Unfractionated heparin platelets

Unfractionated heparin Bleeding, heparin-induced thrombocytopenia Clinical signs of bleeding3 baseline CBC and platelet count aPTT every 6 hours until target then every 24 hours daily CBC platelet count every 2 days (minimum, preferably every day)... 

Xiao Z, Theroux P. (1998) Platelet activation with unfractionated heparin at therapeutic concentrations and comparisons with a low-molecular weight heparin and with a direct thrombin inhibitor. Circulation 97 251-256. 

Heparin may also produce a decrease in platelets (thrombocytopenia) in some patients.13,84 This condition, known commonly as heparin-induced thrombocytopenia (HIT), is less common with LMWHs versus unfractionated heparin, but HIT can occur with any type of heparin treatment.101,145... 

Efficacy and safety oftenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin the ASSENT-3 randomized trial in acute myocardial infarction. Lancet 2001 358 605. LincoffAM, Califf RM, Van De WerfE etal. Mortality at I year with combination platelet glycoprotein llb/llla inhibition and reduced-dose fibrinolytic therapy vs conventional fibrinolytic therapy for acute myocardial infarction GUSTO V randomized trial. JAMA 2002 288 2130. 

Keating FK, Dauerman HL, Whitaker DA, Sobel BE, Schneider DJ. Increased expression of platelet P-selectin and formation of platelet-leukocyte aggregates in blood from patients treated with unfractionated heparin plus eptifibatide compared with bivalirudin. Thromb Res 2006 I 18 361-369. 

Abbreviations aPTT, activated partial thromboplastin time AT, antithrombin HC, heparin cofactor HIT, heparin-induced thrombocytopenia PCI, percutaneous coronary intervention PF, platelet factor UFH, unfractionated heparin. 

The recommendation for UFH is based on documented efficacy in many older mid-sized trials. Meta-analyses showed a clear reduction in Ml and death, but at the cost of an increase in major bleeding rates (35,36). The advantages of LMWH over unfractionated heparin include a better bioavailability, a stronger and longer anti-Xa activity, less platelet activation, and no need for monitoring. A major drawback of standard heparin therapy is the potential risk of heparin-induced thrombocytopenia, which is considerably reduced with LMWH (37). 

Heparin binds to antithrombin (a protease inhibitor that inactivates factors Ha, IXa, Xa and XIa) and markedly accelerates its inhibitory effect on coagulation. In addition, heparin inhibits platelet function, The newer low-molecular-weight heparins augment antithrombin activity preferentially against factor Xa and do not prolong the APTT like standard (unfractionated) heparin does. 

Heparin acts as a catalyst for antithrombin III (AT III), increasing its activity by approximately a thousand times. Antithrombin III is a plasma enzyme that inactivates certain activated serine proteases of the coagulation cascade, most importantly activated factors II (thrombin) and X. The larger heparin species (found in unfractionated heparin) catalyzes the inactivation of activated factors II and X. In contrast, LMWH chiefly inactivates activated factor X. The final effect of both is systemic anticoagulation. Heparin also possesses inherent platelet-aggregating properties and may also induce the production of platelet-aggregating antibodies. Heparin can inhibit aldosterone synthesis. 

Unfractionated heparin (UFH) inhibits platelet aggregation and fibrin formation by accelerating the action of antithrombin, which in turn inactivates factors Ha, IXa, and Xa. The benefit of heparin in UA has been well defined in early trials (48,49). In the RISC trial, a combination of aspirin and heparin reduced the incidence of MI and death during the first five days by 75% when compared with placebo. This result was successfully replicated in several small trials examining the role of heparin in UA. A meta-analysis of these trials revealed a 33% reduction in the combined risk of death or MI in patients treated with aspirin plus heparin compared with those treated with aspirin alone (66). With benefit of heparin clearly established in UA patients, later trials attempted to expand the role of heparin in NSTEMI. 

These drugs have much less plasma protein binding activity than do the higher molecular weight (unfractionated) heparins. These drugs also have decreased binding to platelets, and factors IV and V, thus producing less thrombocytopenia. 

Of 500 patients treated with unfractionated heparin 131 (26%) developed platelet factor 4/heparin antibodies, which... 

Responsibilities for management of chronic and preoperative medication need to be clearly defined and communicated between all involved caregivers. Timely prescription (e.g. treatment of preoperative anemia), reliable continuation (e.g. beta-blockers, aspirin, statins) [2], timely discontinuation (e.g. metformin, platelet inhibitors, new oral anticoagulants), and effective bridging (insulin, unfractionated heparin) of preoperative medications increase patient safety by reducing risks of myocardial ischemia, bleeding and transfusion, and help to avoid case cancellations. 

Therapy, in the short term, is with intravenous unfractionated or subcutaneous low molecular weight heparin. Aspirin, given in low doses between 50 and 100 mg per day, is sufficient to diminish platelet-vessel interaction. Alternatives include 100-200 mg of sulphinpyrazone once or twice a day or dipyridamole where 100 mg four times a day can be used on its own or between 25 and 75 mg combined with aspirin three times a day. More recently thiopy-ridines, as a class, has been shown to have equivalence at 250 mg twice a day. In hyperhomocysteinaemia the risk is reduced by 5 mg of folate and 100 mg of vitamin Bg daily, with addition of oral vitamin Bi2 of less clearly defined benefit. The effect of this intervention requires re-assay at 3-monthly intervals, following standard methionine challenge, to ensure that suitable suppression has been achieved in the plasma amino acid level (Table 5). 

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