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Counterpoint: lack of evidence for echocardiography screening in athletes
  1. Elizabeth Dineen1,
  2. Jordan Prutkin2
  1. 1 Medicine/Cardiology, University of California Irvine, Irvine, California, USA
  2. 2 Medicine/Cardiology, University of Washington, Seattle, Washington, USA
  1. Correspondence to Dr Jordan Prutkin, Medicine/Cardiology, University of Washington, Seattle, WA 98103, USA; jprutkin{at}cardiology.washington.edu

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Prevention of sudden cardiac death (SCD) in athletes continues to be a major focus for sports medicine health professionals. While the incidence is low, the consequences can be devastating. Over the years, our understanding of SCD aetiologies and the ability to identify those at higher risk for SCD continues to improve. The preparticipation examination (PPE) is critical to this mission. While the necessity of a PPE is not questioned, the key elements of the PPE continue to fuel an ever-evolving debate.

The history and physical (H&P) are a cornerstone of the PPE at all levels. There is debate whether to incorporate the 12-lead ECG as part of this screening process. This is based on the idea that the H&P alone may not be enough to fully ascertain diseases associated with SCD. It is supported by many studies, including one of 3620 high school athletes in which the American Heart Association 14-element PPE H&P was found to have decreased sensitivity, specificity and positive predictive value for conditions associated with SCD compared with an ECG (18.8% vs 87.5%, 68% vs 97.5% and 0.3% vs 13.6%, respectively).1 There is concern, however, regarding variability in ECG interpretation and available follow-up resources, so this may not be the best choice for all communities. Thus, American guidelines endorse inclusion of the ECG at the discretion of individual medical entities based on regional athlete risk and resources.2 Importantly, some cardiovascular disease phenotypes do not manifest until later in life and therefore may have a normal initial PPE. Additionally, some conditions, such as catecholaminergic polymorphic ventricular tachycardia or anomalous coronary artery, may not be elucidated from the PPE or resting ECG. PPE screening efficacy is further complicated by the fact that autopsy-negative (structurally normal heart) sudden unexpected death is a leading cause for SCD.3

In this issue of Heart, Niederseer and colleagues4 propose incorporation of the transthoracic echocardiogram into the athlete PPE to better identify those at increased risk for SCD. Their algorithm recommends one echocardiogram during adolescence and one after age 35, given the different SCD aetiologies in these age cohorts. They further suggest that echocardiograms can be time efficient and cost-effective for SCD screening. While we respect this opinion, we believe the current evidence is not robust enough to support a widespread screening echocardiogram as part of every athlete’s PPE.

There is no doubt that performing an echocardiogram will increase the number of identified cardiac pathologies, many of which may require long-term follow-up. Data supporting the role for screening echocardiogram as a means to identify athletes at increased risk for SCD are limited, especially when done in addition to ECG. One study of 3100 male soccer players aged 6–17 showed that the addition of a screening echocardiogram identified 56 cardiac conditions, though only two had a condition associated with an increased risk for SCD (both with hypertrophic cardiomyopathy), and the ECG was abnormal in both.5 Modaff and colleagues added a screening echocardiogram to their PPE process and found 16 out of 1525 athletes with a normal PPE H&P had an abnormal echocardiogram.6 Overall, 95% of the athletes had a normal echocardiogram, and only three out of the total 2898 screened athletes were restricted from sport based on echocardiogram findings (apical hypertrophic cardiomyopathy, dilated ascending aorta and bidirectional atrial septal defect with right ventricular dysfunction). A separate study of over 2000 male soccer players, mean age of 12 years, had a 4.5% prevalence of pathological echocardiogram findings. All conditions requiring sport restriction were initially flagged either by abnormal PPE H&P and/or abnormal screening ECG.7 Overall, it is clear that the addition of an echocardiogram in younger cohorts identifies cardiovascular disease processes that may require long-term follow-up such as a bicuspid aortic valve, though at present, the echocardiogram does not appear to significantly increase the chances of elucidating diseases associated with SCD risk more than that which can be found by other means. Of note, certain individuals have been found to have a higher incidence of SCD (black athletes, males, basketball players),3 and the screening echocardiogram could have a role for decreasing SCD. Full endorsement would depend on results of adequately powered future studies in this subset.

The authors appropriately separate masters athletes (over age 35) from the younger cohort. Based on raw numbers, there is a higher incidence of SCD in this age range due to an increased prevalence of undiagnosed coronary artery disease (CAD). As such, exercise testing is often recommended prior to initiation or increasing intensity of an exercise programme, especially in those with known cardiovascular risk factors. However, a baseline screening echo is unlikely to discover a significant prevalence of wall motion abnormalities, and it is likely that a lipid profile adds more to risk stratification than the evaluation of aortic plaques as Niederseer et al suggest. In addition, until there are further data to support it, we suspect a low yield for detecting cardiomyopathies or silent myocarditis in the masters athletes. We recognise that recent European guidelines incorporate an echocardiogram as part of the risk stratification of patients with known CAD prior to exercise participation,8 but this would not be considered a screening echo in an asymptomatic athlete. Overall, the expected incremental benefit of a screening echo, especially from a cost-effectiveness perspective, is likely low in this population.

We must also highlight the resources required for mass screening echocardiograms. First, specialised personnel are required for performing and interpreting the athlete’s echocardiogram given the nuances of the athletic heart. Given the concerns some have regarding quality of ECGs for screening, we would expect this only to be magnified with the addition of complete echocardiograms. In order to address the issues of time efficiency and cost, the authors suggest a focused echocardiogram, which generally refers to a physician’s use of handheld ultrasound to help answer a specific clinical question. The American Society of Echocardiography guideline on focused echocardiogram supports its use to detect chamber enlargement and hypertrophy, ventricular function, pericardial effusion and inferior vena cava size, but they also note the test’s shortcomings for identifying disease processes such as hypertrophic cardiomyopathy and regional wall motion abnormalities.9 In addition, it can often be challenging even for skilled sonographers to quickly find the coronary arteries to assess for anomalies, one of the main situations where an echo is better than ECG or H&P. Therefore, brief, focused echocardiograms may miss key diagnoses associated with SCD. In addition, these echocardiograms are often not saved for review by others, in contrast to a printed or electronic ECG.

In conclusion, the echocardiogram has a significant role in the secondary evaluation of abnormal history, physical and ECG findings but we do not think it should be used widely for initial screening. We agree that it can pick up structural heart conditions that will need long-term follow-up. However, the purpose of athletic screening should be to pick up life-threatening conditions which could lead to SCD when triggered by exercise or else we would recommend screening all adolescents and adults. Until we have more concrete evidence, we believe the screening echocardiogram does not appear to improve SCD risk stratification in athletes more than the current standard of practice.

References

Footnotes

  • Twitter @BethDineenDO

  • Contributors Both authors contributed to this work and met the criteria for authorship.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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