ventricular myocardium. Circulation 55: 455–462, 1977.
Kuppersmith J. Shiang H, Litwak RS, Herman MV: Electrophysiologic effects of verapamil in canine myocardial ischemia. Am J Cardiol 37:149, 1976 (abstr).
Elharrar J, Gaum WE, Zipes DP: Effect of drugs on conduction delay and incidence of ventricular arrhythmias induced by acute coronary occlusion in dogs. Am J Cardiol 39: 544–549, 1977.
Smith HJ, Singh BN, Nisbet HD, et al: Effect of verapamil on infarct size following experimental coronary occlusion. Cardiovasc Res 9: 569–578, 1975.
Nayler W, Grau A, Slade A: A protective effect of verapamil on hypoxic heart muscle. Cardiovasc Res 10: 650–662, 1976.
Dudel J, Peper K, Rudel R: Effect of tetrodotoxin on the membrane current in cardiac muscle (Purkinje fibers). Pfluegers Arch 295: 213–226, 1967.
Gettes LS, Reuter H: Slow recovery from inactivation of inward currents in mamalian myocardial fibers. J Physiol 240: 703–724, 1974.
El-Sherif, N: Electrophysiologic basis of procainamide therapeutic and toxic effects on ischemia-related reentrant ventricular arrhythmias. Am J. Cardiology 43:429, 1979 (abstr).
Wellens HJJ, Bär FWHM, Lie KI, Düren DR, Dohmen KJ: Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia. Am J Cardiol 40: 579–585, 1977.
Rosen MR, Hoffman BF: Mechanisms of action of antiarrhythmic drugs. Circ Res 32: 1–8, 1973.
Kohlhardt M, Bauer B, Kranse H, Fleckenstein A: Differentiation of the transmembrane Na and Ca channels in mammalian cardiac fibers by use of specific inhibitors. Pfluegers Arch 335: 309–322, 1972.
Cranefield PF, Aronson RS, Wit AL: Effect of verapamil on the normal action potential and on a calcium-dependent slow response of canine Purkinje fibers. Circ Res 34: 204–216, 1974.
Watanabe AM, Besch HR Jr: Subcellular myocardial effects of verapamil and D-600: Comparison with propranolol. J Pharmacol Exp Ther 191: 241–251, 1974.
Wit AL, Cranefield PF: The effects of verapamil on the sino-atrial and atrioventricular nodes of the rabbit and the mechanism by which it arrests reentrant AV nodal tachycardia. Circ Res 35: 413–425, 1974.
Angus JA, Richmond DR, Dhumma-Upakorn P, Cobbin LB, Goodman AH: Cardiovascular action of verapamil in the dog with particular reference to myocardial contractility and atrioventricular conduction. Cardiovasc Res 10: 623–632, 1976.
Danile P, Hordoff AJ, Delphin Es, Rosen MR: Verapamil effects on blood superfused Purkinje fibers: Evidence for direct and catecholamine-mediated actions. Am J Cardiol 41:417, 1978 (abstr).
Nawrath H, Ten Eick RE, McDonald TF, Trautwein W: On the mechanism underlying the action of D-600 on slow inward current and tension in mamalian myocardium. Circ Res 40: 408–414, 1977.
Carmeliet E: Cardiac transmembrane potentials and metabolism. Circ Res 42: 577–587, 1478.
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El-Sherif, N., Gomes, J.A.C., Kelen, G.J., Khan, R.G., Kang, P.S., Zeiler, R.H. (1980). Electrophysiological, Biochemical and Pharmacological Aspects of Reentrant Ventricular Arrhythmias in the Late Myocardial Infarction Period. In: Kulbertus, H.E., Wellens, H.J.J. (eds) Sudden Death. Developments in Cardiovascular Medicine, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-8834-7_7
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DOI: https://doi.org/10.1007/978-94-009-8834-7_7
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