Abstract
It has been known for more than a century that in experimental animals acute ischemia produced by occlusion of a major coronary artery frequently results in the occurrence of ventricular fibrillation within several minutes after the onset of ischemia [1]. The same study also states that sudden release of a coronary artery occlusion may induce fibrillation. It is of interest to note that the reason for undertaking this experimental study was the clinical observation that the only pathologic finding in humans who died suddenly (“strong, well-fed individuals in the prime of their life, who during a walk, at the opera or during a meal, as if struck by lightning, suddenly collapsed and within a few minutes stopped living” [1]) was sclerosis of the coronary arteries. The hypothesis put forward to explain these dramatic events was that cardiac metabolism produces substances that are harmful; normally these substances are washed away by the coronary circulation, and only on their accumulation when coronary flow stops are they able to exert a noxious influence.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Cohnheim, J. and von Schulthess-Rechberg, A. 1881. Ueber die Folgen Kranzarterieinvers-chliessung fuer das Herz Virchows Arch. 85:503–537.
Kennel, W.B. and Thomas, H.E. 1982. Sudden coronary death: The Framingham Study. Ann. NY Acad. Sci. 382:3–21.
Lown, B. 1979. Sudden cardiac death: the major challenge confronting modern cardiology. Am. J. Cardiol. 43:313–329.
Trolese-Mongheal, Y., Duchesne-Marulluz, P., Trolese, J.F., et al. 1985. Sudden death and experimental acute myocardial infarction Am. J. Cardiol. 56:677–681.
Bolli, R., Fisher, D.J., and Entman, W.L. 1986. Factors that determine the occurrence of arrhythmias during acute myocardial ischemia. Am. Heart J. 111:261–270.
Meesmann, W. 1982. Early arrhythmias and primary ventricular fibrillation after acute myocardial ischemia in relation to pre-existing collaterals. In Early Arrhythmias Resulting from Myocardial Ischemia, J.R. Parratt, ed., pp. 93–112, London, MacMillan.
Curtis, M.J., MacLeod, B.A., and Walker, M.J.A. 1987. Models for the study of arrhythmias in myocardial ischemia and infarction: the use of the rat. J. Mol. Cell. Cardiol. 19:399–419.
Manning, G.W., McEachern, CG., and Hall, G.E. 1939. Reflex coronary artery spasm following sudden occlusion of other coronary branches. Arch. Intern. Med. 64:662–674.
Bolli, R., Myers, M.L., Zhu, W-X, and Roberts, R. 1986. Disparity of reperfusion arrhythmias after reversible myocardial ischemia in open chest and conscious dogs J. Am. Coll. Cardiol. 7:1047–1056.
Skinner, J.E., Lie, J.T., and Entman, M.L. 1975. Modification of ventricular fibrillation latency following coronary artery occlusion in the conscious pig: the effects of psychological stress and beta-adrenergic blockade. Circulation 51:656–667.
Skinner, J.E. 1987. How the head rules the heart, in Life Threatening Arrhythmias During Ischemia and Infarction, D.J. Hearse, A.S. Manning, and M.J. Janse, eds., pp. 135–151, New York, Raven Press.
Schwartz, P.J. and Stone, H.L. 1982. The role of the autonomic nervous system in sudden coronary death. Ann. NY Acad. Sci. 382:162–180.
Martin, C. and Meesmann, W. 1985. Antiarrhythmic effect of regional myocardial chemical sympathectomy in the early phase of coronary artery occlusion in dogs. J. Cardiovasc. Pharmacol. 7:576–580.
Harris, A.S. 1950. Delayed development of ventricular ectopic rhythm following experimental coronary occlusion. Circulation 1:1381–1328.
Lynch, J.J. and Lucchesi, B.R. 1987. How are animal models best used for the study of antiarrhythmic drugs? in Life Threatening Arrhythmias During Ischemia and Infarction, D.J. Hearse, A.S. Manning, and M.J. Janse, eds., pp. 169–196, New York, Raven Press.
Janse, M.J. and Kléber, A.G. 1981. Electrophysiological changes and ventricular arrhythmias in the early phase of myocardial ischemia Cir. Res. 49:1064–1081.
