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Left ventricular wall stress normalization in chronic pressure-overloaded heart: A mathematical model study

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Author: Segers, P. · Stergiopulos, N. · Schreuder, J.J. · Westerhof, B.E. · Westerhof, N.
Type:article
Date:2000
Source:American Journal of Physiology - Heart and Circulatory Physiology, 3 48-3, 279
Identifier: 235700
Keywords: Health · Aging · Heart-arterial interaction · Varying elastance · Windkessel · Artery · Heart left ventricle enddiastolic pressure · Heart left ventricle filling pressure · Heart left ventricle hypertrophy · Heart left ventricle overload · Heart output · Heart ventricle compliance · Mathematical model · Prediction · Adaptation, Physiological · Blood Pressure · Cardiac Output · Chronic Disease · Computer Simulation · Diastole · Humans · Hypertension · Hypertrophy, Left Ventricular · Models, Cardiovascular · Reproducibility of Results · Stress, Mechanical · Systole

Abstract

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) to normalize systolic wall stress (σ(s)) in chronic pressure overload. However, LV filling pressure (P(v)) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall stress (σ(d)) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventriculararterial interaction in hypertension-induced LVH. We assessed model parameters for normotensive controls and applied arterial changes as observed in hypertensive patients with LVH (resistance +40%, compliance -25%) and assumed 1) no cardiac adaptation, 2) normalization of σ(s) by LVH, and 3) normalization of σ(s) by LVH and increase in P(v), such that σ(d) is normalized as well. In patients, systolic and diastolic blood pressures increase by ~40%, cardiac output (CO) is constant, and wall thickness increases by 30-55%. In scenarios 1 and 2, blood pressure increased by only 10% while CO dropped by 20%. In scenario 2, LV wall thickness increased by only 10%. The predictions of scenario 3 were in qualitative and quantitative agreement with in vivo human data. LVH thus contributes to the elevated blood pressure in hypertension, and cardiac adaptations include an increase in P(v), normalization of σ(s), and preservation of CO in the presence of an impaired diastolic function.