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The papers presented here have indicated that low molecular weight heparins are efficacious and cost effective in the treatment of unstable angina and non-Q wave myocardial infarction. Amendments to the classification, ongoing risk assessment, and duration and appropriate treatment are all areas of the management of these conditions which were highlighted in this symposium as needing further research.
The classification of unstable angina based on clinical description remains valid. It is likely that further refinements and expansions to the classification will be made in the future, on the basis of the balance of five separate causal factors (thrombosis, arterial obstruction, coronary artery vasospasm or vasoconstriction, inflammation, and increased myocardial oxygen demands). Eventually, a system of aetiological classification may be expected to be added to the current system.
A variety of methods are available to identify patients at increased risk of further ischaemia. The 12 lead ECG is universally used and provides much valuable information, with ST segment depression being closely linked to a poor prognosis. Biochemical methods for risk assessment are also now well established, although not as widely used as they might be. Raised serum troponin T or troponin I concentrations indicate that an episode of ischaemia severe enough to cause myocardial cell necrosis has occurred, and such patients are at high risk of further episodes. Raised serum troponin concentrations provide no information about the cause of the ischaemia, but indicate the need for further investigations to establish the aetiology.
Measurement of C reactive protein (CRP) concentrations is both cheap and easy to perform and provides valuable prognostic information. There is a strong argument for CRP measurement in all patients with unstable angina and non-Q wave MI. A combination of inflammation (indicated by raised concentrations of CRP) and microinfarction (indicated by raised troponin T) is a very strong predictor of poor prognosis. Approximately 50% of patients in whom both CRP and troponin T are raised go on to develop acute MI.
For all biochemical tests, the timing of measurements is critical; troponin T or I may not yet have been released into the circulation in the very early stages after an ischaemic attack, and misleading results can be obtained if reliance is placed on a single early blood sample. Measuring CRP less than two days after admission may help to avoid confusing changes secondary to the index event and changes indicating an ongoing inflammatory process.
Although it is possible to identify clearly patients at high risk of further ischaemia, the most appropriate management for such patients has not yet been determined.
The follow up results from the ESSENCE trial show a reduction in the event rate at one year after short term treatment with enoxaparin. However, it is obviously not possible for treatment given during the acute phase to prevent all late events in a high risk population. The pathological process in unstable angina continues over a period of several weeks, and the optimum duration of treatment needs to be established.