Copyright © 1994 by the European Society of Cardiology.
© 1994 The European Society of Cardiology
Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase
Istituto di Cardiologia dell'Universita' degli Studt, Centro di Studio per te Ricerche Cardiovascolari del Consigtio Nazionale delle Ricerche Fondazione I Monzino', IRCCS, Milano, Italy
Received 13 July 1993; revised 3 December 1993; .
Correspondence: Dr Alessandro Salvioni, Istituto di Cardiologia dell'Universita di Milano. Via Parea 4, 20138 Milano, Italy
Abstract
The purpose of this study was to investigate whether, to what extent, and through which mechanisms intravenous heparin, administered before and after streptokinase, affects the plasma levels of D-dimer and fibrinogen in myocardial infarction. Data concerning mortality and incidence of coronary recanalization in patients receiving heparin and thrombolytic therapy after acute myocardial infarction are controversial; furthermore, the mechanisms through which heparin acts in combination with thrombolytic therapy are unclear. Thirty-eight patients with acute myocardial infarction treated with streptokinase were considered. Nineteen of them received, immediately before the beginning of thrombolytic treatment, a bolus of heparin (100 U. kg1 intravenously) and, 2 h later, intravenous heparin in doses raising the partial thromboplastin time to 2-2.5 times the normal value (Group 1); the remaining 19 did not receive anticoagulant treatment (Group 2). Multiple determinations of plasma D-dimer and fibrinogen levels were obtained in all patients before, and in the seven days following thrombolytic treatment. Six hours after streptokinase, fibrinogen decreased from 304 ± 34 to 61 ± 34 mg. dt1 in Group 1 and from 312 ± 29 to 38 ±21 mg. dt1 in Group 2 (P<002 versus Group 1). The same difference between groups persisted at the 12th and at the 18th hour. D-dimer values, from 0-5 ± 01 \ig. dl1 in Group 1 and 04 ±01 fig. dt1 in Group 2, increased at the 1st hour to 37.2 ± 36.5 fig. dt1 and 52.2 ± 39.8 µg. dl1, respectively. A peak value was reached in both groups at the 6th hour, which was followed by a slow decrease. A significant difference between the two groups (P<0.05) was observed at the 1st, 2nd, 4th and 6th hour. An inverse correlation between maximal changes of fibrinogen and of D-dimer was found in both groups (r= 0.89, P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2).
The relationship between D-dimer and fibrinogen variations after streptokinase and changes induced by heparin, support the hypothesis that the decrease of fibrinogen, following thrombolysis, is not only the consequence of its direct degradation, but also the result of its transformation by streptokinase into fibrin, fibrin cross-linked (with facilitation of thrombogenic condition) and then into the stable catabolite, D-dimer. These data confirm a thrombogenic effect of streptokinase therapy; this tendency can be limited by prompt use of high doses of heparin.
Key Words: Myocardial infarction • thrombolytic therapy • fibrinogen • D-dimer • heparin
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