Rapid rule out of acute myocardial infarction using undetectable levels of high-sensitivity cardiac troponin.

BACKGROUND: We examined whether undetectable levels of high-sensitivity cardiac Troponin (hs-cTn) can be used to rule out acute myocardial infarction (AMI) with a single blood draw at presentation to the emergency department (ED). METHODS AND RESULTS: In a prospective multicenter study we used 4 different hs-cTn assays (hs-cTnT Roche, and hs-cTnI Siemens, hs-cTnI Beckman Coulter and hs-cTnI Abbott) in consecutive patients presenting with acute chest pain. The final diagnosis of AMI was adjudicated by two independent cardiologists using all available data including serial hs-cTnT levels. Mean follow up was 24 months. Among 2072 consecutive patients with available hs-cTnT levels, 21% had an adjudicated diagnosis of AMI. Among AMI patients, 98.2% had initially detectable levels of hs-cTnT (sensitivity 98.2%, 95%CI 96.3%-99.2%, negative predictive value (NPV) 98.6%, 95%CI 97.0%-99.3%). Undetectable levels of hs-cTnT ruled out AMI in 26.5% of patients at presentation. The NPV was similar with the three hs-cTnI assays: among 1180 consecutive patients with available hs-cTnI (Siemens), the NPV was 98.8%; among 1151 consecutive patients with available hs-cTnI (Beckman Coulter), the NPV was 99.2%; among 1567 consecutive patients with available hs-cTnI (Abbott), the NPV was 100.0%. The percentage of patients with undetectable levels of hs-cTnI was similar among the three hs-cTnI assays and ranged from 11.4% to 13.9%. CONCLUSIONS: Undetectable levels of hs-cTn at presentation have a very high NPV and seem to allow the simple and rapid rule out of AMI. This criteria applies to much more patients with hs-TnT as compared to the investigated hs-cTnI assays.

Risk stratification in patients with unstable angina using absolute serial changes of 3 high-sensitive troponin assays.

BACKGROUND: It is unknown whether unstable angina (UA) results in previously nondetectable low-level myocardial necrosis. We compared the pattern of myocardial necrosis between patients with UA, acute myocardial infarction (AMI), and noncardiac chest pain (NCCP) using 3 high-sensitive cardiac troponin (hs-cTn) assays. METHODS: In a multicenter study, we enrolled 842 unselected patients with acute chest pain in the emergency department. Roche hs-cTnT, Beckman Coulter hs-cTnI, and Siemens hs-cTnI were determined in a blinded fashion at presentation and after 1, 2, 3, and 6 hours. The final diagnosis was adjudicated by 2 independent cardiologists. RESULTS: A change in hs-cTn of ≥2 ng/L within the first hour after presentation as assessed with Roche hs-cTnT, Beckman Coulter hs-cTnI, and Siemens hs-cTnI was observed in 26%, 31%, and 32% of patients with UA (n = 115) compared with 91%, 92%, and 96% in patients with AMI (n = 120) and 12%, 23%, and 16% in patients with NCCP (n = 415; P < .001 for all comparisons between UA and AMI, P > .05 for all comparisons between UA and NCCP). In patients with UA, such a 1-hour change in hs-cTn of ≥2 ng/L was associated with an increased risk of death or AMI during the 30-day follow-up (P = .003, .03, .03) and 2-year follow-up (P < .001, .002, and .006). CONCLUSIONS: In marked contrast to patients with AMI, most patients with UA do not exhibit relevant hs-cTn changes. The minority of UA with hs-cTn changes, however, has a significantly worse short- and long-term outcome.

Patients with acute coronary syndrome and normal high-sensitivity troponin.

BACKGROUND: Failure to identify patients with acute coronary syndrome (ACS) is a serious clinical problem. The incidence, characteristics, and outcome of ACS patients with normal high-sensitivity cardiac troponin T (hs-cTnT) levels at presentation are unknown. METHODS: In a prospective multicenter study, hs-cTnT was determined in a blinded fashion in 1181 consecutive patients presenting with acute chest pain to the emergency department. The final diagnosis of ACS was adjudicated by 2 independent cardiologists. Patients were followed for 12 months. RESULTS: ACS was the adjudicated diagnosis in 351 patients (30%), including 187 patients with acute myocardial infarction (AMI) and 164 patients with unstable angina (UA). At presentation, hs-cTnT was normal (<.014 ug/L) in 112 ACS patients (32%), including 11 patients (6%) with AMI and 101 patients (62%) with UA (P <.001). Multivariable analysis revealed previous statin treatment, younger age, preserved renal function, and the absence of ST deviation on the electrocardiogram as independently associated with normal hs-cTnT levels. Mortality rates in ACS patients with normal hs-cTnT level were 0.0% at 30 days, 0.0% at 90 days, and 2.0% (95% confidence interval, 0.5-7.9) at 360 days, which was significantly lower than in ACS patients with elevated hs-cTnT level at presentation (17.5% at 360 days, P <.001). Conversely, AMI rates at 360 days was higher in ACS patients with normal versus elevated hs-cTnT levels (P=.004). CONCLUSION: Almost one third of ACS patients have normal hs-cTnT levels at presentation, mostly patients with UA. ACS patients with normal hs-cTnT have a very low mortality, but an increased rate of AMI during the subsequent 360 days.