Abstract
Sudden release of a coronary artery occlusion is known to be a potent arrhythmogenic stimulus, often leading to ventricular fibrillation [1–4]. Although this phenomenon has been the subject of intense laboratory investigation, assessment of its clinical relevance has been difficult. The majority of patients with acute myocardial infarction undergoing coronary thrombolysis and/or angioplasty, or even those patients with Prinzmetal’s angina have not experienced significant reperfusion arrhythmias. This is not surprising as experimental data derived from dog studies suggest that the prevalence of reperfusion arrhythmias is related to a range of values for different variables that, if not satisfied, would minimize the expression of such arrhythmias. Practical considerations may reduce the risk for certain factors, such as duration of occlusion, myocardium at risk, and magnitude of reflow during reperfusion, resulting in a nominal risk for most patients [1–5]. Nonetheless, as patient access to thrombolytic therapy is accelerated, the duration of occlusion may be shortened, and expression of these arrhythmias may actually increase. More important, interaction among variables may occur, thereby altering the relationship between prevalence of arrhythmia and the value of a particular variable, so that expression of this arrhythmia may increase.
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References
Tennant, R., and Wiggers, C.J. 1935. The effect of coronary occlusion on myocardial contraction. Am. J. Physiol. 112:351–361.
Balke, C.W., Kaplinsky, E., Michelson, E.L., et al. 1981. Reperfusion ventricular tachyarrhythmias: correlation with antecedent coronary artery occlusion tachyarrhythmias and duration of myocardial ischemia. Am. Heart J. 101:449–456.
Battle, W.E., Naimi, S., Avitall, B., et al. 1974. Distinctive time course of ventricular vulnerability to fibrillation during and after release of coronary ligation. Am. J. Cardiol. 34:42–47.
Manning, A.S., and Hearse, D.J. 1984. Reperfusion-induced arrhythmias: mechanisms and prevention. J. Mol. Cell. Cardiol. 16:497–518.
Austin, M., Wenger, T.L., Harrell, F.E. Jr., et al. 1982. Effect of myocardium at risk on outcome after coronary artery occlusion and release. Am. J. Physiol. 243:H340–H345.
Naito, M., Michelson, E.L., Kmetzo, J.J., et al. 1981. Failure of antiarrhythic drugs to prevent experimental reperfusion ventricular fibrillation. Circulation 63:70–79.
Sheridan, D.J., Penkoske, P.A., Sobel, B.E., and Corr, P.B. 1980. Alpha adrenergic contributions to dysrhythmias during myocardial ischemia and reperfusion in cats. J. Clin. Invest. 65:161–171.
Stephenson, S.E. Jr., Cole, R.K., Parrish, T.F., et al. 1960. Ventricular fibrillation during and after coronary artery occlusion: incidence and protection afforded by various drugs. Am. J. Cardiol. 5:77–87.
Stewart, J.R., Burmeister, W.E., Burmeister, J., and Lucchesi, B.R. 1980. Electrophysiologic and antiarrhythmic effects of phentolamine in experimental coronary artery occlusion and reperfusion in the dog. J. Cardiovasc. Pharmacol. 2:77–91.
Stockman, M.B., Verrier, R.L., and Lown, B. 1979. Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion. Am. J. Cardiol. 43:233–238.
Jennings, R.B., Sommers, H.M., Smyth, G.A., et al. 1960. Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog. Arch. Pathol. 70:68–78.
Lederman, S.N., Wenger, T.L., Harrell F.E. Jr., and Strauss, H.C. 1987. Effects of different paced heart rates on canine coronary occlusion and reperfusion arrhythmias. Am. Heart J. 113:1365–1369.
Corr, P.B., Shayman J.A., Kramer, J.B., and Kipnis, R.J. 1981. Increased a-adrenergic receptors in ischemic cat myocardium: a potential mediator of electrophysiological derangements. J. Clin. Invest. 67:1232–1236.
