Epicardial deformation and left ventricular wall mechanisms during ejection in the dog.

Significant differences between epicardial and endocardial systolic stress in the wall of the left ventricle (LV) have been predicted by various models of LV mechanics. Yet a model incorporating transmural differences in fiber orientation and torsion, defined as a rotation of the apex with respect to the base around the long axis of the LV, predicts transmural equalization of stress and shortening along the fiber direction during the ejection phase. this equalization is due to an interplay between torsion and myocardial contraction. To assess the model hypothesis, predicted epicardial deformation during the ejection phase was compared with that measured experimentally. For this purpose 45 sets of measurements were performed in four open-chest dogs using a triangular array of inductive gauges for the assessment of epicardial circumferential strain (epsilon c), base-to-apex strain (epsilon z), and shear angle (gamma). Changes in shear angle are directly related to LV torsion. LV end-diastolic pressure was varied over a wide range (0-15 mmHg) by volume loading and bleeding. In the control state, the slope of the shear angle vs. volume strain curve (volume strain = 2 epsilon c + epsilon z), which is related to contraction, was found to be 0.74 +/- 0.10 (mean +/- SD). This compares reasonably wih the mathematical model prediction of a slope of 0.67. Due to an interplay between torsion and contraction, left ventricular fiber stress and fiber shortening might be uniformly distributed across the wall.

In vivo cinematographic analysis of behavior of the aortic valve.

In open-chest dogs direct-cinematographic high-speed recordings of aortic valve movement were made using a thin flexible fiberscope. Simultaneously ECG, ascending aortic flow (electromagnetically), and the pressures in the aorta, left ventricle, and left atrium were recorded. Replacement of blood by a transparent liquid (Tyrode solution) was done with two roller pumps, one connected to the left atrium and the other to the femoral artery. Free outflow occurred through a cannula in the pulmonary artery. Comparison of the film frames with the aortic flow signals revealed that 1) the valve was completely open at the moment that aortic flow had reached about 75% of its maximum value; 2) the opening time was 32 ms; 3) valve closure started before the onset of aortic flow deceleration; 4) at least 80% of the closure was completed before aortic flow becomes zero; 5) complete valve closing coincided with the moment of maximum backflow in the valve; 6) the shape of the valvular orifice at complete opening was almost circular; and 7) fluid viscosity had no significant effect on valve closure.