Evaluation of new methods for the selective measurement of fibrin and fibrinogen degradation products.
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Biomedical subjects
F Bonechi
Publications and source records attributed to F Bonechi.
Blood clotting active drugs in long-term post-myocardial infarction treatment.
Oral anticoagulants have been used for over three decades in long-term post-myocardial infarction treatment. The cumulated results of the early clinical trials showed a reduction of general mortality of 20%. The reduction reached 60% when trials with adequate anti-coagulant treatment were considered. The most recent study (Sixty Plus Study 1980), a very well designed and conducted study with optimal anticoagulant dosage, reported a 2-year reduction in total mortality of 43% (p less than 0.017 vs. controls) and a reduction of reinfarction of 64.1% (p less than 0.0002). However, the incidence of major hemorrhagic episodes (27 vs. 3) and of definite intracranial hemorrhages (8 vs. 1) was very high in the treatment group with 6 deaths vs. 1 due to hemorrhage. An alternative way for controlling blood clotting activation and thrombin generation appears to be low-dose heparin treatment. In a randomized controlled clinical trial heparin administered in low doses (12,500 i.u. daily by subcutaneous route) reduced the reinfarction rate by 63% (p less than 0.05 vs. controls) and general mortality by 47% (p less than 0.05) over 2 years. Even the frequency of the fatalities attributable to thromboembolic events was significantly decreased. No hemorrhagic complication occurred in any patients. Oral anticoagulants and low-dose heparin appears to be equally effective in secondary prevention of myocardial infarction. However, low-dose heparin treatment appears to be free from the elevated risk of major hemorrhages related to oral anticoagulants and does not require any blood clotting check.
Anticoagulants↗
Decrease in frequency of anginal episodes by control of thrombin generation with low-dose heparin: a controlled cross-over randomized study.
Increased thrombin generation is frequently associated with an increase in anginal activity. A cross-over, single-blind, completely randomized study was planned in order to evaluate whether the control of thrombin generation affected the increase in anginal activity. After discharge from the hospital, 24 patients (18 men and 6 women, aged 40 to 69 years) suffering from spontaneous angina were followed up to 12 months and were alternatively treated during two consecutive 6-month periods with calcium heparin, 12,500 IU by the subcutaneous route, or with placebo by the intramuscular route, in addition to the usual antianginal medications. Thrombin generation and clinical activity of angina were assessed every 15 days by measuring fibrinopeptide A (FPA) plasma levels and by grading in three classes (symptomless, mildly symptomatic, and severely symptomatic) the anginal activity on the basis of the number and the time concentration of the ischemic attacks and ECG changes. Low-dose heparin treatment significantly reduced both the FPA plasma level (from 4.1 +/- 3.7 to 2.3 +/- 1.8 ng/ml, p less than 0.001) and the clinical activity of angina. During heparin treatment, the frequency of the observations in the severely and mildly symptomatic classes decreased, respectively, by 53% and by 30%, whereas that in the symptomless class increased by 23% (p less than 0.001) in comparison with the period on placebo. Present results indicate that the control of thrombin generation obtained by low-dose heparin treatment favorably affects the degree of anginal activity in patients with spontaneous angina.
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