Abstract
Ventricular hypertrophy is a common consequence of most forms of heart disease. There is usually a period of compensated hypertrophy, often lasting many years in humans, but eventually there may be decompensation with congestive heart failure [1, 2]. During the compensated stage the increased wall thickness remains constant, and in concentric hypertrophy due to pressure overloads, the wall stress tends to be normal [2–4]. Because peak systolic wall tension is a good predictor of myocardial oxygen demand [5], the resting hypertrophied ventricle has an increased oxygen consumption in proportion to its increased mass. With exercise or sympathetic stimulation, its oxygen consumption will rise in proportion to the increased heart rate, contractility, and systolic pressure that result. If, however, the ventricle dilates, either because of excessive stresses placed on it or because of myocardial depression from drugs or surgical procedures, then the decreased mass:volume ratio will be associated with an increased peak wall stress [2]. Consequently, the myocardial oxygen demand will rise out of proportion to pressures and heart rates.
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© 1989 Kluwer Academic Publishers
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Hoffman, J.I.E. (1989). Coronary circulation, cardiac hypertrophy, and myocardial ischemia. In: Safar, M.E., Fouad-Tarazi, F. (eds) The Heart in Hypertension. Developments in Cardiovascular Medicine, vol 98. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0941-0_22
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DOI: https://doi.org/10.1007/978-94-009-0941-0_22
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-6913-7
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