Transmural differences in systolic wall thickening were analyzed in 13 conscious dogs by implanting sonomicrometers to continuously measure total wall thickness (WT) and outer WT approximately half the distance through the myocardium at a closely adjacent location. Inner WT was derived by subtraction of outer WT from total WT. Outer wall measurements spanned, on average, the outer 44 +/- 10% (+/- SD) of the wall; derived inner wall measurements spanned the remaining 56 +/- 10%. At rest the fractional contribution (FC) of the outer wall to total systolic wall thickening was 29 +/- 9%, which was significantly less than the FC of the inner wall, 71 +/- 9%. These data are in good agreement with simplified modeling of a cross section of the left ventricle as two concentric rings that predicts that the FC of inner and outer halves of the wall should be approximately 67 and 33%, respectively. During treadmill exercise, the extent of both inner and outer thickening increased significantly (30 and 29%, respectively) but the relative FC of the inner and outer wall remained the same. The data indicate that systolic wall thickening is nonuniform and that this nonuniformity remains constant during the increased inotropic and chronotropic stimulation associated with exercise.

Relationships between regional myocardial perfusion and transmural function, both during treadmill exercise and at rest, were examined in conscious dogs with varying degrees of coronary stenosis produced by a hydraulic occluder. In 13 dogs we measured myocardial blood flow with microspheres (10-12 microns in diameter) and regional systolic wall thickening (%). During exercise with coronary stenosis, myocardial blood flow was characterized by nonuniform distribution, and associated with regional dysfunction. The relationships between normalized myocardial blood flow and normalized %wall thickening during exercise with coronary stenosis were linear, with significantly different slopes (mean myocardial blood flow: y = 1.23x - 0.16, r = 0.93; subendocardial myocardial blood flow: y = 1.50x - 0.02, r = 0.86; subepicardial myocardial blood flow: y = 0.83x - 0.18, r = 0.87). To fill the gap between available subendocardial and subepicardial data during exercise with coronary stenosis and control points, however, would require nonlinear components. In 10 of the dogs, coronary stenosis at rest was also produced to compare regional myocardial blood flow - %wall thickening relations at rest with those during steady state exercise. The absolute mean myocardial blood flow - %wall thickening relation during exercise with coronary stenosis (y = 11.6x - 1.9, r = 0.90) was significantly shifted rightward from the resting relation (y = 25.3x -2.1, r = 0.80). However, when changes in %wall thickening were plotted vs. myocardial blood flow per beat, the relationships at rest and exercise were nearly superimposable. Likewise, relations between normalized myocardial blood flow and changes in %wall thickening at rest and exercise were not significantly different. We conclude: %wall thickening during exercise is directly related to changes in mean myocardial blood flow but is related in nonlinear fashion to changes in subepicardial and subendocardial myocardial blood flow; %wall thickening may provide a reliable index of the relative transmural flow distribution during exercise as well as at rest; during brief bouts (5-8 minutes) of exercise with coronary stenosis, the relationship between stabilized regional contractile dysfunction and level of myocardial blood flow per beat is the same as that during coronary stenosis at rest.

No abstract

No abstract