Quantification of the Contribution of Cardiac and Arterial Remodeling to Hypertension

Abstract

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. ) and contractile properties of the heart muscle (LV contractility). The 2 main mechanical afterload parameters that determine systolic blood (SBP) and pulse pressure (PP) are total peripheral resistance (R) and total arterial compliance (C). 1,2 Arterial blood pressure is thus determined by a limited number of cardiac and arterial mechanical factors. In hypertension, each of these parameters may change and thus contribute, to a different degree, to the elevated blood pressure.Blood pressure in hypertension, measured in vivo, reflects the combined effects of alterations in cardiac and arterial parameters. In this work, we use a mathematical heart-arterial interaction model 1 to unravel and quantify the specific contribution of arterial and cardiac changes. Cardiac and arterial model parameters for normotensive control subjects and for hypertensive patients with different LV adaptation patterns were taken directly from the literature or calculated from data given in the literature. 3 The effect of individual changes in arterial and cardiac properties in hypertension was evaluated, and the relative contribution of cardiac and arterial remodeling to the increase in SBP was quantitatively assessed. Methods Heart-Arterial Interaction ModelAortic blood pressure is computed with a heart-arterial interaction model 1 (Figure 1). Heart function is described with a time-varying elastance model 4 and is coupled to a 4-element lumped-parameter windkessel model that represents the arterial load. 5 The systemic arterial model parameters are total peripheral resistance (R), total arterial compliance (C), total inertance (L), and aortic characteristic impedance (Z 0 ). Time-varying elastance is calculated as E(t)ϭP LV / (V LV ϪV d ), where P LV and V LV are LV pressure and vol...

The arterial Windkessel

“…The four-element Windkessel has been used by Segers [51,[53][54][55] and Burattini [5]. In practice it turns out that the inertance is very difficult to estimate which is an argument to prefer the three-element Windkessel.…”

“…Several studies have been reported on ventriculo-arterial coupling. In these studies Windkessel models of the arterial system have been used [10,52,54,55]. The Windkessel as load is preferred in this type of analysis since more extensive models are awkward to work with.…”

Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity

“…[15] Another choice for the value of total arterial compliance would lead to different R-R L,ao solutions in the 3 subgroups. To assess the impact of this assumption, extra simulations are done with all parameters kept constant, except that C is increased and decreased by 50%.…”

“…Therefore, these data must be estimated in an indirect way. Fixed values are assumed for L (0.005 mm Hg·s 2 /mL) and Z 0 (0.033 mm Hg·s/mL), [15] 2 parameters that have been shown to have limited impact on pressure and flow. [14] It is further assumed that total arterial compliance does not differ between the subgroups, being 1.15 mL/mm Hg, a value that we have found in another study for age-matched hypertensive patients.…”

“…[14] It is further assumed that total arterial compliance does not differ between the subgroups, being 1.15 mL/mm Hg, a value that we have found in another study for age-matched hypertensive patients. [15] The impact of total arterial compliance on hemodynamics will be further assessed. 2 , is taken as the optimal parameter set.…”