Exercise-induced troponin I elevation is associated with alterations in regional longitudinal strain

Abstract

Abstract Background Mechanisms of exercise-induced troponin elevation in healthy individuals are unclear. This study aimed to determine if exercise-induced cardiac troponin elevation (cTn) is associated with alterations in the myocardial response to physical stress. Methods This study assessed regional and global myocardial function by strain echocardiography at rest and following exercise of increasing workloads in individuals with either a high- or a normal cTnI response to exercise. High-cTnI responders (n=34) were individuals with a previous exercise-induced cTnI level above the 92.5% limit (cTnI > 200 ng/L) in the NEEDED population (n= 1002). Normal-cTnI responders comprised 25 reference individuals with a post-exercise cTnI < 200 ng/L. All study participants were healthy individuals with normal CT coronary angiography. The first exercise was a cardiopulmonary exercise test (CPET) of 43 (40,45) minutes. The second exercise was a 91 km recreational mountain bike race of 230 (210, 245) minutes. Myocardial function was assessed by echocardiography before and within 10 minutes and 24 hours after both exercises. Results Study individuals were 51±10 years old, and 46 (74 %) were male. At baseline, there were no differences between the High- and Normal-cTnI responders regarding demographics, training condition, cardiac risk factors, peak oxygen consumption and conventional echocardiographic parameters. Maximal cTnI levels 3 hours after exercise were significantly higher in the High- compared with Normal-cTnI responders: CPET: cTnI 13 (9-32) vs 9 (5-17) ng/L (p 0.027) and Race: cTnI: 101 (76-198) vs 37 (25-69) ng/L (p <0.001). Following exercise, there were no differences in global ventricular function between the two groups, assessed as left ventricular (LV) global longitudinal strain (GLS) and right ventricular (RV) GLS. When comparing regional longitudinal strain between the two groups, High-cTnI responders had significantly lower regional strain values in the anteroseptal segments following both exercises (p-values 0.005-0.041, 8-14% relative difference, Figure 1 and 2). The changes were more profound after the most intensive exercise (the Race). Conclusion High-cTnI responders have larger reductions in post-exercise systolic longitudinal strain in anteroseptal segments than Normal -cTnI responders. The reduction in regional strain was most profound following the highest workload (the Race). These findings suggest that highly elevated exercise-induced cTnI levels may reflect vulnerable regional alterations in the myocardial response to increasing workloads.Figure 1CPETFigure 2Race