title: Mechanics of left ventricular relaxation, early diastolic lengthening, and suction investigated in a mathematical model.
abstract: We investigated the determinants of ventricular early diastolic lengthening and mechanics of suction using a mathematical model of the left ventricle (LV). The model was based on a force balance between the force represented by LV pressure (LVP) and active and passive myocardial forces. The predicted lengthening velocity (e') from the model agreed well with measurements from 10 dogs during 5 different interventions (R = 0.69, P < 0.001). The model showed that e' was increased when relaxation rate and systolic shortening increased, when passive stiffness was decreased, and when the rate of fall of LVP during early filling was decreased relative to the rate of fall of active stress. We first defined suction as the work the myocardium performed to pull blood into the ventricle. This occurred when contractile active forces decayed below and became weaker than restoring forces, producing a negative LVP. An alternative definition of suction is filling during falling pressure, commonly believed to be caused by release of restoring forces. However, the model showed that this phenomenon also occurred when there had been no systolic compression below unstressed length and therefore in the absence of restoring forces. In conclusion, relaxation rate, LVP, systolic shortening, and passive stiffness were all independent determinants of e'. The model generated a suction effect seen as lengthening occurring during falling pressure. However, this was not equivalent with the myocardium performing pulling work on the blood, which was performed only when restoring forces were higher than remaining active fiber force, corresponding to a negative transmural pressure.
authors.affiliation: Department of Cardiology, Oslo Univ. Hospital, Rikshospitalet, Norway. Espen.Remme@medisin.uio.no
authors.forename: Espen W
authors.initials: EW
authors.lastname: Remme
authors.forename: Anders
authors.initials: A
authors.lastname: Opdahl
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D003971:Diastole / Q000502:physiology*; D004285:Dogs; D023421:Models, Animal; D008962:Models, Theoretical; D009200:Myocardial Contraction / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*