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In special circumstances, deviating from the recommendations with regard to competitive sports may be justified, especially for activities such as golf or bowling.

Ultimately, the decision lies with the treating specialist, who needs to consider all findings. Especially in asymptomatic relatives without any sign of subclinical disease (normal ECG and echocardiogram) with a positive genotype, a decision in favor of competitive sports may be justified (not in long QT syndrome [LQTS], catecholaminergic polymorphic ventricular tachycardia [CPVT], laminopathy [LMNA], and arrhythmogenic right ventricular cardiomyopathy [ARVC]).

In routine clinical practice, most patients are not professional athletes but children and adults who, at most, exercise to an average extent, and their quality of life is not restricted by not being able to pursue competitive sports. A relatively common exception to this rule, however, are adolescents, in whom the pertinent question concerns being allowed to play association soccer. Circumspect weighing-up of the risks and benefits, and, if required, psychological treatment, are of the utmost importance in this setting.

Since intense sports activities are a controllable, recognized risk factor, this should be communicated to persons affected by inherited cardiac arrhythmias (1).

The variable penetrance of the disorders described should not per se be used as an argument in favor of competitive sports. There are signs that in persons with the genotype who are primarily asymptomatic, competitive physical activities—especially those that entail high dynamic stress—may affect the course of their condition negatively. This is undisputed for most forms of LQTS or CPVT, and there is evidence that this may exert a negative influence on the course of structural cardiac disorders, such as ARVC, or, in the case of cardiomyopathy due to mutations in the LMNA gene. Studies have shown that intense dynamic exercise, which was stopped an average of 15 years before the disorder manifested, constitutes a predictor for an unfavorable clinical course (2, 3).

DOI: 10.3238/arztebl.2012.0236b

Dr. med. Britt-Maria Beckmann, Prof. Dr. med. Stefan Kääb

Medizinische Klinik und Poliklinik I,
Ludwig Maximilians Universität München

Stefan.kaab@med.uni-muenchen.de

Conflict of interest statement
Professor Kääb and Dr Beckmann have received third-party funding for research projects. ANR SCD Gene: 01 KU0907, M4 innovative therapeutic strategies for cardiac arrhythmias and drug safety: 01 EX 1021 E, NGFN Plus: 01 GS 0838.

1.
Maron BJ, Zipes DP: Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol 2005; 45: 1318–21. CrossRef MEDLINE
2.
Gerull B, Heuser A, Wichter T, et al.: Mutations in the desmosomal protein plakophilin-2 are common in arrhythmogenic right ventricular cardiomyopathy. Nat Genet 2004; 36: 1162–4. CrossRef MEDLINE
3.
Pasotti M, Klersy C, Pilotto A, et al.: Long-term outcome and risk stratification in dilated cardiolaminopathies. J Am Coll Cardiol 2008; 52: 1250–60. CrossRef MEDLINE
4.
Beckmann BM, Pfeufer A, Kääb S: Inherited cardiac arrhythmias:
diagnosis, treatment and prevention. Dtsch Ärztebl Int 2011; 108(37): 623–34. VOLLTEXT
1.Maron BJ, Zipes DP: Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol 2005; 45: 1318–21. CrossRef MEDLINE
2.Gerull B, Heuser A, Wichter T, et al.: Mutations in the desmosomal protein plakophilin-2 are common in arrhythmogenic right ventricular cardiomyopathy. Nat Genet 2004; 36: 1162–4. CrossRef MEDLINE
3. Pasotti M, Klersy C, Pilotto A, et al.: Long-term outcome and risk stratification in dilated cardiolaminopathies. J Am Coll Cardiol 2008; 52: 1250–60. CrossRef MEDLINE
4.Beckmann BM, Pfeufer A, Kääb S: Inherited cardiac arrhythmias:
diagnosis, treatment and prevention. Dtsch Ärztebl Int 2011; 108(37): 623–34. VOLLTEXT

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