alpha-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 L V function. The role of infarct-related artery (IRA) stenosis and superimpo sed changes in coronary vasomotor tone in maintaining LV dysfunction must b e elucidated. Methods and Results-Forty patients underwent diagnostic angiography 24 hour s after thrombolysis, Seventy-two hours after thrombolysis, the culprit les ion was dilated with coronary stenting. During angioplasty, LV function was monitored by transesophageal echocardiography, Percent regional systolic t hickening was quantitatively assessed before PTCA, soon after stenting, 15 minutes after stenting, and after phentolamine 12 mu g/kg IC (n=10), the al pha(1)-blocker urapidil 600 mu g/kg IV (n=10), or saline (n=10), Ten patien ts pretreated with beta-blockers received urapidil 10 mg IC. Coronary stent ing significantly improved thickening in IRA-dependent and in non-IRA-depen dent myocardium (from 27+/-15% to 38+/-16% and from 40+/-15% to 45+/-15%, r espectively). Simultaneously, TIMI frame count decreased from 39+/-11 and 4 0+/-11 in the IRA and non-IRA, respectively, to 23+/-10 and 25+/-7 (P<0.05) . Fifteen minutes after stenting, thickening worsened in both IRA- and non- IRA-dependent myocardium (to 19+/-14% and 28+/-14%, 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 36+/-17% and 4 1+/-14% in IRA and to 48+/-11% and 49+/-17% in non-IRA myocardium respectiv ely, and TIMI frame count decreased to 16+/-6 and to 17+/-5, respectively. Changes were attenuated with beta-blocker pretreatment. Conclusions-Our finding that alpha-adrenergic blockade attenuates vasoconst riction and postischemic LV dysfunction supports the hypothesis of an impor tant role of neural mechanisms in this phenomenon.