The increased risk of new cardiac events associated with elevated troponin in patients with a clinical suspicion of NSTEACS can be attributed to clinical and pathological features associated with abnormal troponin results including underlying severe coronary stenosis; culprit lesion thrombosis; downstream embolization with microinfarction; and in some patients, total coronary occlusion, a large MI, and reduced left ventricular function (Fig. 5). The subgroup of patients without troponin elevation consists partly of those
Coronary artery disease
• t prevalence of significant stenoses
■ More complex lesions
• t prevalence of intra coronary thrombi
■ Impaired coronary flow rate and tissue level perfusion
• Potential origin of ventricular arrhythmias
• At higher levels of troponin [f size)
cause of reduced left ventricular function
Fig. 5. Summary of suggested mechanisms behind prognostic value of troponin in NSTEACS.
without significant atherosclerotic coronary artery disease (CAD), whose symptoms often have noncardiac causes, and partly of patients with CAD, whose symptoms might be caused by an increase in oxygen demand or a decrease in oxygen supply unrelated to coronary thrombosis. The probability of significant coronary stenosis rises considerably at any detectable level of troponin elevation, and the likelihood of an unstable plaque with thrombus and downstream microembolization, impairment of coronary flow, and tissue-level perfusion increases (Fig. 6) (13,37). The latter mechanisms also explain why treatment with antithrombin or platelet inhibitors is protective mainly in patients with elevated troponin. Low-level increases in troponin are usually not associated with a completed infarction in the territory at risk but reflect unstable plaque and thrombus in the culprit vessel that confer a higher risk of causing further myocardial damage. In patients with higher elevations of troponin, a greater proportion will have a persistent occlusion of the culprit coronary vessel and may have completed the infarction in the jeopardized territory, leading to lower risk ofnew myocardial injury in the same territory. However, the larger infarct size is associated with reduced left ventricular function and, thus, higher mortality (13).
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