Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

Abstract

To determine the essential mechanism of increased systolic wall motion, i.e., hyperkinesis, in a nonischemic region (NIR) during acute ischemia, we simultaneously evaluated global and regional function ofthe excised, cross-circulated canine left ventricle connected to a volume servo pump before and after coronary occlusion. Regional areas were determined with pairs of orthogonal subendocardial sonomicrometers in the ischemic region (IR) and NIR. 468increased systolic segment shortening in a nonischemic region that correlated well with an increase in enddiastolic segment length and interpreted the increased shortening as a manifestation of a compensatory operation of the Frank-Starling mechanism. Thereafter, an increase in systolic segment shortening or wall thickening in a nonischemic region has been shown by many others5 8i and has been ascribed to either compensatory operation of the Frank-Starling mechanism or increased sympathetic activity. More recent studies by Lew et al.9 14 and Smalling et al. 15 have attributed the increased segment shortening to a combination of the Frank-Starling mechanism and mechanical unloading due to an intraventricular interaction between the ischemic and nonischemic regions. However, all these studies were performed in hearts in situ in which acute ischemia is usually accompanied by compensatory operation of the Frank-Starling mechanism and myocardial function is regulated by various neurohumoral mechanisms. This has made it difficult to separate the effects of the Frank-Starling mechanism and neurohumoral factors from other CIRCULATION by guest on

Application of three-dimensional speckle tracking echocardiography to assess left ventricular regional work using wall tension-regional area loop

“…In their study, regional work for the remote area moderately decreased because LV end-systolic pressure reduced and end-systolic wall tension decreased. In the other study where LV end-diastolic volume increased to keep a stroke volume constant, they found regional work for the remote area increased (9). In our study, regional work for the remote area did not change because the change of regional endocardial surface area during a cardiac cycle for the remote area increased because of hypercontraction despite the decrease in LV pressure and wall tension at end systole.…”

“…However, their method may not be appropriate as a direct measure of LV regional work, because it is only a unidirectional measurement (8). LV regional work can be reasonably assessed from the integral of wall tension with respect to the area of each region, i.e., area within a wall tension-regional area (T-A) loop (7,9,24). A previous study determined regional areas by pairs of orthogonal sonomicrometers placed on the LV endocardial surface in dogs (8).…”

Depressed contractile function due to canine mitral regurgitation improves after correction of the volume overload.

“…Tension = pressure (P) X radius (r), thus tension times area = (P X r) x r2 = PX r3 (r3 has the same units as volume) P X V, the more familiar expression of stroke work. The accuracy of RW calculated by this method was validated by Goto et al (55) in the excised cross-circulated heart using a volume servo pump system.…”

Contribution of asynchrony and nonuniformity to mechanical interaction in normal and stunned myocardium

“…During ischemia, three independent factors have been identified to contribute to mechanical interaction: 1) changes in sympathetic tone, 2) the Frank-Starling mechanism, and 3) direct myocardial unloading (2,7,8,10,12,16,17,20,23,28,30). The proposed mechanism to explain mechanical interaction during ischemia is discussed for the present experimental conditions.…”