Electrocardiographic Interpretation in Athlete Screening
Electrocardiographic Interpretation in Athlete Screening
The correct differentiation of physiological adaptation owing to sustained and intensive exercise from an inherited or congenital cardiac pathology is paramount in order to correctly identify athletes at risk of SCD. The key finding from the current study is that the prevalence of an abnormal ECG was significantly reduced to 5.3% when using the 2014 Refined Criteria compared with the 2013 Seattle Criteria (11.6%) and the 2010 ESC recommendations (22.3%), respectively, while all three ECG interpretation criteria proved 100% sensitive, identifying all cases of serious cardiac pathology.
Our results demonstrate that when using the 2010 ESC recommendations, almost one in five Arabic, one in three black and one in five Caucasian athletes would require further investigation due to an abnormal ECG. These high false-positive rates certainly reinforce concerns voiced by the cardiovascular screening sceptics. While the ESC recommendations are based upon consensus rather than scientific evidence, the Seattle Criteria modified its ECG interpretation criteria by applying evidence that (1) accounted for the impact of African-Caribbean ethnicity upon the electrocardiographic patterns seen in athletes and (2) by raising the QTc thresholds (≥470 ms men and ≥480 ms women) that would trigger further evaluation. By incorporating these two electrocardiographic features, our study demonstrates that 172 (6.9%) athletes would be spared further investigation, helping to lower (p<0.0001) the prevalence of abnormal ECGs by 48% compared with the ESC recommendations. This compares favourably with a recent investigation involving elite Caucasian athletes from Australia. Our data, however, demonstrate that almost 1 in 10 Arabic, 1 in 6 black and 1 in 11 Caucasian athletes would still require further investigation using the Seattle Criteria, primarily due to the presence of RAE (31.8%), LAE (13.1%), LAD (5.2%), RAD (3.1%) and RVH (1.4%), either in isolation or in association with a recognised training-related ECG change.
Using HCM, arrhythmogenic right ventricular cardiomyopathy (ARVC) and pulmonary hypertension populations as a comparison group, both Zaidi et al and Gati et al have demonstrated that in asymptomatic athletes, the presence of RAE, LAE, LAD, RAD and RVH either in isolation or in association with a recognised training-related ECG change correlates extremely poorly with serious cardiac pathology. Despite this, consensus opinion for the inclusion of these ECG parameters in both the ESC recommendations and the Seattle Criteria comes from the fact that these anomalies, in particular LAE, are common ECG features in HCM. In HCM, however, they usually coexist with multitude of other ECG abnormalities such as T-wave inversion, Q-waves and ST-segment depression. Excluding these ECG parameters forms the basis of the Refined Criteria improving specificity and reducing the prevalence of an abnormal ECG in our cohort to 5.3% overall. More strikingly, the Refined Criteria significantly improved the abnormal ECG prevalence in black athletes to just 10% (vs 29.9% ESC and 16.6% Seattle Criteria), while it was further reduced to 3.6% and 2.1% in Arabic and Caucasian athletes, respectively.
Our study identified seven athletes (0.4%) with HCM, with the prevalence in black athletes five times greater than Arabic athletes (0.9% vs 0.2%). No Caucasian athlete was diagnosed with HCM. HCM is cited as the leading cause of sudden death in young athletes, particularly within the black population. Importantly, all three ECG interpretation guidelines identified all seven HCM athletes with 100% sensitivity. Our incidence rates in the present study from a cohort of 1718 athletes who underwent systematic ECG and echocardiography are similar to those reported in previous screening studies involving black and Arabic athletes, who report a disease incidence of 1% and 0.5%, respectively. While the incidence of HCM in black athletes is still approximately nine times higher than that observed in Caucasian athletes, our Arabic athletes now report similar HCM incidence rates to that of Caucasians, estimated at 0.1%.
A further 29 (1.2%) athletes were identified as having a congenital/valvular abnormality. Specifically, bicuspid aortic valve (n=7, 0.3%), mitral valve prolapse (n=3, 0.1%), mild aortic regurgitation (n=5, 0.2%), mitral regurgitation (mild) (n=2, 0.1%), atrial septal defect (n=6, 0.2%) and one case of dextrocardia (0.04%); all picked up through auscultation. None of these athletes was restricted from competition. Only one of these cases was identified via an abnormal ECG (dextrocardia). This poor sensitivity underscores the importance of a physical examination within the cardiovascular screening remit.
Our results are based on observational cross-sectional data. The potential for a false-negative result exists even though 90–95% of individuals with HCM and 80% with ARVC exhibit ECG abnormalities. Furthermore, without serial examination over many years, it is near impossible to ascertain whether asymptomatic athletes without a family history of SCD presenting with isolated LAD/RAD or LAE/RAE would later go on to develop a cardiomyopathy. Second, our population was exclusively men, limiting the application of our data to the female athletic population.
In the present study, one athlete, a 27-year-old black football player from South America, died unexpectedly. At the time of pre-participation screening, the athlete reported no cardiovascular symptoms and no family history of SCD. ECG and echocardiography were strictly normal. The athlete self-presented to the emergency department complaining of severe abdominal pain and died several hours later. An autopsy was performed, but the report has not been made available to the authors.
