Key result
Mathematical modeling of hypertension-induced LVH suggests that cardiac adaptations include increased venous filling pressure to normalize end-diastolic wall stress and preserve cardiac output.
Mathematical modeling suggests that in hypertension-induced LVH, cardiac adaptation involves not only increased wall thickness to normalize systolic stress, but also increased venous filling pressure to normalize diastolic stress and preserve cardiac output.
We studied heart-arterial interaction in hypertension-induced left ventricular hypertrophy (LVH) using a LV time-varying elastance model coupled to a 4-element lumped parameter model of the systemic arterial system. After assessing cardiac and arterial model parameters for normotensive control subjects, we applied arterial changes as observed in hypertensive patients with LVH (resistance +40%; compliance -25%) and assumed (i) no cardiac adaptation; (ii) LVH normalizes systolic wall stress (/spl sigma//sub s/); (iii) LVH normalizes /spl sigma//sub s/ and venous filling pressure (P/sub v/) increases such that end-diastolic wall stress (/spl sigma//sub d/) is normalized as well. Human in vivo data show that in hypertensives with LVH, systolic and diastolic blood pressure increase by about 40% while cardiac output is constant and wall thickness increases by 30-55%. In both (i) and (ii), blood pressure increased by only 10% while cardiac output dropped by 20%. In (ii), LV wall thickness increased by only 10%. In contrast, the predictions of (iii) were in qualitative and quantitative agreement with in-vivo human data. We conclude that besides an increase in LV mass and wall thickness, normalizing /spl sigma//sub s/, cardiac adaptations further consist of an increase in P/sub v/, normalizing /spl sigma//sub d/ and preserving cardiac output in the presence of an impaired diastolic function.
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Segers et al. (2005) studied Hypertension-induced left ventricular hypertrophy. Mathematical modeling of arterial changes vs. Normotensive control model parameters was evaluated on Blood pressure, cardiac output, and LV wall thickness. Mathematical modeling of hypertension-induced LVH suggests that cardiac adaptations include increased venous filling pressure to normalize end-diastolic wall stress and preserve cardiac output.
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