~um~ary: ~he effect of heparin on blood viscosity was ~nvestl~ated In a group of patients with acute myocardial mfarctlon (AMI) and preinfarction angina (PA), whose blood viscosity was elevated. Viscosity was measured with Cannon, Fenske, and Routine viscometers. Kinematic viscosity, bath and whole blood, plasma, and serum viscosity were determined as well as dependent parameters (fibrinogen, serum proteins, number of platelets, and hematocrit). All of them were found to increase, and it was significantly proved that intravenous heparin immediately decreased plasma viscosity, but has a lesser effect on serum and whole blood viscosity. A dose of 1 cc = 50 mg = 5000 IU intravenous heparin, will maintain this decrease for' a month. In our four-week study, I cc Lv. heparin was administered at 6-hour intervals for the first 2 weeks, and 2 cc heparin subcutaneous injections were administered at 12-hour intervals for the next 2 weeks. We found that heparin also decreased fibrinogen, hematocrit, serum alpha2 globulin, and number of platelets. Hyperviscosity, hypercoagulability, and the mcrease of platelet' adhesiveness are some of the most important physiopathological alterations of AMI and PA. The decrease of blood viscosity due to heparin is one of the most important and beneficial effects of it in this pathology.

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Summary: The effects of heparin were studied in a group of 42 patients with preinfarction angina (PA) and acute myocardial infarction (AMI) whose plasma fibrinogen was increased. Plasma fibrinogen was measured by the turbidimetric method in timol turbidimetric units. Statistically significant results proved that heparin reduces the plasma fibrinogen progressively over a treatment period of 6 weeks. During the first three weeks a dose of I cc (50 mg or 5000 IU) was given by intravenous injection at 6-h intervals, this was followed by a dose of 2 cc (100 mg or 10,000 IU) given by subcutaneous injection at 12-h intervals for a further three weeks. Hyperfibrinogenemia is perhaps one of the most important factors in the thrombophilic syndrome, and at the same time it is one of the fundamental physiopathological alterations observed in AMI and PA. Because heparin reduces hyperfibrinogenemia it has a beneficial effect in these diseases.