How should we screen competitive athletes for cardiovascular disease?

The sudden unexpected deaths of young trained athletes are highlyvisible events which have a substantial impact on the physicianand lay communities.¹ Although initially a focal point in theUnited States in the early 1980s, this issue has now becomea matter of concern in most parts of the industrialized world(particularly in Europe). Evidence of this is the highly publicizedrecent sudden deaths of several elite professional athletesfrom Europe, South America, and Africa, including Sergio Serginho(Brazil; football), Sergei Zholtok (Latvia; hockey), Marc-VivianFoe (Cameroon; football), Sergei Grinkov (Russia; skating),Miklos Feher (Hungary; football), Cristiano de Lima, Jr (Brazil;football), and Trevor Borysuk (Canada; hockey), at least oneof whom had a cardiac diagnosis made previously. Interest in athletic     

Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease

To determine the feasibility of detecting cardiovascular disease in a large group of young competitive athletes, a prospective screening evaluation of intercollegiate student athletes was undertaken at the University of Maryland. Initial clinical screening (including personal and family history, physical examination and 12 lead electrocardiogram) was performed in 501 athletes. Ninety of these subjects had positive findings on one or more of the three studies and agreed to further cardiologic evaluation. The vast majority (75 [84%] of 90) had no definitive evidence of cardiovascular disease, although 1 athlete had mild systemic hypertension and 14 (15%) had echocardiographic evidence of relatively mild mitral valve prolapse that had not been previously suspected. In three athletes with relatively mild ventricular septal hypertrophy (14 to 15 mm), it was not possible to discern with absolute certainty whether the wall thickening was a manifestation of hypertrophic cardiomyopathy or secondary to athletic conditioning ("athlete heart"). Therefore, this screening protocol identified no athletes with definite evidence of hypertrophic cardiomyopathy, Marfan's syndrome or other cardiovascular diseases that convey a significant potential risk for sudden death or disease progression during athletic activity. This failure to identify such diseases could have been due to a lack of sensitivity of the screening tests or to the low frequency with which these diseases occur in youthful healthy athletes. A systematic preparticipation screening program (such as the present one) does not appear to be an efficient means of detecting clinically important cardiovascular disease in young athletes.     

Strategies for assessing the prevalence of cardiovascular sudden deaths in young competitive athletes

Background/Objectives

Prevalence/incidence of sudden death due to cardiovascular disease in young competitive athletes has become an important part of the debate over the most effective and practical preparticipation screening strategies for this population. Since event reporting is not mandatory, identification of cases has been achieved largely through publicly available data and internet searches. The accuracy of this methodology has not been studied and deserves scrutiny.

Methods

We assessed recognition of sudden cardiovascular deaths in college (NCAA) athletes with the U.S. National Registry of Sudden Death in Athletes that uses largely public domain sources, and also the NCAA Memorial Resolutions List.

Results

For 2002–2011, 64 total sudden death cases were identified by both sources. The Registry identified 56 cases (88%), including 14 not found in the NCAA List. The NCAA List identified 50 cases (78%), including 8 unrecognized by the Registry (p = 0.16). Failure to initially recognize these 8 deaths using established Registry search mechanisms was due to the absence of key search terms in media reports. Cases not identified by the 2 methodologies did not differ significantly regarding demographics, cause of death, or sport.

Conclusions

Internet-based, public domain methodology is useful and identified more cases of sudden cardiovascular death in college athletes than did the internal list provided by the NCAA. Nevertheless, these findings support the principle that multiple sources are additive and beneficial in identifying the maximum number of sudden death events.     

Cardiovascular assessment of competitive athletes with syncope and inherited abnormalities of the cardiac ion channels

The Italian legislation mandates preventive cardiovascular screeningfor all subjects engaged in competitive athletic activities.¹Such evaluation is performed by physicians with an academictraining in sports medicine, and includes history, physicalexamination, standard 12-lead electrocardiography and a     

Patterns of ventricular tachyarrhythmias associated with training, deconditioning and retraining in elite athletes without cardiovascular abnormalities

