Death heparins

Low-molecular-weight heparins and heparinoids are not recommended in the treatment of acute ischemic stroke.11 A meta-analysis was performed using data from 10 randomized controlled trials.19 A non-significant decrease in combined death and disability and a non-significant increase in case fatality and hemorrhage were seen. A reduction in venous thromboembolic events was observed in acute stroke patients however, there was also an increase in extracranial bleeding. 

Heparin-induced thrombocytopenia A clinical syndrome of IgG antibody production against the heparin-platelet factor 4 complex occurring in approximately 1% to 5% of patients exposed to either heparin or low-molecular-weight heparin. Heparin-induced thrombocytopenia results in excess production of thrombin, platelet aggregation, and thrombocytopenia (due to platelet clumping), often leading to venous and arterial thrombosis, amputation of extremities, and death. 

Low-molecular-weight heparins (LMWHs) may be an alternative to UFH in STE ACS. Enoxaparin may produce a modest benefit over UFH in reducing the risk of death or nonfatal MI. Enoxaparin has not been studied in the setting of primary PCI. 

Quality still remains the No. 1 criteria for any outsourcing activity. Imports from third-party suppliers account for greater than 80% of APIs (active pharmaceutical ingredient) in the United States and 40% of medicinal products, yet the FDA (US Food and Drug Administration) continues to conduct far fewer foreign compared to domestic inspections (Mullin, 2011). Contaminated heparin was judged as the cause of 81 deaths in the United States in 2008. FDA traced the contaminated API to a Chinese supplier (Changzhou SPL Co.). 

The CURE study involved 12,562 patients randomized to receive Plavix (300 mg loading dose followed by 75 mg daily) or placebo and were treated for up to a year. Patients also received aspirin or other standard treatment such as heparin. The results showed that Plavix had a 20% relative risk reduction compared with placebo (582 cases of cardiovascular death, myocardial infarction, or stroke) versus 719 cases for placebo. 

Drug therapy of acute coronary syndromes including unstable angina and non-Q-wave myocardial infarction includes use of aspirin, heparin and anti-ischaemic drugs and is similar in older patients to other age groups. Activation of platelet thromboxane production in the coronary circulation has been demonstrated in unstable angina. The risk of myocardial infarction or death is reduced by approximately 50% by early aspirin therapy in recommended doses of 160-325 mg per day and continued... 

Vitamin K antagonists, such as dicoumarol (8.61, a natural product) and warfarin (8.62), are used as anticoagulants in human therapy (thrombosis, atherosclerosis) and as rat poisons that lead to internal bleeding and death in rodents. Heparin, a polysaccharide consisting of 2-0-sulfonated glucuronic acid and 2-N,6-0-disulfonated glucosamine, is also a widely used anticoagulant, but its effect is connected not with Vitamin K but with enzyme inhibition. 

April 21 The FDA sets the number of deaths from contaminated doses of Heparin at 81. The main ingredient of the blood-thinning drug comes from pig intestines processed in China. 

May 11 The deaths of two patients in Delaware prompt review of the blood-thinner drug Heparin, a drug that caused 81 deaths in 2008 when tainted ingredients were imported from China. 

Heparin is considered a hazardous drug, Heparin may be the leading cause of drug-related deaths in hospitalized patients who are relatively... 

I11 the therapy of deep venous thrombosis, heparin is commonly administered. This drug takes effect immediately to prevent further thrombus formation. However, heparin is regarded as a hazardous drug and possibly may be tlie leading cause of drug-related deaths 111 hospitalized patients who are relatively well. Usually administered intravenously, preferably by pump-dnven infusion at a constant rate rather than by intermittent injections, it sometimes may cause major bleeding, which is particularly hazardous if it is intracranial. The action of heparin can be terminated almost immediately by intravenous injection of protamine sulfate, but where there may be less urgency, vitamin Ki may be used. The vitamin preparation may be administered intravenously, intramuscularly, or subcutaneously. 

Heparin has a strong clearing action on postprandial lipidemia by activating lipoprotein lipase. This has been thought to be associated with an increase in free fatty acid-induced dysrhythmias and death in patients with myocardial infarction. 

GUSTO-V (55) Abciximab + reteplase + heparin versus reteplase + heparin 16,588 Death 30 day... 

Hence in pooled analysis of the randomized clinical trial experience in PCI, including I 1,638 patients (bivalirudin, 5861 heparin, 5777), bivalirudin was associated with a reduction in the incidence of death, Ml, revascularization, and major bleeding (7.8% vs. 10.8%, P< 0.001) at 48 hours (32). Despite a very low event rate, a benefit in terms of mortality was observed (0.01% vs. 0.02%, P = 0.049), whereas reductions for major bleeding were substantial (2.7% vs. 5.8%, P < 0.001). Furthermore, given the lower overall costs of this agent and savings associated with reduced bleeding, the use of bivalirudin remains economically attractive (33). 

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). 

In the ESSENCE trial, the LMWH enoxaparin led to a relative risk reduction of 15% to 16% in the rate of death, Ml, or refractory ischemia as compared to unfractionated heparin at 30 days in UA/NSTEMI patients (38). Nadroparin [FRAXIS study (39)] and dalteparin [FRIC study (40)] did not demonstrate superiority against unfractionated heparin. Human pharmacokinetic data indicate that these differences in clinical efficacy might be explained by different elimination half-lives of antifactor Xa activity (dalteparin 2.8 hours, nadroparin 3.7 hours, enoxaparin 4.1 hours) (41). 

Several direct thrombin inhibitors have been studied in NSTEMI and STEM I patients and were compared to unfractionated heparin. In the GUSTO lib- and OASIS-2 trial (42,43), hirudin was studied versus heparin in patients with ACS. Despite early benefits, no statistical significance could be demonstrated at 30 days. Together with the OASIS-1 data, a combined analysis indicated a 22% relative risk reduction in cardiovascular death or Ml at 72 hours, 17% at 7 days, and 10% at 35 days (42). 

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