Viola Grabs1, Tobias Peres2, Otto Zelger2, Bernhard Haller3, Axel Pressler2, Siegmund Braun4, Martin Halle5, Johannes Scherr2. 1. Department of Prevention, Rehabilitation and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany. Electronic address: grabs@sport.med.tum.de. 2. Department of Prevention, Rehabilitation and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany. 3. Institute for Medical Statistics and Epidemiology, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany. 4. Institute for Laboratory Medicine, Deutsches Herzzentrum Muenchen der Technischen Universitaet Muenchen, Munich, Germany. 5. Department of Prevention, Rehabilitation and Sports Medicine, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany; DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany; Else Kröner-Fresenius-Zentrum, Klinikum rechts der Isar der Technischen Universität München, Munich, Germany.
Abstract
BACKGROUND: Vigorous exercise such as marathon running results in an increased risk of sudden cardiac death. Malignant arrhythmias seem to be the primary cause. However, continuous electrocardiographic monitoring for detection of arrhythmias during a marathon race has not been performed yet. METHODS: Twenty male marathon runners (age 45 ± 8 years) free of cardiovascular disease underwent 24-hour Holter monitoring 5 weeks before a marathon race (baseline). Subsequently, wireless Holter monitoring started immediately before the race, recorded up to 70 hours postrace. Electrocardiograms were analyzed for the presence of arrhythmias. Additionally, cardiac troponin, interleukin-6 (IL-6), and electrolytes were assessed prerace and postrace. RESULTS: At baseline Holter recordings, runners showed a median of 9 (interquartile range 3-25) atrial premature complexes (APCs) and 4 (2-16) ventricular premature complexes (VPCs) per 100,000 beats. Compared to baseline, the number of APCs decreased significantly during and 1 hour after the marathon race (0 [0-3] and 0 [0-0], all P < .001) as well as the number of VPCs during the race (0 [0-0], P = .008). No malignant arrhythmias occurred. Mean postrace levels for troponin and IL-6 were significantly augmented after the race (prerace to postrace: troponin 4 times, IL-6 17 times, all P < .001); however, no significant influence of these biomarkers or electrolytes on the prevalence of arrhythmias was observed (all P > .05). CONCLUSIONS: In this cohort of male runners free of cardiovascular disease, the prevalence of arrhythmias during and after a marathon race was decreased. Arrhythmogenic risk was independent of changes in biomarkers assessing cardiac injury, inflammation, and changes in electrolytes.
BACKGROUND: Vigorous exercise such as marathon running results in an increased risk of sudden cardiac death. Malignant arrhythmias seem to be the primary cause. However, continuous electrocardiographic monitoring for detection of arrhythmias during a marathon race has not been performed yet. METHODS: Twenty male marathon runners (age 45 ± 8 years) free of cardiovascular disease underwent 24-hour Holter monitoring 5 weeks before a marathon race (baseline). Subsequently, wireless Holter monitoring started immediately before the race, recorded up to 70 hours postrace. Electrocardiograms were analyzed for the presence of arrhythmias. Additionally, cardiac troponin, interleukin-6 (IL-6), and electrolytes were assessed prerace and postrace. RESULTS: At baseline Holter recordings, runners showed a median of 9 (interquartile range 3-25) atrial premature complexes (APCs) and 4 (2-16) ventricular premature complexes (VPCs) per 100,000 beats. Compared to baseline, the number of APCs decreased significantly during and 1 hour after the marathon race (0 [0-3] and 0 [0-0], all P < .001) as well as the number of VPCs during the race (0 [0-0], P = .008). No malignant arrhythmias occurred. Mean postrace levels for troponin and IL-6 were significantly augmented after the race (prerace to postrace: troponin 4 times, IL-6 17 times, all P < .001); however, no significant influence of these biomarkers or electrolytes on the prevalence of arrhythmias was observed (all P > .05). CONCLUSIONS: In this cohort of male runners free of cardiovascular disease, the prevalence of arrhythmias during and after a marathon race was decreased. Arrhythmogenic risk was independent of changes in biomarkers assessing cardiac injury, inflammation, and changes in electrolytes.
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