The study aim was to quantify the individual and combined contributions of
both the arterial system and the heart to systolic blood pressure in hypert
ension. We assessed the parameters of a heart-arterial model for normotensi
ve control subjects and hypertensive patients with left ventricular adaptat
ion patterns classified as normal, concentric remodeling, concentric hypert
rophy, 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 resi
stance that arterial stiffening leads to systolic hypertension in concentri
c remodeling and concentric hypertrophy. The contribution of cardiac pump f
unction to the increase in blood pressure depends on cardiac remodeling, hy
pertrophy, 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 hypertrop
hy, the cardiac contribution to the increase in systolic blood pressure is
21%, 65%, and 108%, respectively. We conclude that-along with arterial chan
ges, cardiac remodeling and hypertrophy contribute to hypertension.