| Literature DB >> 25883700 |
Roman Leischik1, Birgit Dworrak1, Peter Foshag1, Markus Strauss1, Norman Spelsberg1, Henning Littwitz1, Marc Horlitz1.
Abstract
Physical activity increases life expectancy and sport is a priori not harmful. Exhausted sporting activity (e.g. endurance running, triathlon, cycling or competitive sport) can lead under individual conditions to negative cardiac remodelling (pathological enlargement/function of cardiac cavities/structures) or in worst case to cardiac arrhythmias and sudden cardiac death (SCD). This individually disposition can be genetically determined or behaviourally/environmentally acquired. Overall competitive young male athletes suffer five-fold higher than non-competitive athletes from sudden death and athletes aged over 30 bear a potential for arrhythmias, atrial fibrillation or a 20-fold higher possibility for SCD as female athletes. Patients with diabetes, coronary disease, obesity or hypertension require different special managements. Screening of cardiorespiratory health for sport activities has a lot of faces. Basically there is a need for indicated examinations or possible preventive measures inside or outside of pre-competition screening. The costs of screening compared to expenditure of whole effort for sporting activities are acceptable or even negligible, but of course dependent on national/regional settings. The various causes and possibilities of screening will be discussed in this article as basic suggestion for an open discussion beyond national borders and settings.Entities:
Keywords: Athletes; Endurance sport; Physical activity; Pre-participation screening
Year: 2015 PMID: 25883700 PMCID: PMC4394910 DOI: 10.14740/jocmr2129w
Source DB: PubMed Journal: J Clin Med Res ISSN: 1918-3003
Distribution of Cardiovascular Causes of Sudden Death in Young Athletes > 12 - 35 Years and General Population of Young People 5 - 35 Years (in %)
| Marijon et al, 2011 [ | Corrado et al, 2003 [ | Solberg et al, 2010 [ | Maron et al, 2007 | Puranik et al, 2005 [ | |
|---|---|---|---|---|---|
| Aortic rupture/dissection | 2 | 1.8 | 4.3 | 2 | 5.4 |
| Aortic stenosis/cong HD | 6 | 4.3 | 5 | ||
| Arrhythmia | 29 | ||||
| ARVC | 4 | 22 | 4 | 1.6 | |
| Channelopathies (QT, WPW) | 12 | 1.8 | 8.7 | 3 | (29?) |
| Coronary artery anomalies | 11 | 3.3 | 17 | 2.1 | |
| Coronary disease | 6 | 18 | 48 | 3 | 24.5 |
| Dilatative CM | 4 | 1.8 | 2 | 5.4 | |
| Hypertrophic CM | 10 | 1.8 | 4.3 | 36 | 5.8 |
| MVP | 2 | 7.3 | 4 | ||
| Myocarditis | 4 | 9 | 22 | 6 | 11.6 |
| Possible HCM | 4 | 8 | |||
| Riva muscle bridge | 2 | 3.6 | 3 | ||
| Unclear | 36 | 1.8 | |||
| Other (endocarditis, clots, etc.) | 7.5 | ||||
| n = 50 | n = 55 | n = 22 | n = 1,435 | n = 241 |
cong HD: congenital heart disease; ARVC: arrhythmogenic right ventricular cardiomyopathy; QT: QT-syndrome (including Romano-Ward syndrome and Jervell-Lange-Nielsen syndrome); WPW: Wolff-Parkinson-White syndrome; CM: cardiomyopathy; HCM: hypertrophic cardiomyopathy; MVP: mitral valve prolapse.
Figure 1Green light: no strict recommendation [14, 21-23] for further examination (in our opinion minimum echocardiography is recommended). Yellow light: borderline changes, potentially further recommendation for evaluation. Red light: further evaluation strong recommended. RBBB: right bundle brunch block; LVH: left ventricular hypertrophy; TWI: T-wave inversion; BAs: black athletes; WAs: white athletes; LBBB: left bundle brunch block; RV: right ventricular; FU: follow-up; VES: ventricular extrasystole.
Figure 2Exercise ECG shows onset of atrial fibrillation in “healthy” athlete (A) or ventricular ectopic beats (B) during exercise (normally “healthy” athlete).
Figure 3(a, b) Left atrium (LA) follow-up 2 years of triathlete with enlargement of LA and atrial fibrillation events. (b, c) Strain curves of left ventricle during atrial fibrillation (c) and 24 h after recovery in sinus rhythm (d). (e, f) Doppler measurement of diastolic function: conventional (e) and using tissue Doppler imaging (TDI).