Effectiveness of Low-Dose Heparin in Prevention of Myocardial Reinfarction

Serneri, Gian Gastone Neri; Gensini, Gianfranco; Carnovali, M; Rovelli, F; Pirelli, Salvatore; Fortini, Alberto

doi:10.1016/s0140-6736(87)90291-1

Cited by 98 publications

(34 citation statements)

References 34 publications

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“…the extent of the lesion, and upon the capacity of the blood to form thrombin. Decreasing this capacity decreases the rate of reinfarction [2,3], while an increase in the capacity to form thrombin, i.e. hypercoaguability as defined by Virchow, is assumed to predispose to thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

Thrombin Generation in Platelet-Rich Plasma as a Tool for the Detection of Hypercoagulability in Young Stroke Patients

Faber

Lodder²,

Kessels³

et al. 2003

Pathophysiol Haemos Thromb

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The time course of the concentration of active thrombin in clotting plasma (the thrombogram) was measured by subsampling from platelet-rich plasma (PRP) and continuous chromogenic measurement of platelet-poor plasma (PPP) in 41 stroke patients under the age of 50, in whom stroke could not be attributed to cardioembolic disease, arterial dissection or vasculitis. A significant increase in the area under the thrombogram (endogenous thrombin potential, ETP) was seen in 23 patients. In 9 of them, ETP was increased in PRP but normal in PPP. High ETP in PRP was significantly associated with stroke, both in the middle and in the highest tercile of the ETP (odds ratio 5.1, range 1.8–15.1, and 3.7, range 1.3–10.3, respectively). A decreased sensitivity to the inhibitory action of thrombomodulin (TM) on thrombin generation was observed in 5 of 37 cases. No further definition of the cause of increased thrombin generation or TM resistance was attempted, except for the role of von Willebrand factor (vWF). ETP in PRP, platelet-derived procoagulant activity and vWF were correlated and higher in patients than in controls (p = 0.002, p = 0.045 and p = 0.0006, respectively). This confirms the correlation between vWF level and stroke at young age found in epidemiological studies. It suggests that the role of vWF in thrombin generation, which has been demonstrated in vitro, may be the underlying mechanism of this correlation. In summary, hypercoagulability, defined as an increased capacity of the platelet plasma system to form thrombin, is found in over half of the patients under 50 years with an otherwise unexplained stroke. Sometimes it is due to increased plasma factor activity, sometimes to an increased procoagulant activity of the platelets.

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Section: Introductionmentioning

confidence: 99%

Thrombin Generation in Platelet-Rich Plasma as a Tool for the Detection of Hypercoagulability in Young Stroke Patients

Faber

Lodder²,

Kessels³

et al. 2003

Pathophysiol Haemos Thromb

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show abstract

“…Likely the effect of inhibition of thrombin generation outweighs the unfavorable effects of vitamin K antagonists, at least when stable and therapeutic intensity anticoagulation is achieved. This is corroborated by the observation that parenteral anticoagulation (12.500 IU unfractionated heparin once daily) with heparin also protects against reinfarction 7. Different experimental studies show that application of the selective thrombin inhibitor dabigatran markedly reduces atherogenesis in susceptible mice (apoE−/− background) and beneficially affects the plaque phenotype 22, 23, 24, 25.…”

Section: Introductionmentioning

confidence: 74%

“…That thrombin plays a role here is strongly suggested by the observation that oral anticoagulation as well as heparin have a preventive action on the reoccurrence of myocardial reinfarction,6, 7 all the more as the effect superimposes on that of aspirin8; nevertheless, the role of thrombin remains rather equivocal. While straightforward risk associations between thrombin generation and thrombosis have been published, also by us, several other studies show inverse relationships (to be discussed below).…”

Section: Introductionmentioning

confidence: 98%

Thrombin Generation and Atherothrombosis: What Does the Evidence Indicate?

Cate

Hemker

2016

JAHA

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“…141,142 One compared heparin in a fixed dose of 12 500 U SC every 12 hours with an untreated control group, and the other used low-dose heparin (5000 U SC every 12 hours) for comparison. In both studies, moderate-dose heparin (12 500 U SC every 12 hours) reduced the incidence of mural thrombosis detected by 2-dimensional echocardiography by 72% and 58%, respectively (PϽ0.05 for each study).…”

Section: Acute MImentioning

confidence: 99%