Increased platelet thromboxane A2/prostaglandin H2 receptors in patients with acute myocardial infarction.
- 1 January 1990
- journal article
- abstracts
- Published by Wolters Kluwer Health in Circulation
- Vol. 81 (1) , 212-218
- https://doi.org/10.1161/01.cir.81.1.212
Abstract
Platelets have been implicated in the formation of occlusive intracoronary thrombi leading to unstable angina pectoris and acute myocardial infarction. Evidence of platelet involvement in these syndromes includes increased thromboxane A2 synthesis during ischemic events and enhanced in vitro sensitivity to agonists. To determine the density and affinity of platelet thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors in patients with acute myocardial infarction and unstable angina pectoris, the maximum number of binding sites (Bmax) per platelet and the dissociation constant (Kd) of the TXA2/PGH2 receptor antagonist, [125I]-PTA-OH, was determined at equilibrium in washed platelets. Patients with acute myocardial infarction had a significantly (p = 0.006) higher Bmax (4,468 +/- 672 sites/platelet, n = 9) compared with controls (2,206 +/- 203 sites/platelet, n = 8). Restudied at a time when the patients' coronary artery disease was clinically stable, Bmax values for the myocardial infarction group had returned to within normal limits. The dissociation constant for [125I]-PTA-OH was not significantly different in the acute myocardial infarction patients compared with controls. In patients with acute myocardial infarction, the duration of chest pain was positively correlated (r = 0.71, p less than 0.02) with the number of [125I]-PTA-OH binding sites (Bmax). In vitro platelet sensitivity to the TXA2/PGH2 mimetic, U46619, was assessed in aggregation studies. The maximal velocity of aggregation (slope) correlated with platelet TXA2/PGH2 receptor number (r = 0.67, p less than 0.001) and was significantly higher (p less than 0.02) in the acute myocardial infarction patients compared with the other study groups. There was no significant difference in the aggregation EC50 values for the thromboxane mimetic U46619 between unstable angina, acute myocardial infarction, and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)Keywords
This publication has 30 references indexed in Scilit:
- Concurrent Morning Increase in Platelet Aggregability and the Risk of Myocardial Infarction and Sudden Cardiac DeathNew England Journal of Medicine, 1987
- Platelet Activation in Unstable Coronary DiseaseNew England Journal of Medicine, 1986
- Coronary Angioscopy in Patients with Unstable Angina PectorisNew England Journal of Medicine, 1986
- Aspirin, Sulfinpyrazone, or Both in Unstable AnginaNew England Journal of Medicine, 1985
- Protective Effects of Aspirin against Acute Myocardial Infarction and Death in Men with Unstable AnginaNew England Journal of Medicine, 1983
- Release of Prostaglandins and Thromboxane into the Coronary Circulation in Patients with Ischemic Heart DiseaseNew England Journal of Medicine, 1981
- Increased fibrinopeptide A formation and thromboxane A2 production in patients with ischemic heart disease: Relationships to coronary pathoanatomy, risk factors, and clinical manifestationsAmerican Heart Journal, 1981
- Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial InfarctionNew England Journal of Medicine, 1980
- Platelet Activation during Exercise-Induced Myocardial IschemiaNew England Journal of Medicine, 1980
- Increased Synthesis of Prostaglandin-E-like Material by Platelets from Patients with Diabetes MellitusNew England Journal of Medicine, 1977