Of note, these scores and others have been designed to predict different types of events over different time periods following an acute coronary syndrome (ACS). The TIMI Risk Score for UA-NSTEMI and the GRACE Risk Score are two assessment tools that integrate both clinical and biomarker data. Elevations in various cardiac biomarkers have now been proven useful in identifying high-risk populations. Demographic and historical features, as well as information collected during the initial evaluation, including physical examination findings and electrocardiographic changes, have been used in simple risk stratification schema. Therefore, risk stratification is an integral part of clinical decision making and may guide the use of more aggressive therapy in those who are likely to derive the greatest benefit.ĭata from observational studies and clinical trials have documented the prognostic usefulness of individual factors for risk stratification. However, many of these treatment options are associated with bleeding, which in turn has been associated with significant morbidity and mortality. Clinical trials have demonstrated the efficacy of multiple pharmacologic agents, including aspirin, adenosine diphosphate (ADP) receptor blockers, glycoprotein (GP) IIb/IIIa inhibitors, unfractionated heparin, low-molecular-weight heparin (LMWH), and direct thrombin inhibitors, as well as an early invasive strategy of management. Such information is important to the patient and family and also allows for more effective triage and allocation of clinical resources. Risk stratification, aimed at providing a more accurate estimate of a patient’s prognosis, is pivotal in the clinical management of patients with UA-NSTEMI. This higher risk has been associated with the increased age and burden of other diseases in patients with UA and NSTEMI. In contrast, long-term risk of death or cardiovascular complications is higher in patients with UA or NSTEMI than in patients with STEMI. Short-term mortality is lower in patients with UA (1.7% at 30 days) as compared with those with NSTEMI or ST-segment elevation myocardial infarction (STEMI 5.1% at 30 days for each). Nonetheless, among patients presenting with UA-NSTEMI, there is substantial heterogeneity in the risk of death and major cardiac ischemic events over time. Thus, treatments for UA and NSTEMI are identical and consist of a combination of anti-ischemic and antithrombotic therapies, and potentially coronary revascularization. Both entities typically share a common pathobiologic basis, development of a severe but nonocclusive coronary artery thrombus superimposed on a recently disrupted vulnerable plaque. If these symptoms are accompanied by release of cardiac biomarkers of necrosis (e.g., creatine kinase MB or cardiac-specific troponin) then the diagnosis of non–ST-segment elevation myocardial infarction (NSTEMI) is made. Unstable angina (UA) is classically defined as ischemic discomfort that occurs at rest (or with minimal exertion), occurs with a crescendo pattern, or is severe and of new onset.
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