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(Hypertension. 2000;36:760.)
© 2000 American Heart Association, Inc.

Scientific Contributions

Quantification of the Contribution of Cardiac and Arterial Remodeling to Hypertension

Patrick Segers; Nikos Stergiopulos; Nico Westerhof

From the Laboratory for Physiology (P.S., N.W.), Institute for Cardiovascular Research, Free University of Amsterdam, the Netherlands; and Biomedical Engineering Laboratory (N.S.), EPFL, Lausanne, Switzerland.

Correspondence to Dr Patrick Segers, Laboratory for Physiology, Institute for Cardiovascular Research, Free University of Amsterdam, Van Der Boechorstlaan 7, 1081 BT Amsterdam, the Netherlands. E-mail patrick.segers{at}navier.rug.ac.be

Abstract—The study aim was to quantify the individual and combined contributions of both the arterial system and the heart to systolic blood pressure in hypertension. We assessed the parameters of a heart–arterial model for normotensive control subjects and hypertensive patients with left ventricular adaptation patterns classified as normal, concentric remodeling, concentric hypertrophy, or eccentric hypertrophy. The present simulations show that vascular stiffening alone increases the pulse pressure without increasing systolic blood pressure. It is only in combination with an increased peripheral resistance that arterial stiffening leads to systolic hypertension in concentric remodeling and concentric hypertrophy. The contribution of cardiac pump function to the increase in blood pressure depends on cardiac remodeling, hypertrophy, or both. In hypertensive patients with a normal left ventricle, the heart is responsible for 55% of the increase in systolic blood pressure. In concentric remodeling, concentric hypertrophy, and eccentric hypertrophy, the cardiac contribution to the increase in systolic blood pressure is 21%, 65%, and 108%, respectively. We conclude that along with arterial changes, cardiac remodeling and hypertrophy contribute to hypertension.

Key Words: hypertrophy • arteries • compliance • models • remodeling