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Background: The purpose of this study was to verify whether endothelin A-antagonist administration at the time of coronary reperfusion preserves postischemic microvasculature and whether myocardial contrast echo (MCE) is able to detect pharmacologically induced changes in microvascular reflow., Methods and Results: Twenty dogs underwent 90 minutes of LAD occlusion (OCC) followed by 180 minutes of reperfusion (RP). Five minutes before LAD reopening, an intravenous bolus (5 mg/kg) of LU 135252 was given in 10 dogs and vehicle in the remaining 10. At baseline (BSL), OCC, and 90 and 180 minutes of RP, microvascular flow (BF) was assessed by microspheres, and MCE was performed with intravenous echo contrast. MCE videointensity and BF were expressed as risk area/control ratio. Myocardial thickness of the risk area was calculated by 2D echo. No differences in BF between the 2 groups were observed at BSL, OCC, and 90 minutes of RP. At 180 minutes of RP, BF was decreased in controls (70+/-7.4% of BSL; P:<0.005 versus BSL) and preserved in LU 135252-treated animals (89+/-4% of BSL; P=NS versus BSL; P<0.05 versus controls). Videointensity at MCE closely followed the changes in BF observed in both groups throughout the protocol. Myocardial thickness at 180 minutes of RP increased to 138.6+/-9.9% of BSL in controls and remained at 108.9+/-7.4% of BSL in treated dogs (P<0.05)., Conclusions: Endothelin A-antagonist treatment at the time of reperfusion significantly limited the progressive decrease in postischemic microvascular reflow and the increase in myocardial thickness. MCE allowed a reliable evaluation of pharmacologically induced changes in microvascular flow.

Background: [corrected] Subendocardial thickening is greater than subepicardial thickening and acute myocardial ischemia mainly impairs the former. Integrated backscatter cyclic variations (IBScv) reflect regional myocardial contractility and are blunted during myocardial ischemia. We hypothesized that stress-induced myocardial ischemia mainly affects subendocardial IBScv., Methods and Results: Multiplane transesophageal echocardiography and simultaneous atrial pacing were performed in 12 patients without coronary artery disease (CAD) and in 25 with significant CAD. In a transgastric 2-chamber view, we calculated IBScv in subendocardium and subepicardium and a heterogeneity index, both at rest and at peak-pacing. In 27 myocardial segments of patients with normal coronary arteries, and in 16 myocardial segments supplied by coronary artery without significant stenosis in patients with CAD, there was a transmural gradient of IBScv at rest and the heterogeneity index did not change during all the protocol steps. In the 53 myocardial segments related to a significantly narrowed coronary artery, the transmural gradient of IBScv, present at rest, significantly decreased at peak-pacing because of subendocardial blunting, but promptly recovered 5 seconds after pacing interruption. Moreover, the myocardial thickening at rest and peak pacing correlated with the subendocardial IBScv behavior and not with the subepicardial one., Conclusions: IBScv are greater in the subendocardium than in the subepicardium. Atrial pacing stress test does not affect IBScv in segments supplied by nonstenotic coronary arteries, whereas it affects segments supplied by diseased coronary arteries, blunting exclusively subendocardial IBScv. Heterogeneity of IBScv intramyocardial changes caused by stress-induced ischemia must be taken into account when using IBScv for investigating myocardial ischemia.