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Circulation, Vol 74, 901-911, Copyright © 1986 by American Heart Association

ARTICLES

Phasic mitral blood flow and regional left ventricular dimensions: possible mechanism of active assist to ventricular filling

BG Bertha and JD Folts

Postsystolic myocardial segment shortening (PSS) has been observed in dogs and humans by means of ultrasonic crystals but has never been studied specifically. In this study, both subendocardial and subepicardial regional function in the basal circumflex and midventricular anterior myocardium (LAD) was studied during late systole and early diastole with ultrasonic crystals. Fifteen open-chest dogs were instrumented with electrocardiographic leads; Millar catheters for measurement of left ventricular pressure, left ventricular dP/dt, and aortic blood pressure; flow probes for determination of aortic and mitral blood flow; and subendocardial and subepicardial crystal pairs to measure subendocardial segment length shortening velocity (dL/dt). Crystal pairs were placed in the subendocardial left oblique mode and the extreme subendocardial right oblique mode (-50 and +50 degrees from equator) in the lateral basal (circumflex, n = 9) and anterior midventricular myocardium (LAD, n = 6). Subendocardial segments showed PSS averaging 34 +/- 7% of the total shortening distance in the circumflex bed and 21 +/- 2% in the LAD bed (p = NS). The rate of subendocardial segment shortening during PSS increased 273 +/- 42.6% (p less than .05) relative to the rate of segment shortening during ejection in the circumflex bed and 126 +/- 40% (p less than .05) in the LAD bed (p = NS). The most rapid diastolic increase in subendocardial length (peak +dL/dt) occurred immediately after subendocardial PSS. Subendocardial diastolic peak +dL/dt occurred after the onset of mitral inflow during the acceleration limb of the rapid ventricular filling phase. Overlying subepicardial segments began lengthening 82 +/- 12 msec before onset of subendocardial segment lengthening in the circumflex bed and 63 +/- 9 msec before subendocardial lengthening in the LAD bed (p less than .05), indicating that the subepicardial segment had begun to lengthen while subendocardial segment shortening continued after end-systole. Onset of early segmental subepicardial lengthening varied with respect to the point of end-systole. Early segmental subepicardial lengthening with subendocardial PSS may be a mechanism by which the rapid filling phase of the left ventricle is actively potentiated by storing potential energy released as early diastolic elastic recoil.