What is the difference between arixtra and heparin

The effects of low molecular weight and standard heparin on calcium loss from fetal rat calvaria. Blood ; Hirsh J. N Engl J Med ; Heparin induced thrombocytopenia: diagnosis and management update. Postgrad Med J ; Chest ;SS. Antibodies to macromolecular platelet factor 4-heparin complexes in heparin-induced thrombocytopenia: a study of 44 cases. Thromb Haemost ; Pfizer Inc.

New York, NY. April Sanofi-Aventis U. Dosing with tinzaparin and nadroparin is less clear, as different formulations may have variable amounts of anti-Xa activity. Dalteparin is typically measured in terms of anti-Xa units, rather than in milligrams. For example, units of dalteparin is roughly equivalent to 50 mg of enoxaparin.

However, the ratio of anti-Xa vs. Recently, some authors have suggested dosing enoxaparin in a more finely graded fashion as shown below for patients with borderline renal function Shaikh This dosing scheme has yet to gain widespread acceptance, but it might be a consideration in very select situations with close monitoring of anti-Xa levels. Numerous recent studies seem to be converging on a dose of 0. This dose has the following advantages: i Twice-daily dosing avoids sub-therapeutic trough levels it's possible that the trough levels are the primary determinant of efficacy.

Correcting the dose for weight increases the likelihood of obtaining target drug levels. Using a single formula is simpler to apply and more closely mirrors the pharmacokinetics of enoxaparin which is linear. For patients with very unusual weight or borderline renal function, consider obtaining an anti-Xa level to monitor the heparin effect.

This is typically done after the third dose, but could probably be done sooner unless renal function is really awful, the trough heparin levels will be low and won't contribute substantially to the following peak level. For twice-daily prophylactic enoxaparin, the target anti-Xa level is 0.

It is provided in relatively fixed doses, usually q24hrs. It works via enhancing anti-thrombin's inhibition of factor Xa. Use of fondaparinux can help avoid unnecessary workup and empiric therapy for possible HIT. Use of 2. Disadvantages of fondaparinux compared to LMWH Fondaparinux has a very long half-life at hours. This can be problematic if the patient needs an urgent procedure or develops bleeding.

Thus, full therapeutic anticoagulation with fondaparinux is not generally very useful in the ICU. Fondaparinux may be more expensive. Possible procedure in near-term. Weight kg: 7. Medscape monograph on fondaparinux. Monitoring generally isn't necessary, but may be indicated in specific situations e. An anti-Xa level may be obtained three hours after a dose of fondaparinux. However, a specific calibration curve should be used for fondaparinux — if doubt exists about which test and cutoff values to use, discuss with the laboratory.

Many hospitals will lack a fondaparinux-calibrated anti-Xa level assay. This has numerous physiologic effects as shown above e. They are active against both fluid-phase and clot-bound thrombin unlike heparin, which acts only on fluid-phase thrombin.

PTT prolongation is generally used to titrate the dose of a direct thrombin inhibitor. INR prolongation is problematic, as this can make it difficult to transition to warfarin.

Assays for clotting factors and fibrinogen may be falsely prolonged causing the lab to register falsely low values. They are not dependent on anti-thrombin III levels Pharmacokinetics are generally more predictable than those of heparin especially bivalirudin, which doesn't bind to plasma proteins. Bivalirudin's short half-life 25 minutes may make it easier to stop, compared to a heparin infusion with half-life close to 45 minutes.

Lack of any reversal agent. This could be problematic for patients with hepatic dysfunction on argatroban — wherein the half-life may be considerable. Bivalirudin has traditionally been used more in the cardiac catheterization laboratory.

Properties of the two agents are compared here: direct thrombin inhibitor pseudo-resistance True resistance doesn't seem to occur with direct thrombin inhibitors because unlike heparin, their pharmacology is more predictable and their efficacy doesn't depend on anti-thrombin III. Pseudo-resistance can occur with both argatroban and bivalirudin Kennedy et al. This is essentially the same as pseudo-heparin resistance discussed above. This creates a dangerous situation where it falsely appears that the patient is resistant.

