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European Heart Journal 1990 11(Supplement G):100-106; doi:10.1093/eurheartj/11.suppl_G.100
Copyright © 1990 by the European Society of Cardiology.
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© 1990 The European Society of Cardiology

Cardiac volume load as a determinant of the response of cardiac mass to antihypertensive therapy

F. H. H. Leenen* and J. Tsoporis{dagger}

Hypertension Unit, University of Ottawa Heart Institute Ottawa, Ontario, Canada

Correspondence: Frans H. H. Leenen, MD, PhD, FRCPC, Hypertension Unit H360, University of Ottawa Heart Institute, Ottawa Civic Hospital, 1053 Carling Avenue, Ottawa, Ontario, Canada, K1Y 4E9

Whereas chronic pressure overload induces left ventricular hypertrophy in a predictable way, the same lowering of systolic blood pressure by different antihypertensive drug classes is not associated with the same regression of LV mass. In particular, arterial vasodilators may not induce regression or even came progression despite persistent decreases in blood pressure. It has been commonly assumed that different activation of non-haemodynamic mechanisms may explain such a dissociation. However, different effects on the other haemodynamic determinant of cardiac mass, cardiac volume overload, have not been taken into account. Our results in normotensive and hypertensive humans and rats indicate that arterial vasodilators induce a pattern of changes in cardiac anatomy, compatible with cardiac volume overload being a major contributor to these changes. Cardiac sympathetic hyperactivity may also contribute, possibly more in hypertension than in normotension.

Key Words: Cardiac hypertrophy • pressure overload • volume overload • antihypertensive drugs • arterial vasodilators

* Supported by a career investigatorship from the Heart and Stroke Foundation of Ontario.

{dagger} Supported by a traineeship from the Heart and Stroke Foundation of Canada.


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