Effects of nontransmural ischemia on inner and outer wall thickening in the canine left ventricle.

The effect of ischemic subendocardial dysfunction on contractile function in the normally perfused subepicardium remains controversial. Accordingly, regional wall thickening (WT) was measured directly in the left ventricle of 10 open-chest dogs using epicardial echocardiography. Two silk sutures, used as echocardiographic targets, were inserted beneath the transducer to a depth of 25.0 +/- 0.7% (subepicardium) and 48.0 +/- 2.7% (midmyocardium) of transmural thickness. A hydraulic cuff, placed around the left anterior descending coronary artery (LAD) was then inflated slowly until transmural WT was reduced to 62 +/- 2% of baseline. Myocardial blood flow (MBF) was not significantly altered in the subepicardial third of the wall; however, flow to the midwall and subendocardial thirds decreased by 39% (p less than 0.001) and 50% (p less than 0.001), respectively. Nontransmural ischemia produced a small but significant decrease in epicardial WT (baseline = 0.77 +/- 0.08 mm, ischemia = 0.69 +/- 0.08 mm; p less than 0.05) and substantially larger decreases in midwall (baseline = 1.66 +/- 0.14 mm, ischemia = 1.03 +/- 0.09 mm; p less than 0.001) and subendocardial WT (baseline = 3.39 +/- 0.34 mm, ischemia = 2.10 +/- 0.26 mm; p less than 0.001). The degree of regional dysfunction was linearly correlated with tissue depth (r = 0.88, p less than 0.001). Thus the degree of dysfunction produced by nontransmural ischemia increased progressively from the subepicardium to the subendocardium, paralleling the pattern of perfusion. We conclude that perfusion, rather than transmural tethering, largely determines subepicardial function in the setting of nontransmural ischemia.