Background: Cardiac troponin T (cTnT) and cTnI are considered cardiac-specific and equivalent in the diagnosis of acute myocardial infarction. Previous studies suggested rare skeletal myopathies as a non-cardiac source of cTnT. We aimed to confirm the reliability/cardiac specificity of cTnT in patients with various skeletal muscle disorders (SMD). Methods: We prospectively enrolled patients presenting with muscular complaints (≥2 weeks) for elective evaluation in four hospitals in two countries. After cardiac work-up, patients were adjudicated into three predefined cardiac disease categories. Concentrations of cTnT/I and resulting cTnT/I mismatches were assessed using high-sensitivity cTnT (hs-cTnT-Elecsys) and three hs-cTnI assays (hs-cTnI-Architect, hs-cTnI-Access, hs-cTnI-Vista), and compared to controls without SMD presenting with adjudicated non-cardiac chest pain to the emergency department (n=3508, mean age 55y, 37% female). In patients with available skeletal muscle biopsies, TNNT/I1-3 mRNA differential gene expression was compared to biopsies obtained in controls without SMD. Results: Among 211 patients (mean age 57y, 42% female), 108 (51%) were adjudicated to having no cardiac disease, 44 (21%) mild and 59 (28%) severe cardiac disease. hs-cTnT/I concentrations significantly increased from patients with no versus mild versus severe cardiac disease for all assays (all p<0.001). hs-cTnT-Elecsys concentrations were significantly higher in patients with SMD versus controls (median 16ng/L (IQR 7-32.5) versus 5ng/L (IQR 3-9), p<0.001) while hs-cTnI concentrations were mostly similar (hs-cTnI-Architect 2.5ng/L (IQR 1.2-6.2) versus 2.9ng/L (IQR 1.8-5.0), hs-cTnI-Access 3.3ng/L (IQR 2.4-6.1) versus 2.7ng/L (IQR 1.6-5.0) and hs-cTnI-Vista 7.4ng/L (IQR 5.2-13.4) versus 7.5ng/L (IQR 6-10)). hs-cTnT-Elecsys concentrations were above the upper-limit of normal (ULN) in 55% of patients with SMD vs 13% of controls (p<0.01). mRNA analyses in skeletal muscle biopsies (n=33), mostly (n=24) from non-inflammatory myopathy and myositis, showed 8-fold upregulation of TNNT2, encoding cTnT (but none for TNNI3, encoding cTnI); versus controls (n=16, pWald <0.001), the expression correlated with pathological disease activity (R=0.59, pt-statistic <0.001) and circulating hs-cTnT concentrations (R=0.26, pt-statistic =0.031). Conclusions: In patients with active chronic SMD, elevations in cTnT concentrations are common and not due to cardiac disease in the majority. This was not observed for cTnI, and may in part be explained by re-expression of cTnT in skeletal muscle.

Background  Perioperative myocardial infarction/injury (PMI) diagnosed by high-sensitivity troponin (hs-cTn) T is frequent and a prognostically important complication of non-cardiac surgery. We aimed to evaluate the incidence and outcome of PMI diagnosed using hs-cTnI, and compare it to PMI diagnosed using hs-cTnT. Methods We prospectively included 2455 patients at high cardiovascular risk undergoing 3111 non-cardiac surgeries, for whom hs-cTnI and hs-cTnT concentrations were measured before surgery and on postoperative days 1 and 2. PMI was defined as a composite of perioperative myocardial infarction (PMIInfarct) and perioperative myocardial injury (PMIInjury), according to the Fourth Universal Definition of Myocardial Infarction. All-cause mortality was the primary endpoint. Results Using hs-cTnI, the incidence of overall PMI was 9% (95% confidence interval [CI] 8–10%), including PMIInfarct 2.6% (95% CI 2.0–3.2) and PMIInjury 6.1% (95% CI 5.3–6.9%), which was lower versus using hs-cTnT: overall PMI 15% (95% CI 14–16%), PMIInfarct 3.7% (95% CI 3.0–4.4) and PMIInjury 11.3% (95% CI 10.2–12.4%). All-cause mortality occurred in 52 (2%) patients within 30 days and 217 (9%) within 1 year. Using hs-cTnI, both PMIInfarct and PMIInjury were independent predictors of 30-day all-cause mortality (adjusted hazard ratio [aHR] 2.5 [95% CI 1.1–6.0], and aHR 2.8 [95% CI 1.4–5.5], respectively) and, 1-year all-cause mortality (aHR 2.0 [95% CI 1.2–3.3], and aHR 1.8 [95% CI 1.2–2.7], respectively). Overall, the prognostic impact of PMI diagnosed by hs-cTnI was comparable to the prognostic impact of PMI using hs-cTnT. Conclusions Using hs-cTnI, PMI is less common versus using hs-cTnT. Using hs-cTnI, both PMIInfarct and PMIInjury remain independent predictors of 30-day and 1-year mortality. Graphic abstract

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IMPORTANCEIn contrast to type 1 myocardial infarction (T1MI) caused by atherothrombosis, characteristics and outcomes of type 2 myocardial infarction (T2MI) caused by supply-demand mismatch are incompletely understood.OBJECTIVE To explore the characteristics and outcomes of patients with T2MI compared with those with T1MI. DESIGN, SETTING, AND PARTICIPANTSIn a prospective, international, multicenter cohort study including 12 emergency departments (EDs) in 5 European countries, unselected patients presenting with acute chest discomfort were enrolled from April 2006 to April 2018. Follow-up was done by telephone or in written form 3, 12, and 24 months after hospital discharge. Data were analyzed from April 2006 to April 2020. INTERVENTIONSThe final diagnoses of T2MI and T1MI were centrally adjudicated according to the Fourth Universal Definition of Myocardial Infarction by 2 independent cardiologists, including the pathophysiological trigger of T2MI.MAIN OUTCOMES AND MEASURES Patient characteristics and outcomes, including 2-year all-cause and cardiovascular mortality and future T2MI and T1MI events. RESULTSOf 6253 included patients, 2078 (33.2%) were women, and the median (IQR) age was 61 (48-74) years. Among 6253 patients with acute chest discomfort, the final adjudicated diagnosis was T2MI in 251 patients (4.0%), with tachyarrhythmia and hypertension responsible for two-thirds of cases, and T1MI in 1027 patients (16.4%). All-cause and cardiovascular mortality were comparable at 2 years (T2MI: adjusted hazard ratio, 1.0; 95% CI, 0.7-1.5; T1MI: adjusted hazard ratio, 0.7; 95% CI, 0.4-1.1). Patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI was more likely among patients with index T2MI compared with patients with index T1MI (hazard ratio, 3.2; 95% CI, 1.4-7.5). Similarly, future T1MI was more likely to occur among patients with index T1MI (hazard ratio, 3.0; 95% CI, 1.2-7.4).CONCLUSIONS AND RELEVANCE Among patients with T2MI, tachyarrhythmia and hypertension were responsible for more than two-thirds of T2MI cases. While T2MI and T1MI had comparable all-cause and cardiovascular mortality at 2 years, patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI occurred 3-fold more frequently among patients with T2MI vs T1MI as the index event. Improved understanding of the specifics of patients with T2MI should help improve management strategies.