title: Quantification of the contribution of cardiac and arterial remodeling to hypertension.
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.
authors.affiliation: Laboratory for Physiology, Institute for Cardiovascular Research, Free University of Amsterdam, the Netherlands. patrick.segers@navier.rug.ac.be
authors.forename: P
authors.initials: P
authors.lastname: Segers
authors.forename: N
authors.initials: N
authors.lastname: Stergiopulos
authors.forename: N
authors.initials: N
authors.lastname: Westerhof
mesh_terms: D001158:Arteries / Q000502:physiology / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D003187:Compliance; D004548:Elasticity; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D008955:Models, Cardiovascular; D014655:Vascular Resistance / Q000502:physiology; D020257:Ventricular Remodeling