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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 (
s) in chronic pressure
overload. However, LV filling pressure (Pv) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall
stress (
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
s by LVH, and 3) normalization of
s by LVH and increase in Pv, such that
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
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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