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During the 1980s, results from the first large scale clinical studies on acute coronary syndrome were rapidly translated into clinical application.1 The development of effective antithrombotic medication brought a significant reduction in morbidity and mortality. However, despite the data showing that new antithrombotic agents such as low molecular weight heparins (LMWHs) offered advantages over placebo, questions remained about how these new drugs compared to each other. Continued improvements in the “standard of care” for acute coronary syndromes, as well as the economic changes in clinical research, have greatly complicated not only the design and execution of large clinical trials studying these new agents, but also the comparability.2 Subtle differences in inclusion and exclusion criteria and in definitions of end points require great caution when interpreting the results.
In spite of these difficulties, the recent clinical trials with LMWHs provide valuable information about the clinical course of unstable angina and allow us to consider this syndrome in a new light. The onset of unstable angina appears to be the precise moment of transition from stable state to non-Q wave myocardial infarction (MI) or Q wave MI. Increasingly sensitive methods of detecting myocardial necrosis, combined with ECG changes, offer the opportunity that in due course acute coronary syndromes will become divided into two groups—Q wave infarct or non-Q wave infarct—and it may mean that unstable angina as a final diagnosis becomes redundant. We describe here the design and results of the LMWH studies, and in particular the TIMI 11A and B trials, and the changes in treatment strategies evolving from these trials.
LMWHs and unstable angina
The rationale for using LMWHs in arterial thrombosis is based on their structural and chemical features. The most important of these is the small size of LMWHs in relation to unfractionated heparin (UFH). LMWHs inhibit factor Xa and …