We tested the hypothesis that lesion rethrombosis after streptokinase reperfusion is related to luminal size of the residual stenosis. Two independent techniques of analyzing coronary angiograms, quantitative coronary angiography and computer-based videodensitometry, were used to estimate the size of the residual lumen immediately after discontinuation of streptokinase. These techniques were selected because they provide independent estimates of cross-sectional area of a lesion with high degrees of reproducibility and minimal observer variability. Twenty-four patients who had undergone successful reperfusion with streptokinase were studied. Seven patients had lesion rethrombosis documented either on a repeat angiogram, at autopsy, or, in one case, by the fact that the patient had an acute transmural infarction resulting in death. Vessel patency was documented by repeat coronary angiography 8 to 14'days after initial streptokinase reperfusion in the other 17 patients. As assessed by quantitative coronary angiography, seven of 13 patients (54%) with minimal luminal crosssectional areas of less than 0.4 mm2 had rethrombosis. None of the 1 1 patients with lumens greater than 0.4 mm2 had rethrombosis. In the 17 patients with vessels that remained patent the size of the residual lesion at repeat catheterization was compared with its size immediately after reperfusion with streptokinase. Over the intervening 8 to 14 day interval, an average percentage increase in minimal crosssectional area of 116 + 34% was observed. In seven patients minimal luminal cross-sectional area more than doubled. Integrated optical density, an index of the severity of coronary stenosis derived from computer-based videodensitometry, was also useful in identifying a subgroup of patients at high risk for rethrombosis of lesion. Sixteen patients were identified as having integrated optical densities less than 2.5, and seven (44%) of these had rethrombosis of their lesions. Among the eight patients with integrated optical densities greater than 2.5, none had rethrombosis. These results show that rethrombosis of the vessel is in part related to the size of the residual lesion immediately after reperfusion with streptokinase. Vessels with residual stenotic cross-sectional areas less than 0.4 mm2 are at high risk for rethrombosis whereas vessels with minimal cross-sectional areas of greater than 0.4 mm2 are unlikely to develop rethrombosis. Furthermore, residual size of the lumen may change significantly during the 8 to 14 days after reperfusion. These changes may be due to remodeling of a ruptured atherosclerotic plaque, resolution of persistent coronary spasm, or lysis of persistent thrombi.Circulation 69, No. 5, 991-999, 1984. AFTER REPERFUSION WITH STREPTOKINASE residual high-grade stenoses are frequently present at the site of the previous obstruction. ' Decisions regarding the definitive care of these patients are based in part on the appearance of these lesions. In particular, treat-

A B S T R A C T We tested the hypothesis that the normal forearm vasoconstrictor response to leg exercise is inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. Forearm vascular responses to supine leg exercise were measured in 10 patients with aortic stenosis and in 2 control groups of 6 patients with mitral stenosis and 5 patients without valvular heart disease.Forearm vasoconstriction occurred during exercise in the control groups. In contrast, forearm blood flow increased and forearm vascular resistance did not change in patients with aortic stenosis. In six patients with aortic stenosis and a history of exertional syncope, forearm vasodilatation occurred during the second minute of leg exercise. Inhibition or reversal of forearm vasoconstrictor responses in aortic stenosis was asscociated with significant increases in left ventricular pressure.In three patients with aortic stenosis and exertional syncope, forearm vasodilator responses to exercise changed to vasoconstrictor responses after aortic valve replacement.The results indicate that forearm vasoconstrictor responses to leg exercise are inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. The observations suggest that reflex vasodilatation resulting from activation of left ventricular baroreceptors may contribute to exertional syncope in patients with aortic stenosis.

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On the basis of animal studies, we postulated that the size of the perfusion field (risk area) of an occluded coronary artery would be an important determinant of outcome in patients with acute myocardial infarction. To test this hypothesis, we measured size of the risk area in 27 patients with acute myocardial infarction by the intracoronary injection of 9fmTc-macroaggregated albumin and gated nuclear imaging. After injection of the albumin spheres (5.3 + 1.4 hr after the onset of chest pain) streptokinase was administered and in 16 of 27 patients (59%) effective thrombolysis was achieved. Since none of the patients had evidence of a prior acute myocardial infarction, the 3 day nuclear left ventricular ejection fraction (LVEF) was considered an index of infarct size. Response to thrombolysis was analyzed according to success