Effect of acetylsalicylate on cardiac and muscular pain induced by intracoronary and intra-arterial infusion of bradykinin in humans

OBJECTIVES This study assessed the algesic activity of bradykinin (BK) in h umans and the effects of acetylsalicylate on muscular and cardiac BK-induce d pain. BACKGROUND Bradykinin is released by the ischemic myocardium and may be inv olved in the genesis of ischemic pain. METHODS Increasing doses of BK (from 30 to 960 ng/min) were randomly infuse d, for periods of 2 min each, into the iliac artery of 10 patients. The sam e protocol was repeated 30 min after the IV administration of 1 g of acetyl salicylate. In eight other patients with coronary artery disease, the same increasing doses of BK, for periods of 2 min each, were infused into the le ft coronary artery. The same protocol was repeated 30 min after the IV admi nistration of 1 g of acetylsalicylate. Time to pain onset and maximal pain severity were obtained. RESULTS Before acetylsalicylate administration, all patients experienced pa in during intra-iliac infusion of BK. After acetylsalicylate, eight patient s did not experience any pain during BK infusion (p = 0.0014), and in the t wo remaining patients, time to pain onset and maximal pain severity were si milar to those recorded before acetylsalicylate. Before acetylsalicylate ad ministration, all patients experienced pain similar to their habitual angin a during intracoronary BK infusion. After acetylsalicylate, six patients di d not experience any pain during BK infusion (p = 0.0098), whereas in the t wo remaining patients time to pain onset and maximal pain severity were sim ilar to those recorded before acetylsalicylate. CONCLUSIONS Intra-iliac infusion of BK causes muscular pain, and its intrac oronary infusion in patients with coronary artery disease causes cardiac pa in, which is similar to their habitual angina. The BK-induced pain is aboli shed or reduced by acetylsalicylate, thus suggesting that acetylsalicylate- sensitive mediators, such as prostaglandins, are involved in its pathogenes is. (C) 1999 by the American College of Cardiology.