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The relationship between exercise-induced troponin elevation and non-obstructive coronary artery disease (CAD) is unclear. This observational study assessed non-obstructive CAD's impact on exercise-induced cardiac Troponin I (cTnI) elevation in middle-aged recreational athletes. cTnI levels of 40 well-trained recreational athletes (73% males, 50 ± 9 years old) were assessed by a high-sensitive cTnI assay 24 h before, and at 3 and 24 h following two high-intensity exercises of different durations; a cardiopulmonary exercise test (CPET), and a 91-km mountain bike race. Workload was measured with power meters. Coronary computed tomography angiography was used to determine the presence or absence of non-obstructive (<50% obstruction) CAD. A total of 15 individuals had non-obstructive CAD (Atherosclerotic group), whereas 25 had no atherosclerosis (normal). There were higher post-exercise cTnI levels following the race compared with CPET, both at 3 h (77.0 (35.3-112.4) ng/L vs. 11.6 (6.4-22.5) ng/L, p < 0.001) and at 24 h (14.7 (6.7-16.3) vs. 5.0 (2.6-8.9) ng/L, p < 0.001). Absolute cTnI values did not differ among groups. Still, the association of cTnI response to power output was significantly stronger in the CAD versus Normal group both at 3 h post-exercise (Rho = 0.80, p < 0.001 vs. Rho = -0.20, p = 0.33) and 24-h post-exercise (Rho = 0.87, p < 0.001 vs. Rho = -0.13, p = 0.55). Exercise-induced cTnI elevation was strongly correlated with exercise workload in middle-aged athletes with non-obstructive CAD but not in individuals without CAD. This finding suggests that CAD influences the relationship between exercise workload and the cTnI response even without coronary artery obstruction., (© 2024 The Author(s). Scandinavian Journal of Medicine & Science In Sports published by John Wiley & Sons Ltd.)

Background: Recent cross-sectional studies have suggested a dose-dependent relationship between lifelong exposure to physical activity and the burden of calcified coronary artery disease (CAD). No longitudinal studies have addressed this concern., Hypothesis: Exercise volume is associated with progression of coronary artery calcium (CAC), defined as ≥10 units increase in CAC score., Methods: Sixty-one recreational athletes who were assessed by coronary computed tomography angiography (CCTA) as part of the NEEDED 2013/14 study were re-assessed 4-5 years later, in 2018., Results: Subjects were 45.9 ± 9.6 years old at inclusion, and 46 (74%) were male. Between 2013 and 2018, the participants reported median 5 (range: 0-20, 25th-75th percentile: 4-6) hours of high-intensity exercise per week. None of the included subjects smoked during follow-up. At inclusion, 21 (33%) participants had coronary artery calcifications. On follow-up CCTA in 2018, 15 (25%) subjects had progressive coronary calcification (≥10 Agatston units increase in CAC). These subjects were older (53 ± 9 vs 44 ± 9 years old, P = .002) and had higher levels of low-density lipoprotein at baseline (3.5 (2.9-4.3) vs 2.9 (2.3-3.5) mmol/L, P = .031) as compared to subjects with stable condition. No relationship was found between hours of endurance training per week and progression of coronary artery calcification. In multiple regression analysis, age and baseline CAC were the only significant predictors of progressive CAC., Conclusion: No relationship between exercise training volume and the progression of coronary artery calcification was found in this longitudinal study of middle-aged recreational athletes., (© 2020 The Authors. Scandinavian Journal of Medicine & Science In Sports published by John Wiley & Sons Ltd.)

Background Copeptin concentrations increase both during acute coronary syndrome and following physical exercise. The relationship between copeptin increase following physical exercise and coronary artery disease (CAD) is uncertain. The aim of this study was to 1) describe the copeptin response following strenuous physical exercise, and 2) investigate the determinants of exercise induced copeptin concentrations, particularly in relation to cardiac biomarkers and CAD. Methods Serum samples were collected from 97 recreational cyclists 24 h before, and immediately, 3 and 24 h after a 91-km bike race. Three subjects were subsequently diagnosed with significant asymptomatic CAD. Delta copeptin concentrations were correlated to patient characteristics and to biomarker concentrations. Results Participants were 42.8 ± 9.6 years, and 76.3% were male. Copeptin concentrations increased to maximal levels immediately after the race and were normalized in > 90% after 3 h. A total of 53% and 39% exceeded the 95th and 99th percentile of the assay (10 and 19 pmol/L) respectively. In multivariate models, race time, serum sodium, creatinine and cortisol were significant predictors of copeptin levels. There was no correlation between changes in copeptin and changes in cardiac biomarkers (hs-cTnI, hs-cTnT and BNP). Copeptin concentrations were normal in the subjects with asymptomatic CAD. Conclusions The moderate, short-term, exercise induced copeptin increase observed in the present study was not related to hs-cTn or BNP levels. Copeptin was normal in three asymptomatic recreational athletes with significant CAD. [ABSTRACT FROM AUTHOR]

Introduction: Early rule out of NSTEMI is essential in patients presenting with chest pain. Hypothesis: A novel ultra-sensitive (us) troponin (cTn) assay might have higher diagnostic accuracy compared to high sensitive (hs) cTnT and cTnI assays for early identification of NSTEMI in unselected patients presenting with acute chest pain. Methods: 979 patients admitted to Haukeland University Hospital (Norway) with suspected NSTE-ACS were consecutively included from September 2015 to February 2017. The final diagnosis was adjudicated by two independent cardiologists based on all available clinical, laboratory (i.e. hs-cTnT (Roche Diagnostics)) and imaging data. The samples taken at admission were biobanked and later on also measured for hs-cTnI (Abbott Diagnostics) and a novel ultra sensitive cTnI assay (Singulex Inc. (Sgx)). The following cut off values (i.e. baseline samples taken at admission) was tested for safe rule out of NSTEMI: < 2 ng/L (us-cTnIsgx), < 2 ng/L (hs-cTnIAbbott) and < 5 ng/L (hs-cTnT). The negative predictive value (NPV) for NSTEMI using these cut off values, and the AUC-ROC (Delong test) were compared between the us-cTnIsgx, hs-cTnIAbbott and hs-cTnT assays. Results: The prevalence of NSTEMI was 13%, unstable angina pectoris 11%, non-ACS cardiac disease 8%, non-cardiac chest pain 58% and other diseases 10%. Cardiac troponins were measurable in the baseline sample for 99.9% (us-cTnIsgx), 87% (hs-cTnIAbbott) and 70% (hs-cTnT) of the total cohort, respectively. When we applied the cut off values for rule out as stated above were 0.8% (us-cTnIsgx), 2.3% (hs-cTnIAbbott) and 1.5% (hs-cTnT) of NSTEMI patients incorrectly ruled out. The same cut off values would correctly rule out 51% (us-cTnIsgx), 33% (hs-cTnIAbbott) and 43% (hs-cTnT) of patients with non-cardiac chest pain. The NPV for NSTEMI were 99.7% (us-cTnIsgx), 98.6% (hs-cTnIAbbott) and 99.3% (hs-cTnT). The ROC-AUCs for baseline samples were significantly higher (p value < 0.01) for us-cTnIsgx (AUC 0.95) compared to hs-cTnIAbbott (AUC 0.93) and hs-cTnT (AUC 0.91). Conclusion: The us-cTnIsgx assay showed significant higher diagnostic performance for early rule out of NSTEMI, compared to two commonly used high sensitive troponin assays. [ABSTRACT FROM AUTHOR]