Corr, P.B., Yamada, K.A., and Witkowski, F.X. 1986. Mechanisms controlling cardiac autonomic function and their relation to arrhythmogenesis. In The Heart and Cardiovascular System, H.A. Fozzard et al., eds., pp. 1343–1403 New York, Raven Press.
Wilber, D.J., Lynch, J.J., Montgomery, D.G., and Lucchesi, B.R. 1987. a-adrenergic influences in canine ischemic sudden death: effects of ai-adrenoceptor blockade with prazosin. J. Cardiovasc. Pharmacol. 10:96–106.
Kleber, A.G. 1983. Resting membrane potential, extracellular potassium activity, and intracellular sodium activity during acute global ischemia in isolated perfused guinea pig hearts. Circ. Res. 52:442–450.
Ferrier, G.R., Moffat, M.P., and Lukas, A. 1985. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion: studies on isolated canine ventricular tissues. Circ. Res. 56:184–194.
Ferrier, G.R., Moffat, M.P., Lukas, A., and Mohabir, R. 1985. A model of ischemia and reperfusion: effect of potassium concentration of electrical and contractile responses of canine Purkinje tissue. In Cardiac Electrophysiology and Arrhythmias, pp. 325–330, New York, Grune and Stratton.
Hayashi, H., Ponnambalam C, and McDonald, T.F. 1987. Arrhythmic activity in re-oxygenated guinea pig papillary muscles and ventricular cells. Circ. Res. 61:124–133.
Yee, R., Brown, K.K., Bolster, D.E., and Strauss, H.C. 1988. The relationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusion. J. Clin. Invest. 82:225–233.
Hamill, O.P., Marty, A., Neher, E., et al. 1981. Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches. Pflugers Arch. 391:85–100.
Hill, J. A., Coronado, R., and Strauss, H.C. 1988. Reconstitution and characterization of a calcium-activated channel from heart. Circ. Res. 62:411–415.
Wier, W.G., Cannell, M.B., Berlin, J.R., et al. 1987. Cellular and subcellular heterogeneity of [Ca2+]i in single heart cells revealed by fura-2. Science 235:325–328.
Cannell, M.B., Wier, W.G., Berlin, J.R., et al. 1986. Free intracellular calcium in normal and calcium-overloaded rat heart cells: digital imaging fluorescent microscopy using fura-2. Biophys. J. 49:466a.
Yue, D.T., Marban, E., and Wier, W.G. 1986. Relationship between force and intracellular [Ca2+] in tetanized mammalian heart muscle. J. Gen. Physiol. 87:223–242.
Valdeolmillos, M., and Eisner, D.A. 1985. The effects of ryanodine on calcium-overloaded sheep cardiac Purkinje fibers. Circ. Res. 56:452–456.
Lauer, M.R., Rusy, B.F., and Davis, L.D. 1984. H+-induced membrane depolarization in canine cardiac Purkinje fibers. Am. J. Physiol. 247:H312-H321.
Kass, R.S., Lederer, W.J., Tisien, R.W., and Weingart, R. 1978. Role of calcium ions in transient inward currents and aftercontractions induced by strophanthidin in cardiac Purkinje fibers. J. Physiol. (Lond.) 281:187–208.
Grinwald, P.M. 1982. Calcium uptake during post-ischemic reperfusion in the isolated rat heart: Influence of extracellular sodium. J. Mol. Cell. Cardiol. 14:359–365.
Wilde, A. A.M., and Kleber, A.G. 1986. The combined effects of hypoxia, high K\ and acidosis on the intracellular sodium activity and resting potential in guinea pig papillary muscle. Circ. Res. 58:249–256.
Balasubramanian, V., McNamara, D.B., Singh, J.N., and Dhalla, N.S. 1973. Biochemical basis of heart function. X. Reduction in the Na+-K+-stimulated ATPase activity in failing rat heart due to hypoxia. Can. J. Physiol. Pharmacol. 51:502–510.
