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BackgroundProlonged aerobic exercise such as marathon running produces supraphysiological hemodynamic stress that can potentially affect the athlete's cardiac homeostasis. While cardiac structural and functional adaptations in professional athletes are well characterized, only a limited information is available for recreational runners undergoing this supraphysiological stress.MethodsPremarathon and post-marathon echocardiography was performed in 50 recreational marathon runners [age 40.8 ± 7.5 years, 44 (88%) males; running distance 42.195 km]. All the runners received 4-month training for the marathon. The baseline echocardiogram and N-terminal B-type natriuretic peptide (NT-proBNP) were obtained before training, whereas the post-marathon study was performed within 10 days (7.27 ± 0.92 days) of completion of marathon. Two-dimensional speckle-tracking echocardiography was used for characterizing the changes in myocardial mechanics.ResultsThere was a significant reduction in heart rate post-marathon, whereas the levels of NT-proBNP increased significantly (86.0 ± 9.5 pg/ml vs 106.5 ± 24.2 pg/ml, p = 0.001). The left ventricular (LV) end-diastolic volume (61.8 ± 16.5 ml vs 72.8 ± 5.1 ml, p < 0.001), LV mass (120.2 ± 30.0 gm vs 160.3 ± 43.0 gm, p < 0.001), and LV ejection fraction (64.9 ± 5.6% vs 72.0 ± 5.7%, p < 0.001) also increased significantly. However, there was a significant attenuation in LV global longitudinal (−19.3 ± 2.71% vs −16.5 ± 4.6%, p = 0.003) and circumferential strain (−17.2 ± 2.41% vs −15.2 ± 2.6%, p = 0.001) post-marathon. The LV global radial strain showed a nonsignificant reduction.ConclusionRecreational marathon runners have reduced longitudinal and circumferential shortening of the left ventricle with elevation of NT-proBNP. However, the LV ejection performance remains maintained because of an increase in the LV end-diastolic volume and mass. These changes suggest the possibility of “myocardial fatigue” occurring in response to supraphysiological hemodynamic stress of marathon running.

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Background Low-flow, low-gradient severe aortic stenosis (LFLGAS) is a common clinical entity and is associated with poor prognosis. Increased left ventricular (LV) afterload is one of the mechanisms contributing to low LV stroke volume index (SVi) in these patients. Aortic stiffness is an important determinant of LV afterload, but no previous study has evaluated its relationship with LVSVi in patients with AS. Methods Fifty-seven patients (mean age 66 ± 8 years, 71.9% men) with severe AS [aortic valve area (AVA) < 1.0 cm 2 ] undergoing aortic valve replacement (AVR) were included in this study. Echocardiographic parameters of AS were correlated with carotid-femoral pulse wave velocity (cfPWV), a measure of aortic stiffness, derived using PeriScope® device. Results Mean AVA was 0.63 ± 0.17 cm 2 with mean and peak transvalvular gradient 56.5 ± 18.8 mmHg and 83.2 ± 25.2 mmHg, respectively. Nearly half (26 of 57, 45.6%) of the subjects had SVi <35 mL/m 2 , indicative of low-flow severe AS. These subjects had lower AVA, lower aortic valve gradient, and LV ejection fraction. CfPWV was numerically lower in these subjects [median 1467 (interquartile range 978, 2259) vs 1588 (1106, 2167)] but the difference was not statistically significant ( p = 0.66). However, when analyzed as a continuous variable, cfPWV had significant positive correlation with SVi (Pearson's r 0.268, p = 0.048) and mean aortic valve gradient (Pearson's r 0.274, p = 0.043). Conclusions In patients with severe AS undergoing AVR, aortic stiffness measured using cfPWV is not a determinant of low-flow state. Instead, an increasing cfPWV tends to be associated with increasing transvalvular flow and gradient in these patients.

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