Miocardiopatía del atleta

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Abstract

La práctica de los deportes de alto nivel es cada vez más común. En el presente trabajo se revisa una serie de conceptos sobre la muerte súbita en atletas y cómo se puede incluir el concepto de "miocardiopatía del atleta" en el conocimiento disponible hasta la fecha. La prevalencia de muerte súbita en atletas es mayor que en la población general (1.5:100,000 contra 0.2:100,000 respectivamente). Esta diferencia puede ser secundaria a ciertos cambios miocárdicos derivados del ejercicio de resistencia. Consistentemente se han estado describiendo cambios anatómicos y funcionales de predominio ventricular derecho que semejan a una displasia arritmogénica, lo que da lugar a la hipótesis de que el ejercicio de resistencia de alto nivel puede inducir una forma de miocardiopatía que explica un cierto número de casos de muerte súbita en atletas. Los profesionales de la salud deben conocer esta posibilidad de riesgo en atletas entrenados, al tiempo que deben estimular la realización de ejercicio moderado regular como una práctica saludable en la población general.

Translated abstract

High performance sports practice is more common every day. In the present work we evaluate several concepts regarding sudden death among athletes and the recently described "Athlete's cardiomyopathy". The prevalence of sudden death among athletes is higher than among the general population (1.5:100,000 versus 0.2:100,000 respectively). This difference can be related to myocardial changes derived from endurance exercise. There are consistent descriptions of anatomical and functional changes, more specific to the right ventricle that simulate an arrhythmogenic right ventricular dysplasia/cardiomyopathy. This can originate the hypothesis that such a cardiomyopathy can explain a certain number of sudden deaths among athletes. As healthcare professionals we have to be aware of this possibility among trained athletes, although we must continue to encourage moderate physical activity as a healthy behaviour among the general population.

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Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006.

D Kathryn Tierney, Joseph J Doerer, C Haas … (2009)

Sudden deaths in young competitive athletes are highly visible events with substantial impact on the physician and lay communities. However, the magnitude of this public health issue has become a source of controversy. To estimate the absolute number of sudden deaths in US competitive athletes, we have assembled a large registry over a 27-year period using systematic identification and tracking strategies. A total of 1866 athletes who died suddenly (or survived cardiac arrest), 19+/-6 years of age, were identified throughout the United States from 1980 to 2006 in 38 diverse sports. Reports were less common during 1980 to 1993 (576 [31%]) than during 1994 to 2006 (1290 [69%], P<0.001) and increased at a rate of 6% per year. Sudden deaths were predominantly due to cardiovascular disease (1049 [56%]), but causes also included blunt trauma that caused structural damage (416 [22%]), commotio cordis (65 [3%]), and heat stroke (46 [2%]). Among the 1049 cardiovascular deaths, the highest number of events in a single year was 76 (2005 and 2006), with an average of 66 deaths per year (range 50 to 76) over the last 6 years; 29% occurred in blacks, 54% in high school students, and 82% with physical exertion during competition/training, whereas only 11% occurred in females (although this increased with time; P=0.023). The most common cardiovascular causes were hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%). In this national registry, the absolute number of cardiovascular sudden deaths in young US athletes was somewhat higher than previous estimates but relatively low nevertheless, with a rate of <100 per year. These data are relevant to the current debate surrounding preparticipation screening programs with ECGs and also suggest the need for systematic and mandatory reporting of athlete sudden deaths to a national registry.

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Long-term outcome associated with early repolarization on electrocardiography.

Tuomas Kerola, H Rissanen, M. Juhani Junttila … (2009)

Early repolarization, which is characterized by an elevation of the QRS-ST junction (J point) in leads other than V(1) through V(3) on 12-lead electrocardiography, has been associated with vulnerability to ventricular fibrillation, but little is known about the prognostic significance of this pattern in the general population. We assessed the prevalence and prognostic significance of early repolarization on 12-lead electrocardiography in a community-based general population of 10,864 middle-aged subjects (mean [+/-SD] age, 44+/-8 years). The primary end point was death from cardiac causes, and secondary end points were death from any cause and death from arrhythmia during a mean follow-up of 30+/-11 years. Early repolarization was stratified according to the degree of J-point elevation (> or = 0.1 mV or > 0.2 mV) in either inferior or lateral leads. The early-repolarization pattern of 0.1 mV or more was present in 630 subjects (5.8%): 384 (3.5%) in inferior leads and 262 (2.4%) in lateral leads, with elevations in both leads in 16 subjects (0.1%). J-point elevation of at least 0.1 mV in inferior leads was associated with an increased risk of death from cardiac causes (adjusted relative risk, 1.28; 95% confidence interval [CI], 1.04 to 1.59; P=0.03); 36 subjects (0.3%) with J-point elevation of more than 0.2 mV in inferior leads had a markedly elevated risk of death from cardiac causes (adjusted relative risk, 2.98; 95% CI, 1.85 to 4.92; P<0.001) and from arrhythmia (adjusted relative risk, 2.92; 95% CI, 1.45 to 5.89; P=0.01). Other electrocardiographic risk markers, such as a prolonged QT interval corrected for heart rate (P=0.03) and left ventricular hypertrophy (P=0.004), were weaker predictors of the primary end point. An early-repolarization pattern in the inferior leads of a standard electrocardiogram is associated with an increased risk of death from cardiac causes in middle-aged subjects. 2009 Massachusetts Medical Society

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

Tomas G Neilan, James L Januzzi, Elizabeth Lee-Lewandrowski … (2006)

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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Author and article information

Journal

Journal ID (publisher-id): rmc

Title: Revista mexicana de cardiología

Abbreviated Title: Rev. Mex. Cardiol

Publisher: Asociación Nacional de Cardiólogos de México, Sociedad de Cardiología Intervencionista de México (México, DF, Mexico )

ISSN (Print): 0188-2198

Publication date (Print and electronic): June 2014

Volume: 25

Issue: 2

Pages: 109-117

Affiliations

[05] Aguascalientes Aguascalientes orgnameSociedad Cardiovascular y del Metabolismo México

[02] Tijuana Baja California Norte orgnameHospital Ángeles orgdiv1Servicio de Cardiología México

[04] Querétaro orgnameInstituto de Corazón de Querétaro México

[03] Guanajuato orgnameInstituto Mexicano del Seguro Social orgdiv1Hospital de Alta Especialidad México

[01] Querétaro Querétaro orgnameHospital Médica TEC 100 orgdiv1División de Medicina Interna México

[06] orgnameHospital Español de México orgdiv1Laboratorio de Electrofisiología Clínica

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Publisher ID: S0188-21982014000200005 Publisher ID: S0188-2198(14)02500200005

SO-VID: 4bb8c1e5-7052-43b7-ad61-a9b098ce6d88

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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

Miocardiopatía del atleta Translated title: Athlete's cardiomyopathy

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Most cited references 122

Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006.

Long-term outcome associated with early repolarization on electrocardiography.

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

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