An intracoronary infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the "infarct-related vessel." In seven patients reperfusion was established (25 +/- 21 min, mean +/- SD) at which time CA diameter was reduced by 77 +/- 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 +/- 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 +/- 32%; this value was less (P less than 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further "cleanup" can be achieved by prolonging streptokinase infusion.
Nitroglycerin and nitroprusside are known to differ in their relative degree of systemic arterial and venous dilation. Nitroglycerin has been shown to be a potent large-vessel coronary dilator, but the effects of nitroprusside on coronary artery size are unclear. Accordingly, we studied coronary artery angiographic responses to both nitroprusside and nitroglycerin in 12 patients. Diameters Of left coronary artery segments were measured by quantitative angiography before and during an intravenous infusion of nitroprusside and after sublingual nitroglycerin when both drugs were administered in doses adjusted to achieve reductions in aortic pressure. Dilation of the left coronary artery was observed after nitroprusside and after nitroglycerin. Degrees of dilation were similar in the various left coronary artery segments after either nitroprusside or nitroglycerin. In general, segments located more proximally dilated less than those located more distally after either agent. We conclude that both nitroprusside and nitroglycerin are potent dilators of large epicardial and of smaller intramuscular coronary artery segments. The magnitude of dilation of all measured left coronary artery segments appeared remarkably similar with nitroprusside and nitroglycerin given in doses that produced a similar reduction in aortic pressure.
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