outpatient assessment) and need for objective testing. 15-18 The use of these tools has been shown to facilitate clinical decisions (for example, hospital admission vs. Comprehensive prognostic tools that integrate patient history, signs and symptoms, electrocardiographic findings, and hs-cTn results exist 14 and are part of standard clinical assessment in hospitals in Australia, New Zealand, and some European countries. A pragmatic way out of this dilemma would be the management of patients according to their cardiac risk. The difficulty of defining UA is in part related to the fact that symptoms poorly correlate with the presence of both unstable coronary plaques and hs-cTn levels. 11 Conversely, higher hs-cTn levels are associated with high-risk atheroma features in patients clinically regarded as having stable angina. 8,9 Plaque ruptures may occur days or weeks before the onset of ischemic symptoms 10 and have been found in patients who died from non-cardiac causes. Angiographic studies have revealed thrombus or plaque ruptures in up to 17% of patients with putative stable angina. 3Īpart from the overlap between UA and NSTEMI, the assignment of patients to a diagnostic category is also complicated by an overlap existing between UA and high-risk stable angina. Controls (patients with hs-cTnT <14 ng/L, no significant coronary stenosis, and discharged without a specified diagnosis) were used as reference. 3įigure 1: Risk of Major Cardiovascular Events in Patients With Non-ST-Segment Elevation ACSĪnalyses were adjusted for admission year, hospital, age, sex, current smoking, hypertension, diabetes, previous MI, heart failure, previous stroke, ST-segment depression, estimated glomerular filtration rate, and in-hospital coronary revascularization. Notably, patients with UA have worse outcomes compared with patients without overt cardiac disease regardless of whether the diagnosis is strictly based on criteria outlined in the guidelines or on the clinical impression (Figure 1). This introduces substantial subjectivity. Given the lack of a specific biomarker criterion, the exact definition of UA remains elusive. These issues may have contributed to the fact that 60% of the patients with UA from the above-mentioned registry study had a maximum hs-cTnT level above the 99th percentile of 14 ng/L. A significant change may also be absent in late presenters with true non-ST-segment elevation MI (NSTEMI) in whom hs-cTn levels have reached a plateau phase. 7 These patients may be labelled with UA if typical symptoms are present. Chronic hs-cTn elevation is commonly found in the elderly and patients with cardiovascular comorbidities or renal failure. 6 Accordingly, patients with unstable symptoms and hs-cTn levels either below the 99th percentile or hs-cTn levels above the 99th percentile but without a significant change in serial samples (delta) could be regarded as having UA. The definition of UA in major guidelines relies on the clinical presentation together with biomarker results that do not fulfill the criteria of MI: 4,5 a cTn level above the 99th percentile together with a significant rise and/or fall. Why does UA appear to be frequently diagnosed when hs-cTn assays are available? Does this reflect the difficulties that clinicians encounter when adapting to hs-cTn results or shortcomings of current diagnostic classifications? This unexpected finding raises several questions. 3 At some of the hospitals reporting data to the registry, the incidence of UA exceeded 20%. 2 However, a Swedish registry-based cohort study recently demonstrated that 15% of 21,398 patients with non-ST-segment elevation ACS who were diagnosed with hs-cTnT were still regarded as having UA. 1 It has been expected that with the introduction of high-sensitivity (hs) cTn assays, UA would become, if not extinct, a rarity. Among US patients admitted in 2003 with non-ST-segment elevation ACS, the incidence of UA was 42% that percentage has decreased considerably since then. The clinical manifestations of acute coronary syndrome (ACS) include myocardial infarction (MI) with and without ST-segment elevation and unstable angina (UA), the latter traditionally regarded as an entity without elevated cardiac troponin (cTn) levels.
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