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      Long-Term Assessment of Electrocardiographic and Echocardiographic Findings in Norwegian Elite Endurance Athletes

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          Abstract

          Objectives: The long-term outcome and clinical significance of athlete’s heart has been debated and more longitudinal data are needed. We present a prospective 15 years’ follow-up study of ECG and echo findings in elite endurance athletes following the end of their competitive career. Methods: Clinical evaluation, ECG, ambulatory Holter recording and echocardiography were performed in 30 top-level endurance athletes with a mean age of 24 years with follow-up 15 years later. All had then ended their competitive career, but still performed recreational sports activities. Results: No clinical events were reported. Average resting heart rate was unchanged (53.5 ± 10 at baseline and 55.4 ± 11 at follow-up, p = n.s.), complex ventricular arrhythmias did not occur and the number of ventricular premature beats (VPBs) were 0.4 ± 0.8/h at baseline and 3.8 ± 10/h at follow-up (p = n.s.). In a subgroup of 4 subjects with >100 VPBs per hour at follow-up left ventricular mass was increased compared to the others (p < 0.03). Furthermore, regression of sino-atrial (SA) and atrioventricular (AV) blocks was shown. There were no cases of atrial flutter or fibrillation. There was a slight reduction in mean left ventricular wall thickness (9.9 ± 1.2 vs. 9.5 ± 1.4 mm, p < 0.05) and a highly significant reduction of relative wall thickness (0.38 vs. 0.35, p < 0.001). Left ventricular end-diastolic volume (68 ± 6 vs. 70 ± 7 ml ml/m<sup>2</sup>, p = n.s.) and left ventricular mass (109 ± 19 vs. 107 ± 19 g/m<sup>2</sup>, p = n.s.) were unchanged when corrected for body surface area and ejection fraction (EF) increased (60 ± 7 vs. 67 ± 6%, p < 0.01). Parameters of left ventricular diastolic function were normal both at baseline and follow-up. Conclusions: There was no evidence of deleterious cardiac effects of previous top-level endurance athletic activity at 15 years’ follow-up.

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          Most cited references25

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          Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon.

          Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction. We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler-derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, > 60% of participants had increased cTnT > 99th percentile of normal (> 0.01 ng/mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (> or = 0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P 45 miles/wk, athletes who trained < or = 35 miles/wk demonstrated increased pulmonary pressures, right ventricular dysfunction (mid strain 16+/-5% versus 25+/-4%, P<0.001), myocyte injury (cTnT 0.09 versus < 0.01 ng/mL, P<0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P<0.001). Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.
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            Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists.

            Significant brady- and tachyarrhythmias may occur in active endurance athletes. It is controversial whether these arrhythmias do persist after cessation of competitive endurance training. Among all 134 former Swiss professional cyclists [hereafter, former athletes (FAs)] participating at least once in the professional bicycle race Tour de Suisse in 1955-1975, 62 (46%) were recruited for the study. The control group consisted of 62 male golfers matched for age, weight, hypertension, and cardiac medication. All participants were screened with history, clinical and echocardiographic examination, ECG, and 24 h ECG. The time for the last bicycle race of FAs was 38 +/- 6 years. The mean age at examination was 66 +/- 6 years in controls and 66 +/- 7 years in FAs (P = 0.47). The percentage of study participants with >4 h current cardiovascular training per week was identical. QRS duration (102 +/- 20 vs. 95 +/- 13 ms, P = 0.03) and corrected QTc interval (416 +/- 27 vs. 404 +/- 18, P = 0.004) were longer in FAs. There was no significant difference in the number of isolated atrial or ventricular premature complexes, or supraventricular tachycardias in the 24 h ECG; however, ventricular tachycardias tended to occur more often in FAs than in controls (15 vs. 3%, P = 0.05). The average heart rate was lower in FAs (66 +/- 9 vs. 70 +/- 8 b.p.m.) (P = 0.004). Paroxysmal or persistent atrial fibrillation or flutter was reported more often in FAs (P = 0.028). Sinus node disease (SND), defined as bradycardia of 2.5 s (6 vs. 0%), was more common in FA (16%) than in controls (2%, P = 0.006). Observed survival of all FAs was not different from the expected. Among FAs, SND occurred significantly more often compared with age-matched controls, and there is trend towards more frequent ventricular tachycardias. Further studies have to evaluate prevention of arrhythmias with extreme endurance training, the necessity of regular follow-up of heart rhythm, and management of arrhythmias in former competitive endurance athletes.
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              Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning.

              The clinical significance and long-term consequences of left ventricular (LV) hypertrophy associated with intensive athletic conditioning remain unresolved. We prospectively evaluated 40 elite male athletes who had shown marked LV cavity enlargement of > or = 60 mm, wall thickness of > or = 13 mm, or both in a longitudinal fashion with serial echocardiograms, initially at peak training (age 24 +/- 4 years) and subsequently after a long-term deconditioning period (1 to 13 years; mean, 5.6 +/- 3.8). After detraining, LV cavity dimension decreased by 7% (61.2 +/- 2.9 to 57.2 +/- 3.1 mm; P or = 60 mm) in 9 athletes (22%); in contrast, wall thickness returned to normal in each athlete. Multiple regression analysis demonstrated that approximately 50% of the incomplete reduction in cavity dimension was explained by increased body weight and recreational physical activity performed during the follow-up period. No athlete had developed cardiac symptoms, impaired exercise performance, or evidence of LV dysfunction. LV remodeling was evident after long-term detraining, with significant reduction in cavity size and normalization of wall thickness. Resolution of cavity enlargement was, however, incomplete in most cases, and substantial chamber dilatation persisted in >20% of athletes. The possibility that this residual LV hypertrophy, apparently part of the athlete's heart syndrome, may have future long-term clinical implications in some individuals cannot be excluded with certainty.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2009
                January 2009
                22 August 2008
                : 112
                : 3
                : 234-241
                Affiliations
                aDepartment of Heart Diseases, Haukeland University Hospital, Bergen, bDepartment of Circulation and Medical Imaging, University of Science and Technology, Trondheim, cDepartment of Cardiology, Rikshospitalet University Hospital, Oslo, and dHeart and Lung Centre, Ullevaal University Hospital, Oslo, Norway; eMinneapolis Heart Institute Foundation, Minneapolis, Minn., USA
                Article
                151435 Cardiology 2009;112:234–241
                10.1159/000151435
                18719347
                d10efdb2-022a-404a-b5fb-6e6dbe366533
                © 2008 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 19 July 2007
                : 24 February 2008
                Page count
                Figures: 1, Tables: 3, References: 56, Pages: 8
                Categories
                Original Research

                General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Electrocardiography,Elite endurance athletes,Echocardiography

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