ABC | Volume 112, Nº3, March 2019

Original Article Castro et al Troponin I after acute coronary syndrome Arq Bras Cardiol. 2019; 112(3):230-237 Figure 1 – Kaplan-Meier curve for all-cause mortality according to hs-cTnI tertile measured 25 to 90 days after acute coronary syndrome. 1.0 0.8 0.6 0.4 0.2 0.0 0 500 1000 1500 2000 2500 Time (days) Probability of survival p < 0.001 by the Log-rank test 1st tertile 2nd tertile 3rd tertile 1st tertile 179 173 162 109 33 3 2nd tertile 171 157 147 98 39 5 3rd tertile 175 149 131 90 43 5 Numbers at risk elevated levels of circulating cardiac troponins are general markers of higher risk for death in different populations, independently of age and comorbidities. Some aspects of our study should be highlighted. First, it was conducted at a community-based hospital with no in-house cardiology staff; this type of medical care is received by many ACS patients in Brazil, but few prognostic studies have been published in this setting. Second, our sample size and long-term follow-up make this one of the largest studies with prognostic biomarkers in ACS patients in Brazil. In addition, because we searched for the death records of all patients who could not be contacted during follow-up, our analysis of all-cause mortality was not significantly affected by selection bias. This study has some limitations. As in all single-center studies, outcomes in both groups could have been influenced by local practices. Since coronary interventions were not performed on-site, data regarding type of revascularization (if any) were not accessible for most patients and could not be accounted for in our Cox model. We also did not have data about the proportion of patients presenting with STEMI who received reperfusion therapy. Additionally, adherence to guideline recommended therapies for ACS was suboptimal in our cohort. Lastly, even though we used standardized assays to measure all troponin levels in the subacute phase of ACS, these were not the same assays used on admission of these patients to the hospital; this precluded further analyses of evolutive trends in hs-cTnI levels through time. Despite these limitations, our findings could demonstrate an association between elevated levels of hs-cTnI and worse outcomes in this highly admixed population. Conclusions Elevated levels of hs-cTnI in the stabilized phase after an ACS event are associated with higher all-cause and cardiovascular mortality that is independent from comorbidities, renal function and left ventricular ejection fraction. These findings may potentially enhance risk stratification of post-ACS patients in the ambulatory setting. Author contributions Conception and design of the research: Castro LT, Bittencourt MS, Lotufo PA, Bensenor IM; acquisition of data: Castro LT, Santos IS, Goulart AC, Lotufo PA, Bensenor IM; analysis and interpretation of the data: Castro LT, Santos IS, Goulart AC, Pereira AC, Staniak HL, Bittencourt MS, Bensenor IM; statistical analysis: Castro LT, Santos IS, Goulart AC, Bittencourt MS, Bensenor IM; writing of the manuscript: Castro LT, critical 234