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Shortening of oblique left ventricular (LV) fibers results in torsion. A unique relationship between volume and torsion is therefore expected, and the effects of load and contractility on torsion should be predictable. However, volume-independent behavior of torsion has been observed, and the effects of load on this deformation remain controversial. We used magnetic resonance imaging (MRI) with tagging to study the relationships between load and contractility, and torsion. In ten isolated, blood-perfused canine hearts, ejection was controlled by a servopump: end-diastolic volume (EDV) was controlled by manipulating preload parameters and end-systolic volume (ESV) by manipulating afterload using a three-element windkessel model. MRI was obtained at baseline, two levels of preload alteration, two levels of afterload alteration, and dobutamine infusion. An increase in EDV resulted in an increase in torsion at constant ESV (preload effect), whereas an increase in ESV resulted in a decrease in torsion at constant EDV (afterload effect). Dobutamine infusion increased torsion in association with an increase in LV peak-systolic pressure (PSP), even at identical EDV and ESV. Multiple regression showed correlation of torsion with preload (EDV), afterload (ESV), and contractility (PSP; r = 0.67). Furthermore, there was a close linear relationship between torsion and stroke volume (SV) and ejection fraction (EF) during load alteration, but torsion during dobutamine infusion was greater than expected for the extent of ejection. Preload and afterload influence torsion through their effects on SV and EF, and there is an additional direct inotropic effect on torsion that is independent of changes in volume but rather is force dependent. There is therefore potential for the torsion-volume relation to provide a load-independent measure of contractility that could be measured noninvasively.

Diastolic ventricular interaction is associated with septal shift and deformation, the consequences of which have not been fully assessed. A model was therefore developed to describe the mechanisms involved in interaction between the ventricles under different loading conditions. We assumed a circular cardiac minor-axis geometry surrounded by a pericardial membrane with the left ventricle (LV) and septum described by three layers. To define the equilibrium condition, we required the net force-balance at the right ventricular (RV)-LV intersection points to equal zero. The model was tested with and without consideration of bending forces associated with a change of curvature of a thick-walled structure. Model results were compared with data from animal experiments subjected to aortic and pulmonary constriction. LV and RV end-diastolic pressures as well as pericardial pressure were measured. In six dogs, septal segment length was measured using sonomicrometry, and in seven dogs, endocardial curvature was measured using echocardiography. Model and experimental results show that 1) with severe RV loading, septal inversion occurs at a negative transseptal gradient, and 2) the end-diastolic septal segment length continues to shorten after septal inversion during pulmonary constriction. Model simulation suggests that bending moments account for the septal curvature at zero transseptal pressure. In addition, the model predicts the shift in the pressure-area relationship of each ventricle by a change in loading of the opposite ventricle and predicts that large transmural gradients in stress and strain are associated with septal inversion. Thus the model and the experimental data agree and describe the important factors that modulate diastolic septal mechanics during acute differential ventricular loading.

The ventricular septum attaches to the insertion points of the ventricular free walls, separates, and is shared by both the left (LV) and right (RV) ventricles. Changes in the transseptal pressure gradient (PTS, the difference between LV and RV pressures) will change the stress in the septum and, therefore, the length of the septal segment (Ls). However, since most of the septal myocardial fibers are continuous with those of LV free wall and the septum appears to be an integral part of LV, one might also expect that if the LV transmural pressure (Plvtm; the difference between LV and pericardial pressure) is raised, Ls would increase even in the absence of any change in PTS. Therefore, we hypothesized that at end diastole, Ls depends on both Plvtm and PTS. To test this hypothesis, we measured Ls (sonomicrometry), LV and RV pressures (micromanometers), and pericardial pressure (flat liquid-containing balloon) in seven anesthetized open-chest dogs. Plvtm was increased through volume loading, whereas PTS was maintained constant at 10, 5, 0, -5, -10, and -15 mmHg by adjusting the degree of constriction of the pulmonary artery or aorta. These procedures were performed first with pericardium reapproximated and then after the pericardium had been opened widely. At each controlled PTS level, Ls increased linearly with the increase in Plvtm. Both the slope and the intercept of this Ls-Plvtm relation were affected by PTS in a nonlinear fashion. (ABSTRACT TRUNCATED AT 250 WORDS)