Discussion
The correct differentiation of physiological adaptation owing to sustained and intensive exercise from an inherited or congenital cardiac pathology is paramount in order to correctly identify athletes at risk of SCD. The key finding from the current study is that the prevalence of an abnormal ECG was significantly reduced to 5.3% when using the 2014 Refined Criteria compared with the 2013 Seattle Criteria (11.6%) and the 2010 ESC recommendations (22.3%), respectively, while all three ECG interpretation criteria proved 100% sensitive, identifying all cases of serious cardiac pathology.
Our results demonstrate that when using the 2010 ESC recommendations, almost one in five Arabic, one in three black and one in five Caucasian athletes would require further investigation due to an abnormal ECG. These high false-positive rates certainly reinforce concerns voiced by the cardiovascular screening sceptics. While the ESC recommendations are based upon consensus rather than scientific evidence, the Seattle Criteria modified its ECG interpretation criteria by applying evidence that (1) accounted for the impact of African-Caribbean ethnicity upon the electrocardiographic patterns seen in athletes and (2) by raising the QTc thresholds (≥470 ms men and ≥480 ms women) that would trigger further evaluation. By incorporating these two electrocardiographic features, our study demonstrates that 172 (6.9%) athletes would be spared further investigation, helping to lower (p<0.0001) the prevalence of abnormal ECGs by 48% compared with the ESC recommendations. This compares favourably with a recent investigation involving elite Caucasian athletes from Australia. Our data, however, demonstrate that almost 1 in 10 Arabic, 1 in 6 black and 1 in 11 Caucasian athletes would still require further investigation using the Seattle Criteria, primarily due to the presence of RAE (31.8%), LAE (13.1%), LAD (5.2%), RAD (3.1%) and RVH (1.4%), either in isolation or in association with a recognised training-related ECG change.
Using HCM, arrhythmogenic right ventricular cardiomyopathy (ARVC) and pulmonary hypertension populations as a comparison group, both Zaidi et al and Gati et al have demonstrated that in asymptomatic athletes, the presence of RAE, LAE, LAD, RAD and RVH either in isolation or in association with a recognised training-related ECG change correlates extremely poorly with serious cardiac pathology. Despite this, consensus opinion for the inclusion of these ECG parameters in both the ESC recommendations and the Seattle Criteria comes from the fact that these anomalies, in particular LAE, are common ECG features in HCM. In HCM, however, they usually coexist with multitude of other ECG abnormalities such as T-wave inversion, Q-waves and ST-segment depression. Excluding these ECG parameters forms the basis of the Refined Criteria improving specificity and reducing the prevalence of an abnormal ECG in our cohort to 5.3% overall. More strikingly, the Refined Criteria significantly improved the abnormal ECG prevalence in black athletes to just 10% (vs 29.9% ESC and 16.6% Seattle Criteria), while it was further reduced to 3.6% and 2.1% in Arabic and Caucasian athletes, respectively.
Identification of pathology
Our study identified seven athletes (0.4%) with HCM, with the prevalence in black athletes five times greater than Arabic athletes (0.9% vs 0.2%). No Caucasian athlete was diagnosed with HCM. HCM is cited as the leading cause of sudden death in young athletes, particularly within the black population. Importantly, all three ECG interpretation guidelines identified all seven HCM athletes with 100% sensitivity. Our incidence rates in the present study from a cohort of 1718 athletes who underwent systematic ECG and echocardiography are similar to those reported in previous screening studies involving black and Arabic athletes, who report a disease incidence of 1% and 0.5%, respectively. While the incidence of HCM in black athletes is still approximately nine times higher than that observed in Caucasian athletes, our Arabic athletes now report similar HCM incidence rates to that of Caucasians, estimated at 0.1%.
A further 29 (1.2%) athletes were identified as having a congenital/valvular abnormality. Specifically, bicuspid aortic valve (n=7, 0.3%), mitral valve prolapse (n=3, 0.1%), mild aortic regurgitation (n=5, 0.2%), mitral regurgitation (mild) (n=2, 0.1%), atrial septal defect (n=6, 0.2%) and one case of dextrocardia (0.04%); all picked up through auscultation. None of these athletes was restricted from competition. Only one of these cases was identified via an abnormal ECG (dextrocardia). This poor sensitivity underscores the importance of a physical examination within the cardiovascular screening remit.
Limitations
Our results are based on observational cross-sectional data. The potential for a false-negative result exists even though 90–95% of individuals with HCM and 80% with ARVC exhibit ECG abnormalities. Furthermore, without serial examination over many years, it is near impossible to ascertain whether asymptomatic athletes without a family history of SCD presenting with isolated LAD/RAD or LAE/RAE would later go on to develop a cardiomyopathy. Second, our population was exclusively men, limiting the application of our data to the female athletic population.
In the present study, one athlete, a 27-year-old black football player from South America, died unexpectedly. At the time of pre-participation screening, the athlete reported no cardiovascular symptoms and no family history of SCD. ECG and echocardiography were strictly normal. The athlete self-presented to the emergency department complaining of severe abdominal pain and died several hours later. An autopsy was performed, but the report has not been made available to the authors.
