Lack of platelet-activating factor release during reversible myocardial ischaemia

Eur Heart J. 1992 Dec;13(12):1641-4. doi: 10.1093/oxfordjournals.eurheartj.a060118.

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 (delta ST = -1.8 +/- 0.2 mm) and lactate excretion in the coronary sinus (percent lactate extraction decreased from 20 +/- 6% to -15 +/- 9%). Thromboxane B2 was produced causing a positive transmyocardial gradient (from 88 +/- 154 pg.ml-1 baseline to 1770 +/- 1407 pg.ml-1 at the peak) but there was no PAF 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: PAF was not detected in coronary sinus, whereas percent lactate extraction decreased from 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.

MeSH terms

  • Angina Pectoris / blood
  • Angioplasty, Balloon, Coronary
  • Humans
  • Myocardial Ischemia / blood*
  • Platelet Activating Factor / analysis*
  • Platelet Activating Factor / metabolism
  • Thromboxane B2 / blood

Substances

  • Platelet Activating Factor
  • Thromboxane B2