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      International recommendations for electrocardiographic interpretation in athletes

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          Abstract

          Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport. A variety of mostly hereditary, structural, or electrical cardiac disorders are associated with SCD in young athletes, the majority of which can be identified or suggested by abnormalities on a resting 12-lead electrocardiogram (ECG). Whether used for diagnostic or screening purposes, physicians responsible for the cardiovascular care of athletes should be knowledgeable and competent in ECG interpretation in athletes. However, in most countries a shortage of physician expertise limits wider application of the ECG in the care of the athlete. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from distinctly abnormal findings suggestive of underlying pathology. Since the original 2010 European Society of Cardiology recommendations for ECG interpretation in athletes, ECG standards have evolved quickly over the last decade; pushed by a growing body of scientific data that both tests proposed criteria sets and establishes new evidence to guide refinements. On 26-27 February 2015, an international group of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle, Washington, to update contemporary standards for ECG interpretation in athletes. The objective of the meeting was to define and revise ECG interpretation standards based on new and emerging research and to develop a clear guide to the proper evaluation of ECG abnormalities in athletes. This statement represents an international consensus for ECG interpretation in athletes and provides expert opinion-based recommendations linking specific ECG abnormalities and the secondary evaluation for conditions associated with SCD.

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          Most cited references83

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          Etiology of Sudden Death in Sports: Insights From a United Kingdom Regional Registry.

          Accurate knowledge of causes of sudden cardiac death (SCD) in athletes and its precipitating factors is necessary to establish preventative strategies.
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            Long-term outcome associated with early repolarization on electrocardiography.

            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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              Incidence of sudden cardiac death in National Collegiate Athletic Association athletes.

              The true incidence of sudden cardiac death (SCD) in US athletes is unknown. Current estimates are based largely on case identification through public media reports and estimated participation rates. The purpose of this study was to more precisely estimate the incidence of SCD in National Collegiate Athletic Association (NCAA) student-athletes and assess the accuracy of traditional methods for collecting data on SCD. From January 2004 through December 2008, all cases of sudden death in NCAA student-athletes were identified by use of an NCAA database, weekly systematic search of public media reports, and catastrophic insurance claims. During the 5-year period, there were 273 deaths and a total of 1 969 663 athlete participant-years. Of these 273 deaths, 187 (68%) were due to nonmedical or traumatic causes, 80 (29%) to medical causes, and 6 (2%) to unknown causes. Cardiovascular-related sudden death was the leading cause of death in 45 (56%) of 80 medical cases, and represented 75% of sudden deaths during exertion. The incidence of SCD was 1:43 770 participants per year. Among NCAA Division I male basketball players, the rate of SCD was 1:3100 per year. Thirty-nine (87%) of the 45 cardiac cases were identified in the NCAA database, only 25 (56%) by use of public media reports, and 9 (20%) from catastrophic claims data. SCD is the leading medical cause of death and death during exercise in NCAA student-athletes. Current methods of data collection underestimate the risk of SCD. Accurate assessment of SCD incidence is necessary to shape appropriate health policy decisions and develop effective strategies for prevention.
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                Author and article information

                Journal
                European Heart Journal
                Oxford University Press (OUP)
                0195-668X
                1522-9645
                February 20 2017
                February 20 2017
                :
                :
                Article
                10.1093/eurheartj/ehw631
                28329355
                653297d0-6428-4d65-8a8b-d6e7c666e5f7
                © 2017
                History

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