Abstract
The left ventricle (LV) in hypertension has to pump against a chronically increased workload, so that a priori, we would expect LV hypertrophy (LVH) to be an inevitable consequence of hypertension. Yet the reported prevalence of LVH in human hypertension is relatively low, much more so than in animal models. The first part of this chapter considers possible reasons for the apparent paradox. Similarly, if we regard LVH as a physiological response to hypertension, LV myocardial function would be expected to be either normal or enhanced. But here too there is no consensus, with divergent conclusions based on studies in humans and animals. The experimental conditions under which LV function has often been compared, probably contribute to the above differences. For example, the performance of the normal and LVH heart have often been assessed under different loading conditions, as discussed in the second part of the chapter. However, there are problems of oxygen delivery through the coronary circulation, which ultimately set limits on myocardial performance. The last part of the chapter considers regression of myocardial hypertrophy during anti-hypertensive drug therapy and whether this should be an explicit therapeutic target in management.
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© 1989 Kluwer Academic Publishers
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Korner, P.I. (1989). Cardiac structure and function in animal models and in human hypertension. 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_14
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DOI: https://doi.org/10.1007/978-94-009-0941-0_14
Publisher Name: Springer, Dordrecht
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