Quantifying shear-induced margination and adhesion of platelets in microvascular blood flow.

We tested the usefulness of aspirin (325 mg twice daily), heparin (1000 units per hour by intravenous infusion), and a combination of the two in the early management of acute unstable angina pectoris in a double-blind, randomized, placebo-controlled trial involving 479 patients. The patients entered the study as soon as possible after hospital admission (at a mean [+/- SD] of 7.9 +/- 8.0 hours after the last episode of pain), and the study was ended after 6 +/- 3 days, when definitive therapy had been selected. Major end points--refractory angina, myocardial infarction, and death--occurred in 23, 12, and 1.7 percent of the 118 patients receiving placebo, respectively. Heparin was associated with a decrease in the occurrence of refractory angina (P = 0.002). The incidence of myocardial infarction was significantly reduced in the groups receiving aspirin (3 percent; P = 0.01), heparin (0.8 percent; P less than 0.001), and aspirin plus heparin (1.6 percent, P = 0.003), and no deaths occurred in these groups. There were too few deaths overall to permit evaluation of the effect of treatment on this end point. The combination of aspirin and heparin had no greater protective effect than heparin alone but was associated with slightly more serious bleeding (3.3 vs. 1.7 percent). We conclude that in the acute phase of unstable angina, either aspirin or heparin treatment is associated with a reduced incidence of myocardial infarction, and there is a trend favoring heparin over aspirin. Heparin treatment is also associated with a reduced incidence of refractory angina.

Aspirin, heparin, or both to treat acute unstable angina

Davies, MJ, Thomas AC. Plaque fissuring—the cause of acute myocardial infarction, sudden ischaemic death and crescendo angina. Br Heart J 1985;53:363–373. Davies MJ, Woolf N, et al. Morphology of the endothelium over atheroscleretic plaques in human coronary arteries. Br Heart J 1988;60:459–464. Libby P. Molecular basis of the acute coronary syndromes. Circulation 1993;87:1179–1187. Burke AP, Farb A, Malcom GT, et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997;336:1276–1281. Davies MJ. The composition of coronary artery plaques [editorial]. N Engl J Med 1997;336:1312–1314. Report of a Meeting of Physicians and Scientists, Texas Heart Institute and the University of Texas Medical School at Houston. Lancet 1993;342:1151–1155. Thompson SG, Keinast J, Pyke SDM, et al. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995;332:635–678. DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980;303:16. Fuster V, Chesebro JH. Mechanisms of unstable angina [editorial]. N Engl J Med 1986;315:1023–1025. Chesebro JH, Fuster V. Thrombosis in unstable angina [editorial]. N Engl J Med 1992;327:192–194. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992;326:242–250, 310–318. Hamm CW, Ravkilde J, Gerhardt W, et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med 1992;327:146–150. Théroux P, Ouimet H, McCans J, et al. Aspirin, heparin, or both to treat acute unstable angina. N Engl J Med 1988;319:1105–1111.

Key references: pathology/physiology including thrombosis.

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Key references: pathology/physiology including thrombosis.