Acute coronary syndromes: Predictors of clinical presentation and prognosi

The severity of clinical presentation following coronary plaque disruption is an important determinant of prognosis, yet factors affecting the mode of presentation of acute coronary syndromes (ACS) are not well defined. Similarly, though those at the highest risk benefit the most from various therapeutic strategies, methods of risk stratification following ACS are of limited clinical value primarily because of the low positive predictive power of individual markers of risk. The baseline characteristics of patients presenting to 2 East London Hospitals have been analysed in order to determine factors that influence the severity of ACS. One cohort was followed up for 1 year and a model of incremental risk assessment developed. Presentation with myocardial infarction (MI) rather than unstable angina (UA) is favoured by smoking, advanced age, renal impairment and increased platelet activity all of which increase thrombogenicity. Presentation with UA is favoured by pretreatment with aspirin which reduces thrombogenicity, hypertension which increases myocardial mass and a history of previous coronary syndromes which may promote collateralisation and ischaemic preconditioning. In the context of MI smoking has complex effects, increasing the likelihood of ST elevation but also providing a substrate for successful thrombolysis which reduces the risk of Q wave development. Although not the most severe form of ACS, the incidence of non ST elevation ACS is increasing and the associated morbidity and mortality substantial. In view of this a clinically useful method of risk stratifiying patients with non ST elevation ACS has been developed. Using a cumulative approach clinical data, troponin T concentrations, ST segment monitoring and heart rate variability successfully identified a subgroup of patients whose risk of cardiac death or non-fatal Ml during the first year approached 50%. C reactive protein (CRP) concentrations were not found to be an independent predictor of risk. However, CRP was a univariate predictor of cardiac events in patients not taking aspirin prior to presentation. The mechanism of this interaction is not clear although modification of the acute phase inflammatory responses to myocardial injury may be involved as pretreatment with aspirin was protective against troponin release. In a similar manner, the effects of age, previous ACS and smoking on the severity of ACS were also mirrored in their effects on troponin release in non-ST-elevation ACS. In this same cohort of patients, pretreatment with ACE-inhibitors was also associated with both reduced incidence and magnitude of troponin release. Thus, the clinical presentation of ACS is determined by a range of factors many of which have the potential to influence the haemostatic enviroment at the time of plaque disruption. These factors may play a more important role in determining outcome than therapeutic strategies, such as aspirin and thrombolysis, given after plaque disruption. Those most at risk of subsequent events, who may therefore benefit most from interventional management, are best identified using a cumulative approach to risk stratification.