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Am J Physiol Heart Circ Physiol 279: H1120-H1127, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1120-H1127, September 2000

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

Patrick Segers1, Nikos Stergiopulos2, Jan J. Schreuder3, Berend E. Westerhof4, and Nico Westerhof1

1 Laboratory for Physiology, Institute for Cardiovascular Research, Free University of Amsterdam, and 4 Biomedical Instrumentation, Institute of Applied Physics, Netherlands Organization for Applied Scientific Research, Academic Medical Center, 1081 BT Amsterdam, The Netherlands; 2 Biomedical Engineering Laboratory, Ecole Polytechnique Fédéralé de Lausanne, 1015 Lausanne, Switzerland; and 3 Department of Cardiac Surgery, Ospedale San Raffaele, 20132 Milan, Italy

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) to normalize systolic wall stress (sigma s) in chronic pressure overload. However, LV filling pressure (Pv) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall stress (sigma d) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventricular-arterial 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 sigma s by LVH, and 3) normalization of sigma s by LVH and increase in Pv, such that sigma 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 Pv, normalization of sigma s, and preservation of CO in the presence of an impaired diastolic function.

hypertrophy; heart-arterial interaction; aging; hypertension; varying elastance; windkessel; left ventricle


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