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

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          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 references 25

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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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              Long-lasting sport practice and lone atrial fibrillation.

              To analyse whether the proportion of patients with lone atrial fibrillation engaged in chronic sport practice was higher than that observed in the general population. The records of 1160 patients, seen at the arrhythmia outpatient clinic, were reviewed. A total of 70 patients (6%) suffered lone atrial fibrillation and were younger than 65 years. Thirty two of them had been engaged in long-term sport practice. All patients in the sport group were men as compared to only 50% in the sedentary group (P<0 x 0001). To avoid the confounding effect of sex distribution, women were excluded. Sportsmen started their episodes of atrial fibrillation at a younger age, they had a lower incidence of mild hypertension and their episodes of atrial fibrillation were predominantly vagal in contrast to the sedentary patients. The echocardiographic parameters were similar to those observed in the sedentary patients, but when compared with 20 healthy controls, they showed greater atrial and ventricular dimensions and a higher ventricular mass. The proportion of sportsmen among patients with lone atrial fibrillation is much higher than that reported in the general population of Catalonia: 63% vs 15% (P<0 x 05). Long-term vigorous exercise may predispose to atrial fibrillation. Copyright 2001 The European Society of Cardiology.

                Author and article information

                S. Karger AG
                January 2009
                22 August 2008
                : 112
                : 3
                : 234-241
                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
                151435 Cardiology 2009;112:234–241
                © 2008 S. Karger AG, Basel

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                Figures: 1, Tables: 3, References: 56, Pages: 8
                Original Research


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