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In the context of sepsis, we tested the relationship between echocardiographic findings and Troponin, and their impact on prognosis. In this prospective study, we enrolled 325 septic patients (41% with shock), not mechanically ventilated, between October, 2012 and June, 2019 among those admitted to our High-Dependency Unit. By echocardiography within 24 h from the admission, sepsis-induced myocardial dysfunction (SIMD) was defined as left ventricular (LV) systolic dysfunction (speckle-tracking-based global longitudinal peak systolic strain, GLS, >  - 14%) and/or right ventricular (RV) systolic dysfunction (Tricuspid Annular Plane Systolic Excursion, TAPSE < 16 mm). Troponin I levels were measured upon admission (T0) and after 24 h (T1); it was considered normal if > 0.1 ng/mL. Mortality was assessed at day-7 and day-28 end-points. One-hundred and forty-two patients had normal Troponin level at T0 and T1 (G1), 69 had abnormal levels at T0 or T1 (G2) and 114 showed abnormal Troponin levels at both T0 and T1 (G3). Compared to G1, patients in G3 had worse LV and RV systolic function (GLS  - 11.6 ± 3.4% vs  - 14.0 ± 3.5%, p < 0.001; TAPSE 18 ± 0.5 vs 19 ± 0.5 mm, p = 0.047) and greater day-28 (34% vs 20%, p = 0.015) mortality. In a Cox survival analysis including age, Troponin and SOFA score, mortality was predicted by the presence of SIMD (RR 3.24, 95% CI 1.72-6.11, p < 0.001) with no contribution of abnormal Troponin level. While abnormal Troponin levels were associated with SIMD diagnosed by echocardiography, only the presence of SIMD predicted the short- and medium-term mortality rate, without an independent contribution of increased Troponin levels., (© 2021. Società Italiana di Medicina Interna (SIMI).)

We evaluated the prevalence and prognostic value of left (LV) and right (RV) ventricular systolic dysfunction in the presence of overt and cryptic shock. In this prospective study, between October 2012 and June 2019, we enrolled 354 patients with sepsis, 41% with shock, among those admitted to the Emergency Department High-Dependency Unit. Patients were grouped based on the presence of shock, or by the presence of lactate levels ≥ (LAC +) or < 2 mmol/L (LAC-) evaluated within the first 24 h. By echocardiography performed within 24 h from the admission, LV systolic dysfunction was defined as global longitudinal strain (GLS) > -14%; RV systolic dysfunction as Tricuspid Annular Plane Systolic Excursion (TAPSE) < 16 mm. All-cause mortality was assessed at day-7 and day-28 follow-up. Mean values of LV GLS (-12.3 ± 3.4 vs -12.9 ± 3.8%) and TAPSE (1.8 ± 0.7 vs 1.8 ± 0.5 cm, all p = NS) were similar in patients with and in those without shock. LV GLS was significantly worse in LAC + than LAC- patients (- 11.2 ± 3.1 vs - 12.9 ± 3.7%, p = 0.001). In patients without shock, as well as in those LAC-, LV dysfunction was associated with increased day-28 mortality rate (78% vs 57% in non-survivors and survivors without shock and 74% vs 53% in non-survivors and survivors LAC-, all p < 0.01). LV (RR 2.26, 95% CI 1.37-3.74) and RV systolic dysfunction (RR 1.85, 95% CI 1.22-2.81) were associated with increased 28-day mortality rate in addition and independent to LAC + (RR 1.81, 95% CI 1.15-2.84). In conclusion, LV and RV ventricular dysfunction were independently associated with an increased mortality rate, altogether with the presence of cryptic shock.