Coronel, R., Fiolet, J.W.T., Wilms-Schopman, F.J.G., et al. in press. Distribution of extracellular potassium and its relation to electrophysiologic changes during acute myocardial ischemia in the isolated porcine heart Circulation.
Kléber, A.G. 1984. Extracellular potassium accumulation in acute myocaridal ischemia. J. Mol. Cell. Cardiol. 16:389–394.
Morena, H., Janse, M.J., Fiolet, J.W.T., et al. 1980. Comparison of the effects of regional ischemia, hypoxia, hyperkalemia and acidosis on intracellular and extracellular potentials and metabolism in the isolated porcine heart Circ. Res. 46:634–646.
Wilde, A.A.M. 1988. Myocardial Ischemia and Hypoxia. Effect on Cellular Ionic and Electrical Activity. Ph.D. dessertation. University of Amsterdam.
Kléber, A.G., Riegger, C.B., and Janse, M.J. 1987. Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. Circ. Res. 61:271–279.
Kléber, A.G. and Riegger, C.B. 1987. Electrical constants of arterially perfused rabbit papillary muscle. J. Physiol. (Lond.) 385:307–324.
Kléber, A.G., Janse, M.J., Wilms-Schopman, F.J.G., et al. 1986. Changes in conduction velocity during acute ischemia in ventricular myocardium of the isolated porcine heart. Circulation 73:189–198.
Cardinal, R., Janse, M.J., van Eeden, I., et al. 1981. The effects of lidocaine on intracellular and extracellular potentials, activation and ventricular arrhythmias during acute regional ischemia in the isolated porcine heart. Cir. Res. 49:792–801.
Gettes, L.S. and Reuter, H. 1974. Slow recovery from inactivation of inward currents in mammalian myocardial fibers J. Physiol. (Lond.) 240:703–724.
Downar, E., Janse, M.J., and Durrer, D. 1977. The effect of acute coronary occlusion on subepicardial transmembrane potentials in the intact porcine heart Circulation 56:217–224.
Hill, J.L. and Gettes, L.S. 1980. Effect of acute coronary artery occlusion on local myocardial extracellular K+ activity in swine Circulation 61:768–778.
Capucci, A., Coronel, R., Fabius, M., and Janse, M.J. 1985. Electrophysiologic mechanism of ventricular arrhythmias in acute ischemia: further observations. New Trends in Arrhythmias 1:41–56.
Smeets, J.L.R.M., Allessie, M.A., Lammers, W.J.E.P., et al. 1986. The wavelength of the cardiac impulse and re-entrant arrhythmias in isolated rabbit atrium. Circ. Res. 58:96–108.
Janse, M.J. and van Capelle, F.J.L. 1982. Electrotonic interactions across an inexcitable region as a cause of ectopic activity in acute regional myocardial ischemia. A study in intact porcine and canine hearts and computer models. Circ. Res. 50:527–537.
Pogwizd, S. and Corr, P.B. 1987. Re-entrant and non re-entrant mechanisms contribute to arrhythmogenesis during early myocardial ischemia: results using three-dimensional mapping. Circ. Res. 61:352–371.
Janse, M.J., van Capelle, F.J.L., Morsink, H., et al. 1980. Flow of “injury” current and patterns of excitation during early ventricular arrhythmias in acute regional myocardial ischemia in isolated porcine and canine hearts. Circ. Res. 47:151–165.
Janse, M.J., Kleber, A.G., Capucci, A., et al. 1986. Electrophysiological basis for arrhythmias caused by acute ischemia. Role of the subendocardium. J. Mol. Cell. Cardiol. 18:339–355.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1989 Kluwer Academic Publishers, Boston/Dordrecht/London
About this chapter
Cite this chapter
Janse, M.J. (1989). Arrhythmias in the Early Ischemic Period. In: Rosen, M.R., Palti, Y. (eds) Lethal Arrhythmias Resulting from Myocardial Ischemia and Infarction. Developments in Cardiovascular Medicine, vol 94. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1649-7_16
Download citation
DOI: https://doi.org/10.1007/978-1-4613-1649-7_16
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8916-6
Online ISBN: 978-1-4613-1649-7
eBook Packages: Springer Book Archive