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PubMed · 9561999

Postischemic left ventricular dysfunction is abolished by alpha-adrenergic blocking agents.

L Gregorini·J Marco·C Palombo·M Kozàkovà·G B Anguissola·B Cassagneau·M Bernies·A Distante·I Marco·J Fajadet·A Zanchetti
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Abstract

OBJECTIVES: We sought to evaluate the efficacy of alpha-adrenergic blocking agents in counteracting left ventricular (LV) dysfunction occurring after transient ischemia in humans. BACKGROUND: The mechanisms underlying postischemic LV dysfunction are largely unknown. METHODS: Percutaneous transluminal coronary angioplasty (PTCA) provides a clinical model of ischemia and reperfusion. In 50 patients undergoing coronary stenting for 77+/-5% stenosis, LV function was monitored by transesophageal echocardiography during and 30-min after PTCA. Fifteen minutes after stenting, 15 patients received 12 microg/kg body weight of the alpha-blocker phentolamine intracoronarily, 15 patients received 600 microg/kg of the alpha1-blocker urapidil intravenously, 10 patients received the combination of phentolamine and 1.2 mg of propranolol intracoronarily, and 10 patients received saline. RESULTS: Fifteen minutes after successful coronary dilation, significant contractile dysfunction occurred in previously ischemic and nonischemic myocardium. LV dysfunction was accompanied by an increase in coronary resistance and diffuse vasoconstriction. Alpha-blockers counteracted LV dysfunction and coronary resistance and the increase in vasoconstriction. Phentolamine and urapidil increased global LV shortening from 34+/-9% to 45+/-8% and to 49+/-8%, respectively (p < 0.05). After the administration of propranolol combined with phentolamine, LV dysfunction remained unchanged (34+/-6%), as in control subjects. CONCLUSIONS: LV dysfunction occurs after PTCA, as described in animal models after ischemia. Alpha-blockers abolished LV, macrocirculatory and microcirculatory dysfunction, whereas the alpha-blocker effect was prevented by combining alpha- and beta-blockers. The evidence of diffuse rather than regional dysfunction, together with the opposite effects of alpha- and beta-blockade, supports the hypothesis of neural mechanisms eliciting postischemic LV dysfunction.

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Adrenergic alpha-AntagonistsAgedAngioplasty, Balloon, CoronaryCoronary VesselsEchocardiography, TransesophagealFemaleHemodynamicsHumansMaleMiddle AgedMyocardial IschemiaStentsVascular ResistanceVentricular Dysfunction, LeftJournal ArticleResearch Support, Non-U.S. Gov't

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L Gregorini, J Marco, C Palombo, M Kozàkovà, G B Anguissola, B Cassagneau, M Bernies, A Distante, I Marco, J Fajadet, A Zanchetti. 1998. Postischemic left ventricular dysfunction is abolished by alpha-adrenergic blocking agents.. https://doi.org/10.1016/s0735-1097(98)00055-2

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