Effects of nitroglycerin at therapeutic doses on platelet aggregation in unstable angina pectoris and acute myocardial infarction

• Published in: The American journal of cardiology Vol. 66; no. 7; pp. 683 - 688
• Main Authors: Diodati, Jean, Théroux, Pierre, Latour, Jean-Gilles, Lacoste, Lucie, Lam, Jules Y.T., Waters, David
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.09.1990; Elsevier
• Subjects: Adenosine Diphosphate - pharmacology; Angina Pectoris - drug therapy; Angina, Unstable - blood; Angina, Unstable - drug therapy; Antianginal agents. Coronary vasodilator agents; Biological and medical sciences; Cardiovascular system; Female; Humans; Male; Medical sciences; Middle Aged; Myocardial Infarction - blood; Myocardial Infarction - drug therapy; Nitroglycerin - pharmacology; Nitroglycerin - therapeutic use; Pharmacology. Drug treatments; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors; Platelet Function Tests - methods; Thrombin - pharmacology; Time Factors; Antianginal agent; Human; Infarct; Cardiovascular disease; Angina pectoris; Coronary heart disease; Aggregation; Chemotherapy; Platelet; Treatment; Perfusion; Organic nitrate; Myocardium
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/0002-9149(90)91130-X

The platelet aggregation response to adenosine diphosphate (AOP) and to thrombin was quantified in 10 patients, 5 with unstable angina pectoris and 5 with acute myocardial infarction, before, during and after a 45-minute infusion of nitroglycerin. An impedance aggregometer allowing rapid bedside studies in whole blood was used. The reproducibility of the methods was documented to be within 10%. Doses of nitroglycerin were titrated for a 10 mm Hg decrease in mean arterial blood pressure with mean doses being 1.2 ± 0.2 (standard error of the mean) μg/kg/min. Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 ± 3.6 to 30 ± 6.3 cm 2 (p = 0.007) and by thrombin from 8.9 ± 1.7 to 4.1 ± 0.9 cm 2 (p = 0.003). Peak responses to ADP were decreased from 13.3 ± 1 to 9.1 ± 1.7 ohms (p = 0.005) and to thrombin from 9.3 ± 2 to 5.0 ± 1.2 ohms (p = 0.003). All patients had ≥50% inhibition with 1 agent or the other and the inhibition was >50% with each of the 2 aggregating agents in 6 patients. Analyses performed on blood withdrawn 15 minutes after the discontinuation of nitroglycerin showed a return to baseline before nitroglycerin results. When analyses were delayed and performed on blood preserved at room temperature for 30 minutes, no effect of nitroglycerin could be detected. Thus, bedside platelet aggregation studies document a significant and reversible effect of nitroglycerin at therapeutic doses on platelet function.