Infection and type 2 myocardial infarction: A large observational study from emergency department.

Abstract

Troponin elevation is frequent in patients with acute infection (AI) admitted to emergency unit (EU). Acute infection (AI) has been suggested as a common trigger in type 2 myocardial infarction (T2MI), corresponding to a myocardial oxygen supply-demand mismatch without atherothrombosis. We aim to characterize risk factors of T2MI occurrence and in-hospital mortality among patients admitted to an EU with AI and elevated troponin. Among the medical records of all the patients admitted from January 2014 to December 2016 in a university hospital EU ( n = 82,543), patients with a diagnosis of AI and elevated troponin Ic (≥ 0.10 μg/L)( n = 714) were systematically adjudicated as T2MI in the presence of symptoms or signs of myocardial ischemia (typical chest pain and/or ECG changes). Among the 714 patients included (aged 85, 50% male), 185 (26%) were classified as T2MI, of whom infection site was pulmonary tract ( n = 111), urinary tract ( n = 27), skin ( n = 15), digestive tract ( n = 9) or other or indefinite site ( n = 23). By multivariate analysis, a history of chronic obstructive pulmonary disease (COPD) [OR (95% CI): 0.53 (0.30–0.96)], high temperature [OR: 0.86 (0.74-0.99) per °C] and elevated creatinine (0R 0.998 (0.996–1.000) per μmol/L) were associated with a lower risk of T2MI, whereas age, site of infection, C-reactive protein and troponin rates were not predictors of T2MI. Death rate was similar among patients with or without T2MI (21 vs. 23%, P = 0.6). In contrast, age, troponine, creatinine or C-reactive protein elevations were independent co-variates associated with mortality. Our large real-life study shows that in patients admitted to an EU with AI and troponin elevation, T2MI is a common feature, in the absence of temperature elevation, renal insufficiency or history of COPD. In such patients, inflammatory and cardiac biomarkers levels were independently associated with early mortality.