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

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) t o normalize systolic wall stress (sigma(s)) in chronic pressure overload. H owever, LV filling pressure (Pv) may be elevated as well, supporting the al ternative hypothesis of end-diastolic wall stress (sigma(d)) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial f our-element lumped-parameter model to study ventricular-arterial interactio n in hypertension-induced LVH. We assessed model parameters for normotensiv e controls and applied arterial changes as observed in hypertensive patient s with LVH (resistance +40%, compliance -25%) and assumed 1) no cardiac ada ptation, 2) normalization of sigma(s) by LVH, and 3) normalization of sigma (s) by LVH and increase in P-v, such that sigma(d) is normalized as well. I n patients, systolic and diastolic blood pressures increase by similar to 4 0%, 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 dropp ed by 20%. In scenario 2, LV wall thickness increased by only 10%. The pred ictions of scenario 3 were in qualitative and quantitative agreement with i n vivo human data. LVH thus contributes to the elevated blood pressure in h ypertension, and cardiac adaptations include an increase in P-v, normalizat ion of sigma(s), and preservation of CO in the presence of an impaired dias tolic function.