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(Circulation. 1999;99:482-490.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
-Adrenergic Blockade Improves Recovery of Myocardial Perfusion and Function After Coronary Stenting in Patients With Acute Myocardial Infarction
From Clinique Pasteur, Centre de Cardiologie Interventionelle, Toulouse, France (J.M., I.M., M.B., B.C., I.M.B., J.F.); Clinica Medica Generale, Ospedale Maggiore IRCCS, University of Milano (L.G., G.B.A.), and Clinical Physiology Institute, Pisa (M.K., C.P., A.D.), Italy; and Abteilung für Pathophysiologie, Universitätsklinikum Essen, Germany (G.H.).
Correspondence to Prof Luisa Gregorini, MD, Clinica Medica Generale, Università di Milano, Via Francesco Sforza 35, 20122 Milano, Italy. E-mail luisa.gregorini{at}unimi.it
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
µg/kg IC (n=10), the 
1-blocker urapidil 600 µg/kg IV
(n=10), or saline (n=10). Ten patients pretreated with ß-blockers
received urapidil 10 mg IC. Coronary stenting significantly
improved thickening in IRA-dependent and in non–IRA-dependent
myocardium (from 27±15% to 38±16% and from 40±15% to
45±15%, respectively). Simultaneously, TIMI frame count
decreased from 39±11 and 40±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
41±14% in IRA and to 48±11% and 49±17% in non-IRA
myocardium respectively, and TIMI frame count decreased to
16±6 and to 17±5, respectively. Changes were attenuated with
ß-blocker pretreatment.
Conclusions—Our finding that -adrenergic blockade
attenuates vasoconstriction and postischemic LV dysfunction
supports the hypothesis of an important role of neural mechanisms in
this phenomenon.
Key Words: myocardial infarction • nervous system, autonomic • vasoconstriction • regional blood flow • receptors, adrenergic, alpha
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