Abstract
The myocardial cell hypertrophies as an adaptive response to a mechanical overload. However, cardiac hypertrophy induced by chronic pressure overload results in a variety of structural and functional changes. These include alterations in morphology, metabolism, hemodynamics, contraction, and electrophysiology. Despite these adaptations, or because of these alterations, patients with left ventricular hypertrophy have high risk of cardiovascular morbidity and mortality. Electrophysiological abnormalities may be partly responsible for the increased mortality rate with left ventricular hypertrophy. Several recent clinical studies have demonstrated an increased incidence of ventricular arrhythmias and sudden cardiac death presumably due to ventricular fibrillation or tachycardia in association with left ventricular hypertrophy (1–3). In addition, superimposition of ischemia enhances arrhythmogenesis in hypertrophied hearts. Experimentally, it has been demonstrated that the incidence of ischemia- and reperfusion-induced ventricular fibrillation and sudden death are significantly higher in rats and dogs with left ventricular hypertrophy (4–6). However, the precise mechanisms of electrophysiological abnormalities and enhanced arrhythmogenesis in cardiac hypertrophy remain unsettled.
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References
Levy D, Anderson KM, Savage DD Balkus SA, Kannel WB, Castelli WP (1987) Risk of ventricular arrhythmias in left ventricular hypertrophy ( The Framingham Heart Study). Am J Cardiol 60: 560–565
McLenachan JM, Henderson E, Morris KI, Dargie HJ, (1987) Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med 317: 787–792
Messerli FH, Ventura HO, Elizardi DJ, Dunn FG, Frolisch ED (1984) Hypertension and sudden death: increased ventricular ectopic activity in left ventricular hypertrophy. Am J Med 77: 18–22
Kohya T, Kimura S, Myerburg RJ, Bassett AL (1988) Susceptibility of hypertrophied rat hearts to ventricular fibrillation during acute ischemia. J Mol Cell Cardiol 20: 159–168
Koyanagi S, Eastham G, Marcus ML (1982) Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden death after coronary artery occlusion in conscious dogs. Circulation 65: 1192–1197
Taylor AL, Winter R, Thandroyen F, Murphree S, Buja LM, Eckels R, Pastor P, Kremers M (1990) Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy. Circ Res 67: 501–509
Bassett AL, Gelband H (1973) Chronic partial occlusion of the pulmonary artery in cats: change in ventricular action potential configuration during early hypertrophy. Circ Res 32: 15–26
Tritthart H, Leudcke H, Bayer R, Sterle H, Kauffmann R (1975) Right ventricular hypertrophy in the cat: An electrophysiological anatomical study. J Mol Cell Cardiol 7:163–174
TenEick RE, Houser SR, Bassett AL (1989) Cardiac hypertrophy and altered cellular electrical activity of the myocardium. In: Physiology and Pathophysiology of the Heart, edited by Sperelakis N, Kluwer Academic Publishers, Boston, p. 573–594
Aronson RS (1980) Characteristics of action potentials of hypertrophied myocardium from rats with renal hypertension. Circ Res 47: 443–454
Gulch RW (1980) The effect of chronic loading on the action potential of mammalian myocardium. J Mol Cell Cardiol 12: 425–420
Cameron JS, Myerburg RJ, Wong SS, Gaide MS, Epstein K, Alvarez TR, Gelband H, Guse PA, Bassett AL (1983) Electrophysiologic consequences of chronic experimentally- induced left ventricular pressure overload. J Am Coll Cardiol 2: 481–487
Cameron JS, Linda SM, Kimura S, Kaiser CJ, Campbell DR, Kozlovskis PL, Gaide MS, Myerburg RJ, Bassett AL (1986) Systemic hypertension induces disparate localized left ventricular action potential lengthening and altered sensitivity to verapamil in left ventricular myocardium. J Mol Cell Cardiol 18: 169–175
Ten Eick RE, Bassett AL, Robertson LL (1983) Possible electrophysiological basis for decreased contractility associated with myocardial hypertrophy in the cats: a voltage clamp approach. In: Perspectives in Cardiovascular Research. Myocardial Hypertrophy and Failure, edited by Alpert NR. New York, Raven, vol. 7, p. 245–259
Kleiman RB, Houser SR (1988) Calcium currents in normal and hypertrophied isolated feline ventricular myocytes. Am J Physiol 255 (Heart Circ Physiol 24): H1434–1442
Kleiman RB, Houser SR (1989) Outward currents in normal and hypertrophied feline ventricular myocytes. Am J Physiol 256 (Heart Circ Physiol 25): H1450–1461
Keung EC (1989) Calcium current is increased in isolated adult myocytes from hypertrophied rat myocardium. Circ Res 64: 753–763
Scamps F, Mayoux E, Charlemagne D, Vassort G (1991) Calcium current in single cells isolated from normal and hypertrophied rat heart: Effects of β-adrenergic stimulation. Circ Res 67: 199–208
Cameron JS, Bassett AL, Gaide MS, Wong SS, Lodge NJ, Kozlovskis PL, Myerburg RJ (1987) Cellular electrophysiological effects of coronary artery ligation in chronically pressure overloaded cat hearts. Int J Cardiol 14:155–168
Noma A (1983) ATP-regulated K+ channels in cardiac muscle. Nature 305: 147–148
Cuevas J, Bassett AL, Cameron JS, Furukawa T, Myerburg RJ, Kimura S (1991) Effect of H+ on ATP-regulated K+ channels in feline ventricular myocytes. Am J Physiol 261 (Heart Circ Physiol 30): H755–H761
Cameron JS, Kimura S, Jackson-Burns DA, Smith DB, Bassett AL (1988) ATP–sensitive K+ channels are altered in hypertrophied ventricular myocytes. Am J Physiol 255 (Heart Circ Physiol 24): H1254–H1258
Noma A, Shibasaki T (1985) Membrane current through adenosine-triphosphate-regulated potassium channels in guinea-pig ventricular cells. J Physiol 363: 463–480
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© 1992 Springer-Verlag Tokyo
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Kimura, S., Basseit, A.L., Myerburg, R.J. (1992). Electrophysiological Abnormalities in Cardiac Hypertrophy. In: Yasuda, H., Kawaguchi, H. (eds) New Aspects in the Treatment of Failing Heart. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68219-6_16
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DOI: https://doi.org/10.1007/978-4-431-68219-6_16
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-68221-9
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