Russell, J.M., Boron, W.F., and Brodwick, M.S. 1983. Intracellular pH and Na fluxes in barnacle muscle with evidence for reversal of the ionic mechanism of intracellular pH regulation. J. Gen. Physiol. 82:47–78.
Allen, D.G., and Orchard, C.H. 1987. Myocardial contractile function during ischemia and hypoxia. Circ. Res. 60:153–168.
Deitmer, J.W., and Ellis, D.W. 1980. Interactions between the regulation of the intracellular pH and sodium activity of sheep cardiac Purkinje fibres. J. Physiol. (Lond.) 304:471–488.
Philipson, K.D., Bersohn, M.M., and Nishimoto, A.Y. 1982. Effects of pH on Na+-Ca2+ exchange in canine cardiac sarcolemmal vesicles. Circ. Res. 50:287–293.
Roos, A., and Boron, W.F. 1981. Intracellular pH. Physiol. Rev. 61:296–434.
de Hemptinne, A. 1980. Intracellular pH and surface pH in skeletal and cardiac muscle measured with a double-barrelled pH microelectrode. Pflugers Arch. 386:121–126.
Ellis, D., and Thomas, R.C. 1976. Direct measurement of the intracellular pH of mammalian cardiac muscle. J. Physiol. (Lond.) 262:755–771.
Hoerter, J.A., Miceli, M.V., Renlund, D.G., et al. 1986. A phosphorus-31 nuclear magnetic resonance study of the metabolic, contractile, and ionic consequences of induced calcium alterations in the isovolumic rat heart. Circ. Res. 58:539–551.
Couper, G.S., Weiss, J., Hiltbrand, B., and Shine, K.I. 1984. Extracellular pH and tension during ischemia in the isolated rabbit ventricle. Am. J. Physiol. 247:H916-H927.
Fabiato, A., and Fabiato, F. 1978. Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiac and skeletal muscles. J. Physiol. (Lond.) 276:233–255.
Kentish, J.C. 1986. The effects of inorganic phosphate and creatine phosphate on force production in skinned muscles from rat ventricle. J. Physiol. (Lond.) 370:585–604.
Blanchard, E.M., Pan, B.S., and Solaro, RJ. 1984. The effect of acidic pH on the ATPase activity and troponin Ca2+ binding of rabbit skeletal myofilaments. J. Biol. Chem. 259:3181–3186.
Langer, G.A. 1985. The effect of pH on cellular and membrane calcium binding and contraction of myocardium. Circ. Res. 57:374–382.
Kusoka, H., Porterfield, J.K., Weisman, H.F., et al. 1987. Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts. J. Clin. Invest. 79:950–961.
Colquhoun D., Neher, E., Reuter, H., and Stevens, C.F., 1981. Inward current channels activated by intracellular Ca in cultured cardiac cells. Nature 294:752–754.
Callewaert, G., Vereecke, J., and Carmeliet, E. 1986. Existence of a calcium-dependent potassium channel in the membrane of cow cardiac Purkinje cells. Pflugers Arch. 406:424–426.
Smith, J. S., Coronado, R., and Meissner, G. 1985. Sarcoplasmic reticulum contains adenine nucleotide-activated calcium channels. Nature 316:446–449.
Rousseau, E., Smith, J.S., Henderson, J.S., and Meissner, G. 1986. Single channel and 45Ca2+ flux measurements of the cardiac sarcoplasmic reticulum calcium channel. Biophys.J. 50:1009–1014.
Cannell, M.B., and Lederer, W.J. 1986. The arrhythmic Iti current in the absence of electrogenic sodium-calcium exchange in sheep cardiac Purkinje fibres. J. Physiol (Lond.) 374:201–219.
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Strauss, H.C., Yee, R., Hill, J.A., Wenger, T.L. (1989). Mechanisms of Reperfusion Arrhythmias. 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_5
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DOI: https://doi.org/10.1007/978-1-4613-1649-7_5
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