Copyright © 1992 by the European Society of Cardiology.
© 1992 The European Society of Cardiology
Lack of platelet-activating factor release during reversible myocardial ischaemia



*From the Departments of Cardiology Hôpital Pitié-Salpétrière
the INSERM unit 150, Hôpital Lariboisière Paris
Henri Beaufour Institute, Le Plessis-Robinson France
From the Departments of Hematology, Hôpital Pitié-Salpétrière
Received 17 December 1991; revised 26 May 1992; .
Correspondence G Montalescot, MD, PhD, Catherization Laboratory, Department of Cardiology, Hôpital Pitié-Salpétriére, 47 Bl de l'Hôpital, 75651 Paris Cédex 13, France
Abstract
Platelet-activating factor (PAF) is involved in experimental models of myocardial ischaemia, and PAF infusion can cause thromboxane release. Thromboxane is produced during brief episodes of reversible myocardial ischaemia in patients with coronary heart disease. To learn whether PAF synthesis is associated with thromboxane production in mild myocardial ischaemia, we performed rapid atrial pacing in four patients with angina pectoris which caused chest pain, ST segment depression (
ST= 1·8 ±0·2 mm) andlactate excretion in the coronary sinus (percent lactate extraction decreasedfrom 20 ± 6% to 15±9%). Thromboxane B2 was produced causing a positive transmyocardial gradient (from 88 ± 154 pg . ml1 baseline to 1770 ± 1407 pg . ml1 at the peak) but there was no PA F release into coronary sinus blood. In four other patients we determined whether more pronounced ischaemia could be associated with PAF synthesis. Coronary sinus blood was sampled before and during balloon occlusion of a major coronary artery: PA F was not detected in coronary sinus, whereas percent lactate extraction decreasedfrom 24 + 6% to 63±22% (n = 4). We conclude that PAF plays a minor role in short episodes of reversible ischaemia and does not participate in thromboxane production.
Key Words: Angina pectoris PAF eicosanoids myocardial ischaemia
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