Treatment of acute myocardial infarction with subcutaneous heparin at low doses

Abstract Heparin has been used intensively in the treatment of acute myocardial infarction and preinfarction angina (PA) at full doses as a single drug by us. However, heparin may be used at smaller doses for similar purposes. These doses are not exactly anticoagulant, even though they reduce blood hypercoagulability, and act mainly in an antithrombotic capacity. We studied 529 patients with acute myocardial infarction, of whom 262 were treated with subcutaneous heparin at low doses (5000 IU every 12 h) and 267 received conventional therapy without antithrombotic drugs. Heparin used was Heparina (Abbott) and Liquemine (Roche), in vials with the equivalence 1 cm 3 =50 mg=5000 IU. Blood rheologic factors (thrombo‐elastography, platelet adhesiveness, total blood viscosity, and number of platelets) were determined in all patients, those treated with heparin at low doses and also the control group, before and after the 30‐day treatment period. Diagnosis was based on clinical symptoms, laboratory studies, and electrocardiogram examination. In both the 262 patients treated with heparin at low doses and in the control group of 267 patients, baseline values of rheological factors were high. After 30 days (i.e., after study completion) these high values which are statistically significant compared with normal values, with p<0.0001 for both groups, remained constant in the control group who did not receive heparin. On the contrary, in the group treated with heparin at low doses, all these factors changed. Heparin provides protection against thrombosis by increasing the negative charge of the vessel wall and by other reactions at the endothelial surface. Heparin requires a plasmatic component called antithrombine III. Another important action of heparin is its activity as anti‐Xa which is said to be reason for its antithrombotic effect. When low molecular weight heparin is administered subcutaneously, higher anti‐Xa levels are obtained in blood as compared with those obtained with heparin of high molecular weights. Heparin obtained from intestinal mucosa has a great capacity to potentiate anti‐Xa, which does not occur with heparin of pulmonary origin. Heparin at low doses prevents thrombosis by inhibiting the coagulation cascade, acting selectively on the Xa which join the intrinsic and extrinsic systems. Heparin neutralizes activation of complement in several stages. Treatment of actue myocardial infarction with heparin during 30 days with full anticoagulant doses provides a mortality rate of 6.1%. These high doses were considered to be the reason for bleedings, even though heparin does not produce bleeding when administered correctly, as was the case in our study. With the low heparin doses used in this study subcutaneously during 30 days, there were no cases of bleedings.