a-Adrenergic Blockade Improves Recovery of Myocardial Perfusion and Function After Coronary Stenting in Patients With Acute Myocardial Infarction

Background—AMI reperfusion by thrombolysis does not improve TIMI flow and LV function. The role of infarct-related artery (IRA) stenosis and superimposed changes in coronary vasomotor tone in maintaining LV dysfunction must be elucidated. Methods and Results—Forty patients underwent diagnostic angiography 24 hours after thrombolysis. Seventy-two hours after thrombolysis, the culprit lesion was dilated with coronary stenting. During angioplasty, LV function was monitored by transesophageal echocardiography. Percent regional systolic thickening was quantitatively assessed before PTCA, soon after stenting, 15 minutes after stenting, and after phentolamine 12 mg/kg IC (n510), the a1-blocker urapidil 600 mg/kg IV (n510), or saline (n510). Ten patients pretreated with b-blockers received urapidil 10 mg IC. Coronary stenting significantly improved thickening in IRA-dependent and in non–IRA-dependent myocardium (from 27615% to 38616% and from 40615% to 45615%, respectively). Simultaneously, TIMI frame count decreased from 39611 and 40611 in the IRA and non-IRA, respectively, to 23610 and 2567 (P,0.05). Fifteen minutes after stenting, thickening worsened in both IRAand non–IRA-dependent myocardium (to 19614% and 28614%, P,0.05), and TIMI frame count returned, in both the IRA and non-IRA, to the values obtained before stenting. Phentolamine and urapidil increased thickening to 36617% and 41614% in IRA and to 48611% and 49617% in non-IRA myocardium respectively, and TIMI frame count decreased to 1666 and to 1765, respectively. Changes were attenuated with b-blocker pretreatment. Conclusions—Our finding that a-adrenergic blockade attenuates vasoconstriction and postischemic LV dysfunction supports the hypothesis of an important role of neural mechanisms in this phenomenon. (Circulation. 1999;99:482-490.)