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Biomedical subjects

L F Caprissi

Publications and source records attributed to L F Caprissi.

11 recordsLinked to original sources

Treatment of acute myocardial infarction with subcutaneous heparin at low doses.

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 cm3 = 50 mg = 5000 IU. Blood rheologic factors (thromboelastography, 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Heparin effect on plasma fibrinogen in the thrombophilic syndrome.

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 1 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.

Adult↗

Heparin effect on blood viscosity.

The effect of heparin on blood viscosity was investigated in a group of patients with acute myocardial infarction (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, 1 cc i.v. 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 alpha 2 globulin, and number of platelets. Hyperviscosity, hypercoagulability, and the increase of platelet adhesiveness arae 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.

Adult↗