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

L Gregorini1, J Marco, C Palombo

  • 1Clinica Medica Generale, Ospedale Maggiore-IRCCS, University of Milano, Italy. gregorm@imiucca.csi.unimi.it

Journal of the American College of Cardiology
|April 30, 1998
PubMed
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Alpha-adrenergic blockers effectively treated left ventricular (LV) dysfunction after transient ischemia in patients. Combining alpha- and beta-blockers negated these beneficial effects, suggesting neural mechanisms in postischemic LV dysfunction.

Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Postischemic left ventricular (LV) dysfunction mechanisms remain unclear.
  • Percutaneous transluminal coronary angioplasty (PTCA) serves as a human model for ischemia-reperfusion.
  • LV dysfunction following ischemia is a significant clinical concern.

Purpose of the Study:

  • To assess the efficacy of alpha-adrenergic blocking agents in mitigating LV dysfunction post-transient ischemia.
  • To investigate the role of neural mechanisms in postischemic LV dysfunction.

Main Methods:

  • Fifty patients undergoing coronary stenting for stenosis were studied.
  • Transesophageal echocardiography monitored LV function during and after PTCA.
  • Patients received intracoronary phentolamine, intravenous urapidil, a combination of phentolamine and propranolol, or saline.

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Main Results:

  • Significant LV contractile dysfunction occurred post-PTCA in both ischemic and non-ischemic myocardium.
  • Alpha-blockers (phentolamine, urapidil) counteracted LV dysfunction, increased coronary resistance, and reduced vasoconstriction.
  • Combined alpha- and beta-blockade with phentolamine and propranolol did not improve LV dysfunction.

Conclusions:

  • LV dysfunction post-PTCA mirrors findings in animal ischemia models.
  • Alpha-blockers effectively resolved LV, macrocirculatory, and microcirculatory dysfunction.
  • The opposing effects of alpha- and beta-blockade support a hypothesis of neural mechanisms driving postischemic LV dysfunction.