Ongoing up-titration of the direct thrombin inhibitor in efforts to increase the PTT can cause hemorrhage. Pseudo-resistance may be suspected if: An unusually high dose of direct thrombin inhibitor is required, or if it is impossible to achieve a therapeutic PTT. A baseline reduction in PTT might also support pseudo-resistance. However, it should not be ignored that both groups were also additionally treated with tirofiban [ 12 ] and the total number of patients enrolled was less when compared to the OASIS 5 and 6.

Moreover, the French cohort of NSTEMI patients who were predominantly managed invasively did not show fondaparinux to be superior to enoxaparin in terms of bleeding outcomes [ 3 ]. However, similar to the results of this analysis, mortality was not significantly different between these two anticoagulants. Nevertheless, it was shown that during the propensity score matched cohorts, a lower number of patients used aspirin or clopidogrel before admission.

Finally, the fact that several factors such as co-morbidities, age, use of anti-platelets and anticoagulants, as well as the dosage and whether these blood thinning agents were used before and after admission and the effect of plaque should all be taken into consideration when assessing bleeding risk and other adverse clinical outcomes in such patients.

For example, a recent meta-analysis showed thin-cap fibro-atheroma to be highly associated with culprit plaque rupture [ 13 ]. Therefore, clinical outcomes might vary from study to study due to the influence of such factors. It is among the first meta-analyses comparing enoxaparin with fondaparinux in patients who were being treated for ACS. A low to moderate level of heterogeneity was observed in several of the subgroups analyzing the outcomes, which might be a positive aspect of this analysis.

Randomized patients and patients obtained from observational studies were combined as well as separately analyzed. Classification of bleeding events was vast. Use of other anti-platelets and anticoagulants and other factors might have influenced the results which were obtained. Clinical efficacy and safety of enoxaparin in unselected Swiss patients undergoing primary or elective percutaneous coronary intervention: analysis of the RIVIERA study.

Acta Cardiol. Article PubMed Google Scholar. Efficacy and safety of fondaparinux versus enoxaparin in patients with acute coronary syndromes undergoing percutaneous coronary intervention: results from the OASIS-5 trial.

J Am Coll Cardiol. Impact of fondaparinux versus enoxaparin on in-hospital bleeding and 1-year death in non-ST-segmentelevation myocardial infarction. Phase I findings. N Engl J Med. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate healthcareinterventions: explanation and elaboration.

Measuring inconsistency in meta-analyses. Bauer KA. Fondaparinux sodium: a selective inhibitor of factor Xa. Am J Health Syst Pharm. Mechanism of catheter thrombosis: comparison of the antithrombotic activities of fondaparinux, enoxaparin, and heparin in vitro and in vivo.

Arq Bras Cardiol. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. Fondaparinux vs. J Clin Pharm Ther. Prevalence and predictors of culprit plaque rupture at OCT in patients with coronary artery disease: a meta-analysis. Eur Heart J Cardiovasc Imaging. Routine use of fondaparinux in acute coronary syndromes: a 2-year multicenter experience.

Am Heart J. Comparative evaluation of efficacy, safety and haemostatic parameters of enoxaparin and fondaparinuxin unstable coronary artery disease. J Clin Diagn Res.

Mil Med Res. Download references. All data and materials used in this research are freely available. References have been provided.

PKB, MS and JY were responsible for the conception and design, acquisition of data, analysis and interpretation of data, drafting the initial manuscript and revising it critically for important intellectual content. PKB wrote this manuscript. All authors read and approved the final manuscript. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. You can also search for this author in PubMed Google Scholar.

Correspondence to Jun Yuan. Reprints and Permissions. Bundhun, P. Choosing between Enoxaparin and Fondaparinux for the management of patients with acute coronary syndrome: A systematic review and meta-analysis.

BMC Cardiovasc Disord 17, Download citation. Received : 28 February Accepted : 02 May Published : 08 May Anyone you share the following link with will be able to read this content:.

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