2018
DOI: 10.1016/j.jcmg.2017.09.016
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Myocardial Fibrosis in Competitive Triathletes Detected by Contrast-Enhanced CMR Correlates With Exercise-Induced Hypertension and Competition History

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Cited by 138 publications
(120 citation statements)
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“…Cardiopulmonary exercise testing was performed 3 hours after the baseline CMR to objectify the exercise capacity of the triathletes as previously described. 13 Study exclusion criteria were contraindications for CMR or any systemic disease. None of the triathletes had cardiovascular diseases and all reported no intake of any cardiac or illicit medication.…”
Section: Triathletes and Controlsmentioning
confidence: 99%
“…Cardiopulmonary exercise testing was performed 3 hours after the baseline CMR to objectify the exercise capacity of the triathletes as previously described. 13 Study exclusion criteria were contraindications for CMR or any systemic disease. None of the triathletes had cardiovascular diseases and all reported no intake of any cardiac or illicit medication.…”
Section: Triathletes and Controlsmentioning
confidence: 99%
“…Only few and smaller CMR studies have been done in other patients populations known to develop heart failure. But LGE patterns have been described in patients with uraemia (of whom some also had DM) (21,22), hypertensive cardiomyopathy(23), aortic stenosis(23), atrial brillation (24) and exercise-induced hypertrophy (25). I all studies no typical pattern was found.…”
Section: Discussionmentioning
confidence: 99%
“…47 Taken together, E Tahir and colleagues have to be congratulated for addressing an underestimated entity for the physiological as well as pathological adaptation of the myocardium during exercise, the role of arterial exercise hypertension, although it remains unclear whether the data of three publications are partly overlapping. [1][2][3] Moreover, from a methodological point of view an observational study such as the present one could go further by adding multivariate analyses or, in the case of quantitative data, respectively adjusted regression analyses. Thus, it remains unclear to what extent the conclusions of Tahir et al are limited by obvious differences in baseline parameters (seven years of age and a body mass index of 1.7 kg/m 2 ) between the subjects with and without CMR evidence of cardiac fibrosis as well as hidden differences, for example, the years in competitive endurance performance, which have not been reported.…”
mentioning
confidence: 99%
“…[10][11][12] Explanations for the prevalence of myocardial lesions particularly in male athletes are diverse and include genetic predisposition, gender (females are less affected), risk factors for coronary artery disease and coronary ischaemia itself, acute or reactivated myocarditis, pulmonary artery pressure overload and exercise-induced repetitive micro-injury during prolonged exercise stress. 13,14 However, most importantly the series of data 1,3 adds another potential risk factor to the currently discussed ones, the role of exercise blood pressure on myocardial remodelling and determinant for myocardial injury. The current study has revealed that those athletes with positive LGE had a significantly higher maximal exercise blood pressure (30 mmHg higher compared with LGE negative athletes) at similar maximal exercise capacities between groups.…”
mentioning
confidence: 99%
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