Low-Molecular-Weight Heparins in the Management of Acute Coronary Syndromes

Zed, Peter J.; Tisdale, James E.; Borzak, Steven

doi:10.1001/archinte.159.16.1849

Cited by 51 publications

(11 citation statements)

References 77 publications

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“…Such a situation would be particularly beneficial in conditions such as ischemic heart disease and acute PE. 40,41 In summary, this study is the first to suggest that incorporation of LMWH in PEG-liposomes increases the half-life of the drug. Of the formulations tested, PEG-2000 liposomes were the most efficacious in enhancing pulmonary absorption and prolonging the circulation time of LMWH.…”

Section: Discussionmentioning

confidence: 72%

Inhalable Liposomes of Low Molecular Weight Heparin for the Treatment of Venous Thromboembolism

Bai

Ahsan

2010

Journal of Pharmaceutical Sciences

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Section: Discussionmentioning

confidence: 72%

Inhalable Liposomes of Low Molecular Weight Heparin for the Treatment of Venous Thromboembolism

Bai

Ahsan

2010

Journal of Pharmaceutical Sciences

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“…5,14,17) Similar to UFH, LMWHs exert their anticoagulant activity by activating AT III, but owing to their high content of BCLM, they have less ability to catalyze the inactivation of factor IIa when compared to that of factor Xa, yielding an antifactor Xa : antifactor IIa ratio above 1 and varying from 2:1 to 4:1 among different types of LMWHs. 15) Unfractionated heparin binds nonspecifically to plasma proteins, endothelial cells, and platelets and is sensitive to inactivation by platelet factor 4. In contrast, LMWHs are less frequently bound to plasma proteins, endothelial cells, and platelets and are resistant to inactivation by platelet factor 4.…”

Section: Discussionmentioning

confidence: 99%

Head-to-Head Comparison of Two Different Low-Molecular-Weight Heparins in Acute Coronary Syndrome. A Single Center Experience.

et al. 2002

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SUMMARYLow-molecular-weight heparins (LMWH) of different types have yielded different results when used in the setting of unstable angina (UA) or non Q-wave myocardial infarction (NQMI). We compared the safety and therapeutic efficacy of two different LMWHs, namely dalteparin (Dalt.) and enoxaparin (Enox.), in the acute phase (first 5 days) of UA or NQMI.One hundred and forty-two patients with UA/NQMI were randomly assigned to treatment with either Dalt. [120 IU/kg twice daily by subcutaneous (SC) injection] or Enox.[1 mg/kg twice daily by SC injection]. The occurrence of any one of death, myocardial infarction, or angina recurrence within 5 days of the first LMWH injection was the endpoint of the study. There were 69 patients in the Enox. group (53 males, 16 females, mean age : 60.3±11.9) and 73 patients in the Dalt. group (54 males, 19 females, mean age : 59.6 ±10.3). The baseline characteristics of the patients in the two groups were similar. There were no deaths in either group. Myocardial infarction occurred in two patients in the Dalt. group (4%). Angina recurrence was seen in 11 patients in the Enox. group (16%) and in 11 patients in the Dalt. group (15%). Overall, any of the events that made up the endpoint occurred in 11 (16%) and 14 (19%) patients in the Enox. and Dalt. groups, respectively (P>0.05). The time to occurrence of the first event, however, was significantly longer in the Enox. group (82.3±33.2 versus 37.6±23.4 hours, P=0.007). Thrombocytopenia and allergic reactions were not detected in any patient. Major bleeding was seen in 1 patient in the Enox. group. Minor bleeding occurred in 17 (25%) and 21 (29%) patients in the Enox. and Dalt. groups, respectively (P>0.05).Enoxaparin and dalteparin were found to be equally safe and effective for the early management of UA/NQMI, but enoxaparin appeared to delay the occurrence of MI or angina recurrence as compared to dalteparin in this setting. (Jpn Heart J 2002; 43: 433-442)

