Defective coronary prostaglandin modulation in anginal patients

Gian Gastone Neri Serneri, Gian Franco Gensini, Rosanna Abbate, Sergio Castellani, Francesco Bonechi, Marino Carnovali, Carlo Rostagno, Roberto Piero Dabizzi, Armando Dagianti, Luciano Arata, Francesco Fedele, Carlo Iacoboni, Domenico Prisco

Research output: Contribution to journalArticlepeer-review

Abstract

In order to investigate whether coronary vasodilating prostaglandins (PGl2 and PGE2) have a role in the pathophysiology of myocardial ischemia, 26 patients with angina pectoris and 23 control subjects (nonischemic patients) were studied by assessing coronary hemodynamics and prostaglandin formation in relation to sympathetic stimulation. Following a cold pressor test (CPT), coronary prostaglandin output markedly increased (p <0.001) and coronary vascular resistance (CVR) decreased (p <0.001) in all control subjects. In contrast, in anginal patients prostaglandins in the coronary sinus were undetectable and after CPT prostaglandin output did not increase, whereas CVR paradoxically increased (p <0.001). In control subjects the inhibition of coronary prostaglandin formation (by ketoprofen [1 mg/kg intravenously] or by aspirin [15 mg/kg intravenously]) caused a paradoxical increase of CVR following CPT (p <0.001). In anginal patients the inhibition of prostaglandins further exaggerated the increase of CVR after CPT (p <0.001). These results indicate that coronary vasodilating prostaglandins PGI2 and PGE2 play a role in modulating coronary vascular response to sympathetic stimulation induced by CPT. Their defective production in anginal patients may be responsible for the paradoxical increase in CVR following sympathetic stimulation.

Original languageEnglish
Pages (from-to)12-21
Number of pages10
JournalAmerican Heart Journal
Volume120
Issue number1
DOIs
Publication statusPublished - 1990

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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