Prevention of myocardial platelet deposition and thromboxane release with dipyridamole.

Although current methods of myocardial preservation for coronary bypass surgery provide excellent protection, perioperative ischemic injury persists. Platelet activation and myocardial deposition may contribute to perioperative ischemic injury and early postoperative graft occlusion. Dipyridamole may reduce platelet activation and myocardial deposition and reduce perioperative ischemic injury. A prospective randomized trial was instituted in 40 patients undergoing elective coronary bypass surgery to evaluate the effects of dipyridamole on myocardial platelet and leukocyte deposition and the cardiac release of thromboxane and prostacyclin. Twenty patients received intravenous dipyridamole (0.24 mg/kg/hr) beginning 20 hr before surgery and continuing for 24 hr after surgery. Autologous platelets, leukocytes, and erythrocytes were labeled with 111In, 99mTc, and 51Cr, respectively, and were infused before release of the cross-clamp. Myocardial biopsy samples were obtained 10, 20, and 30 min after aortic declamping and indicated that platelets and leukocytes were deposited in the myocardium during reperfusion. Dipyridamole reduced both platelet (with dipyridamole 1540 +/- 2100 cells/mg, no dipyridamole 14,500 +/- 33,000 cells/mg) and leukocyte deposition (with dipyridamole 16 +/- 32 cells/mg, no dipyridamole 63 +/- 110 cells/mg). Cardiac release of thromboxane B2 (the stable metabolite of thromboxane A2) occurred in the early postoperative period and was reduced by dipyridamole (with dipyridamole 0.039 +/- 0.16 mg/liter, no dipyridamole 0.27 +/- 0.18 micrograms/liter, p less than .05). Dipyridamole reduced cardiac platelet deposition and thromboxane release and may reduce perioperative ischemic injury and early graft occlusion.