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“…A higher safety index allows even higher doses during treatment. In some prevention studies, an increased dose of LMWH was found to be more effective and safer in patients experiencing bleeding complications following UFH administration (Levine et al, 1991;FRISC Study Group, 1996;Zed et al, 1999). Similar results have been obtained from studies dealing with prevention and treatment of both arterial and venous thrombosis (Hull et al, 1991;Prandoni, 1991;Columbus Investigators, 1997;Klein et al, 1997;Hirsh, 1998).…”

Section: Lmwh's In the Prevention Of Arterial Thrombosis -Clinical Stmentioning

confidence: 75%

Heparin and its derivatives in the treatment of arterial thrombosis: a review

Dvořák¹,

Vlašín²,

Dvorakova³

et al. 2010

Vet. Med. - Czech

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Arterial occlusion due to thrombosis caused by ruptured atherosclerotic plaques (Baba et al., 1975) has been recognized as a major cause of morbidity and mortality in western populations. Thrombosis may occur in various sections of arterial circulation, peripheral arteries of the limbs, coronary arteries, brain arteries, or both major and minor vessels within the abdominal cavity. The ultimate consequence is varying degrees of organ failure, mostly of ischemic origin. Arterial thrombosis represents a continuous problem, debilitating patients and decreasing their quality of life. Moreover, along with chronic heart failure, it can significantly decrease patient life expectancy. Arterial thrombosis results in ischemia, with serious systemic consequences, such as metabolic breakdown. The major goal of treatment remains fast and efficient recanalization -surgical, interventional or thrombolytic. To be able to prevent acute reocclusion with severe consequences (rhabdomyolysis, compartment syndrome, excessive tissue necrosis leading to limb amputation, etc.), several adjunctive treatment regimens have been advocated. Among others, thrombin inhibitors and platelet inhibitors have been widely used for both prophylaxis and adjunctive treatment. Direct thrombin inhibitors and antithrombin stimulators have been recognized as typical antithrombotic drugs. Direct (antithrombin-independent) thrombin inhibitors can be divided into two main categories: monovalent, active site inhibitors (argatroban, efegatran, inovastan, melagatran) and bivalent (hirudin, hirugen, hirulog, bivalirudin), while antithrombin stimulators represent standard (unfractionated) heparin (UFH) and its depolymerizing products -low molecular weight heparins (LMWH's). Recently, a clear change in the main use of heparin, as well as low-molecular weight heparins has been advocated representing a shift from treatment and prophylaxis of deep vein thrombosis to prophylaxis of thromboembolic disease following vascular, cardiovascular or orthopedic surgery, treatment of unstable angina and prevention of acute myocardial infarction. The main effect of heparins lies in their anticoagulant activity. Heparins are involved in different pathways of the coagulation cascade with anticoagulant, antithrombotic, profibrinolytic, anti-aggregative, as well as anti-inflammatory effects. Moreover, there is a little doubt about their anti-proliferative and anti-ischemic activity (Penka and Bulikova, 2006). Unlike standard heparin, low-molecular weight heparins do not affect the patient's general coagulation profile. Obviously, the difference in molecular weight results in different pharmacokinetic and pharmacodynamic properties of the agents.Key words: coagulation; arterial thrombosis; standard heparin; low-molecular weight heparins List of abbreviations ABI = axillary/...index, t-PA = tissue-type plasminogen activator, ADP = adenosin diphosphate, AG = angiography, AMI = acute myocardial infarction, APSAC = acylated plasminogen streptokinase activator complex, APTT = acti...

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Low-Molecular-Weight Heparins in the Management of Acute Coronary Syndromes

Cited by 51 publications

References 77 publications

Inhalable Liposomes of Low Molecular Weight Heparin for the Treatment of Venous Thromboembolism

Inhalable Liposomes of Low Molecular Weight Heparin for the Treatment of Venous Thromboembolism

Head-to-Head Comparison of Two Different Low-Molecular-Weight Heparins in Acute Coronary Syndrome. A Single Center Experience.

Heparin and its derivatives in the treatment of arterial thrombosis: a review

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