International, Randomized, Controlled Trial of Lamifiban (a Platelet Glycoprotein IIb/IIIa Inhibitor), Heparin, or Both in Unstable Angina

Acute coronary syndromes (unstable angina and non-Q-wave myocardial infarction) are caused by the rupture of an atherosclerotic plaque, platelet activation, and fibrin deposition resulting in thrombosis. Aspirin and unfractionated heparin have traditionally been the treatments of choice for patients with acute coronary syndromes. Low-molecular-weight heparins offer potential advantages over unfractionated heparin, having proven equally effective for the treatment and prevention of many thromboembolic processes. Recently, a number of randomized controlled trials have been conducted to evaluate the role of low-molecular-weight heparins in the management of patients with unstable angina or non-Q-wave myocardial infarction. The purpose of this article is to review and evaluate the available literature on the use of low-molecular-weight heparins in the management of acute coronary syndromes to establish their role in therapy.

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

Zed¹,

Tisdale²,

Borzak³

1999

Unstable Angina

Ambrose

Dangas²

2000

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.

New Approaches to Diagnosis and Management of Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction

O’Rourke¹,

Hochman²,

Cohen³

et al. 2001

Recently, it has been demonstrated in multiple clinical research studies that non-Q-wave myocardial infarction shares many of the features of unstable angina pectoris and that both diseases initially are managed similarly. Important new antiplatelet drugs (glycoprotein IIb-IIIa inhibitors) and antithrombin agents (low-molecular-weight heparin) are currently recommended for patients with unstable angina pectoris/non-ST-segment elevation MI who are at high or intermediate risk on the basis of symptoms, electrocardiographic findings, and the presence or absence of serum markers (eg, troponin I, troponin T, and creatine kinase-MB). This review provides important information concerning the results of clinical studies of glycoprotein IIb-IIIa inhibitors (tirofiban hydrochloride and eptifibatide) when used with unfractionated heparin in patients with this syndrome or with low-molecular weight heparin (enoxaparin sodium) in similar patients. The Thrombolysis in Myocardial Infarction IIIB, Veterans Affairs Non-Q-Wave Infarction Studies in Hospital, and Fast Revascularization During Instability in Coronary Artery Disease II studies evaluating a conservative, ischemia-guided approach vs an early aggressive approach to such patients are presented, with a practical algorithm for treating such patients.