Cardiac models have proposed tight coupling between the systolic twisting motion of the left ventricle about its longitudinal axis and muscle shortening. Whether a similar relationship holds during diastole is unknown. The present study determined the dynamic twist-radial shortening relationship throughout the cardiac cycle in six in situ canine left ventricles. Radiopaque markers (15-26) were implanted throughout the myocardial midwall in six canine left ventricles. Three-dimensional marker location was determined by computer analysis of biplane cineradiograms (60 frames/s), and the results were transformed to cardiac cylindrical coordinates. Mean chamber twist was defined as the gradient along the long axis of circumferential rotation relative to end diastole. Changes in chamber dimension were indexed by average radial shortening, normalized to span from 0 at end diastole to 1.0 at end systole. During systole, ventricular twist and radial shortening were linearly related with an average slope of -0.058 radians (r = 0.99). However, during early diastolic relaxation there was substantial untwist (48 +/- 20% of total) despite only an approximately 15% increase in mean radial dimension resulting in a much steeper twist-percent shortening relationship (-0.24 radians, r = 0.96). During most of the remainder of diastolic filling, the twist-shortening relation was shallower (-0.02, r = 0.91) than the corresponding systolic relation (P less than 0.05). Thus the twist-radial shortening relation depends on the phase of the cardiac cycle. These data suggest that models of chamber mechanics that incorporate twisting motion need to account for the matrix surrounding the muscles in addition to the shortening and lengthening of the muscle fibers.

A comprehensive model that describes the interaction between the cardiovascular system (CVS) and the intrathoracic pressure (ITP) based on a lumped parameter vascular representation and a time-varying elastance concept for the four cardiac chambers is presented. Special attention is given to two possible mechanisms of interventricular interaction; the constraining effects of the pericardium and direct interventricular interaction that results from the fact that the two ventricles share a common interventricular septum. The response of the CVS to positive and negative perturbations in the ITP and to injection of fluid into the pericardium was simulated and compared with experimental literature data. The results show that 1) the total heart volume is relatively constant throughout the cycle both for ITP of 0 and +15 mmHg, which is consistent with experimental data in dogs, thus suggesting that intrinsic properties of the cardiac chambers rather than a restricting pericardium is the mechanism for that observation. 2) The pericardium has a major role in modifying the transient and steady-state response to a step decrease in the ITP with a transient decrease in left ventricle (LV) end-diastolic volume followed by gradual increase afterwards. 3) The response to sudden injection of fluid into the pericardial space is a larger transient decrease in right ventricle than LV volume, which is consistent with experimental data. 4) Transmission across the septum has a relatively minor role in modifying the response of the CVS to negative pressure. Thus the model reasonably predicts the effects of intrathoracic and pericardial pressures on the circulation in a reflex-blocked animal and provides a means for placing multiple potential mechanisms in proper hierarchial order with regard to contributions to LV and overall CVS function.

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