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Cyclic motion of ischemic ventricular wall area and hydrodynamics of the blood during ejection.

Analysis of dimensional changes of ischemic left ventricular wall segments evidenced a dilation immediately after onset of ejection; thereafter, contraction appears delayed but almost regular. This biphasic systolic wall motion was correlated in a retrospective study to parameters indicating local intramural disorders, intraventricular load changes, and hydrodynamics of the blood during ejection. Hemodynamic data stored on a 16-track tape recorder were analyzed from 12 consecutive experiments in anesthetized dogs in which the left circumflex coronary artery (LCX) was gradually narrowed (coronary flow restriction greater than or equal to 50%). Left ventricular and aortic pressure, aortic blood velocity (v), acceleration/deceleration (dv/dt), and instantaneous stroke volume (m = integral of v*dt), and segment lengths of normal and ischemic myocardial regions (sonomicrometry) were numerically evaluated with 5 msec resolution. Systolic shortening of the intact myocardium correlates with the diminution of the intraventricular volume during ejection (r greater than 0.98). In contrast, ischemic segments dilate early during systole when the blood is accelerated; the extent of dilation depends on the degree of coronary flow reduction. The time course of lengthening coincides with the development of force F = m*dv/dt (r greater than 0.90) originating from regularly contracting parts of the ventricle. During blood deceleration, ischemic wall segments shorten as F turns to negative (r greater than 0.95). Thus, the wall motion of ischemic myocardial regions is modulated by the hydrodynamic force resulting from acceleration and deceleration of blood consecutively impeding and supporting the systolic function of the ischemic myocardium in the course of ejection.