Benefit of adding low molecular weight heparin to the conventional treatment of stable angina pectoris. A double-blind, randomized, placebo-controlled trial.

Melandri, Giovanni; Semprini, Franco; Cervi, Vittorio; Candiotti, N; Palazzini, E; Branzi, Angelo; Magnani, B

doi:10.1161/01.cir.88.6.2517

Cited by 44 publications

(13 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It also increased the template bleeding time consistent with several reports on the antihemostatic effects of LMWH. [29][30][31][32][33][34] The bleeding time test, which remains the most reliable global marker of treatment-induced hemostasis impairment, [22][23][24][35][36][37] was therefore used for the safety assessment of PCA treatment infusion in the equiefficacious dose range. While the absence of significant increase in the bleeding time during PCA infusion does not exclude the possibility of bleeding side effects, 38 the direct comparison between LMWH and PCA strongly suggested that the latter was considerably safer.…”

Section: Discussionmentioning

confidence: 99%

Relative antithrombotic and antihemostatic effects of protein C activator versus low-molecular-weight heparin in primates

Gruber

Marzec

Bush

et al. 2007

Blood

View full text Add to dashboard Cite

The anticoagulant and anti-inflammatory enzyme, activated protein C (APC), naturally controls thrombosis without affecting hemostasis. We therefore evaluated whether the integrity of primary hemostasis was preserved during limited pharmacological antithrombotic protein C activator (PCA) treatment in baboons. The double-mutant thrombin (Trp215Ala/ Glu217Ala) with less than 1% procoagulant activity was used as a relatively selective PCA and compared with systemic anticoagulation by APC and low-molecular-weight heparin (LMWH) at doses that inhibited fibrin deposition on thrombogenic segments of arteriovenous shunts. As expected, both systemic anticoagulants, APC (0.028 or 0.222 mg/kg for 70 minutes) and LMWH (0.325 to 2.6 mg/kg for 70 minutes), were antithrombotic and prolonged the template bleeding time. In contrast, PCA at doses (0.0021 to 0.0083 mg/kg for 70 minutes) that had antithrombotic effects comparable with LMWH did not demonstrably impair primary hemostasis. PCA bound to platelets and leukocytes, and accumulated in thrombi. APC infusion at higher circulating APC levels was less antithrombotic than PCA infusion at lower circulating APC levels. The observed dissociation of antithrombotic and antihemostatic effects during PCA infusion thus appeared to emulate the physiological regulation of intravascular blood coagulation (thrombosis) by the endogenous protein C system. Our data suggest that limited pharmacological protein C activation might exhibit considerable thrombosis specificity. IntroductionSystemic anticoagulants can completely interrupt thrombus formation, but their usefulness is limited because their antithrombotic and antihemostatic activities are mechanistically tied. Highly effective plasma concentrations of systemic anticoagulants, such as those used for temporary thrombo-prophylaxis in interventional cardiology, prevent thrombin generation in both the blood vessel and the wound and can paralyze hemostasis with potentially fatal consequences. Due to safety considerations, the vast majority of patients who receive antithrombotic treatment are not anticoagulated to full efficacy. Thrombotic blood vessel occlusions causing myocardial infarction and ischemic stroke thus continue to contribute to mortality statistics. 1 Until more thrombosis-specific intravascular anticoagulants become available, balancing the potential benefits and risks of systemic anticoagulation remains a critical hurdle for the clinician.Occlusive thrombus formation is naturally down-regulated without bleeding complications most of the time following thrombogenic stimuli, such as blood vessel injuries or infections. It thus seems possible that selective pharmacological enhancement of the natural antithrombotic systems could achieve thrombosis specificity. Enhancement of the endogenous protein C pathway in the vicinity of thrombus formation might offer this wider therapeutic window. Thrombin is the natural protein C activator enzyme that activates protein C on such anatomic surfaces as the endothelial lining of blood vessels. ...

show abstract

Section: Discussionmentioning

confidence: 99%

Relative antithrombotic and antihemostatic effects of protein C activator versus low-molecular-weight heparin in primates

Gruber

Marzec

Bush

et al. 2007

Blood

View full text Add to dashboard Cite

show abstract

“…A lower plasma fibrinogen level can be achieved by reducing cigarette smoking [37], by exercise [38,39] and in diabetic patients probably by improved metabolic control [19,20]. Fibrinogen lowering can also be achieved by heparin [40] or low molecular weight heparin [41] administration. In diabetic patients these results were confirmed for both heparin formulations and moreover for the glucosaminoglycan sulodexide [42].…”

Section: Conclusion: Is It Time For Intervention Trials?mentioning

confidence: 99%

Fibrinogen and diabetes mellitus: is it time for intervention trials?

Ceriello

1997

Diabetologia

View full text Add to dashboard Cite

show abstract

“…This is the first study to demonstrate such an improvement. De creased fibrin formation has been shown by the same group [18] in patients with acute myocardial infarction treated with a high dose of LMWH (parnaparin 12,800 IU anti-Xa once a day) compared to a low dose of par naparin (6,400 IU once a day) or UFH (15,000 IU). Significantly lower levels of fibrinopeptide A (FpA) during the first 8 h after drug administration were observed in the high-dose parnaparin group, compared to the other two groups.…”

Section: Stable Angina and Myocardial Infarctionmentioning

confidence: 82%

Are Low-Molecular-Weight Heparins Useful for the Prophylaxis and Treatment of Arterial Thrombi?

Samama

Combe²,

Ill³

et al. 1996

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

The pharmacologic specificity of low-molecular-weight heparins (LMWHs) has enabled multiple attractive developments in the prophylaxis and treatment of arterial thrombosis. Their high antithrombotic potency associated with a potentially lower induced bleeding risk, the lack of platelet interaction, the prevention of myointimal hyperplasia, and the lower incidence of heparin-induced thrombocytopenia, are major advantages. New studies in cardiology and vascular surgery demonstrate a high efficacy for LMWHs associated with a low risk.

show abstract

Benefit of adding low molecular weight heparin to the conventional treatment of stable angina pectoris. A double-blind, randomized, placebo-controlled trial.

Abstract: Patients with stable angina pectoris may be treated with Parnaparin in addition to aspirin and conventional antianginal medication. Side effects are negligible, and compliance is excellent.

Cited by 44 publications

References 38 publications

Relative antithrombotic and antihemostatic effects of protein C activator versus low-molecular-weight heparin in primates

Relative antithrombotic and antihemostatic effects of protein C activator versus low-molecular-weight heparin in primates

Fibrinogen and diabetes mellitus: is it time for intervention trials?

Are Low-Molecular-Weight Heparins Useful for the Prophylaxis and Treatment of Arterial Thrombi?

Contact Info

Product

Resources

About