Ventricular tachyarrhythmias commonly occur in trained athletes during ambulatory Holter electrocardiography and are usually associated with a benign course. Such arrhythmias have been demonstrated to be sensitive to short periods of athletic deconditioning; however, their response to retraining is not known. Twenty-four hour Holter electrocardiographic monitoring was performed at peak training and after 3 to 6 months of deconditioning and was repeated in the present study after 2, 6, and 12 months of retraining in 37 athletes with frequent and complex ventricular tachyarrhythmias and without cardiovascular abnormalities. These subjects showed partial (101 to 500 ventricular premature complexes [VPCs]/24 hours) or marked (<100 VPCs) reversibility of arrhythmias after deconditioning. Retraining initially resulted in a significant increase in arrhythmia frequency compared with deconditioning (from 280 ± 475 to 1,542 ± 2,186 VPCs; p = 0.005), couplets (0.14 ± 0.42 to 4.4 ± 8.2; p = 0.005), and nonsustained ventricular tachycardia (from 0 to 0.8 ± 1.8; p = 0.02). Subsequently, a progressive reduction was seen in the frequency of all ventricular arrhythmias during the 1 year of training to well below that at the peak training levels (VPCs 917 ± 1,630, couplets 1.8 ± 4.2, and nonsustained ventricular tachycardia 0.4 ± 1.2). Such annual arrhythmia reduction was significantly greater statistically in those athletes with marked reversibility after deconditioning than in the athletes with partial reversibility (69 ± 139 vs 1,496 ± 1,917 VPCs/24 hours, respectively; p = 0.007). No cardiac events or symptoms occurred during 1 year of follow-up. In conclusion, in elite athletes without cardiovascular disease, a resumption in intense training after deconditioning was associated with variable, but prolonged, suppression of ventricular ectopy. The absence of adverse clinical events or symptoms associated with the resumption of training supports the continued eligibility in competitive sports for such athletes and is also consistent with the benign nature of physiologic athlete's heart syndrome.     

The role of modern cardiovascular imaging in (suspected) coronary artery disease in competitive athletes

This overview addresses different non-invasive imaging methods in diagnosing CAD before clearing the athlete for participation in sports activity. Keep in mind the risks and benefits of exercising for the competitive athlete and to use the SCORE-information as a first evaluation tool. It is essential to gather relevant information and to complement anatomical evaluations with functional evaluations. Exercise testing also has an added value in athletes as it will inform both the physician and the athlete on the aerobic fitness of the individual, a key factor in risk assessment.     

How to screen athletes for cardiovascular diseases

The Italian screening protocol has adequate sensitivity and specificity for detection of potentially dangerous cardiovascular diseases, and substantially reduces mortality of young competitive athletes, mostly by preventing sudden cardiac death from cardiomyopathy. The results of the Italian preparticipation evaluation program have significant implications worldwide: this article addresses the efficacy and feasibility of preparticipation screening, essentially based on 12-lead ECG, as has been in practice in Italy for 25 years.     

Risk of competitive sport in young athletes with heart disease

The majority of sudden deaths in young athletes occur in the context of underlying inherited or genetic cardiac disorders. The evaluation of every athlete regarding underlying cardiac disease is impractical and therefore needs to be targeted at those who are at a higher risk. A practical approach would be to channel efforts towards athletes with cardiac symptoms, those with a family history of inherited cardiac disease, and those with a family history of premature sudden death. There are potential pitfalls in the evaluation of young athletes using non-invasive tests when making the distinction between physiological adaptations to exercise and cardiac pathology. Physicians evaluating young athletes need to be aware of the spectrum of physiological adaptations and to be familiar with conditions responsible for sudden death in this population.     

Causes of sudden death in competitive athletes

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.     

The preparticipation cardiovascular screening of competitive athletes: is it time to change the customary clinical practice?

The recent 'Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 update', state that it is not 'either prudent or practical to recommend the routine use of test such as 12-lead ECG' into the preparticipation screening, in contrast to previous Recommendations of the European Society of Cardiology (ESC) and the International Olympic Committee (IOC). This comment was, therefore, prompted by the personal consideration that it is timely and appropriate to clarify the rationale of the European Recommendations, in an effort to achieve an agreement on this controversial issue. The strongest evidence supporting the need for 12-lead ECG into the screening programme is the demonstration for substantial decrease in sudden deaths in screened individuals, compared with not screened ones (i.e. 3.6-0.4 deaths x 100 000 person-years in the period 1979-2004), associated with a concomitant increase in individuals identified with cardiomyopathies (4.4-9.4%). Indeed, implementation of the 12-lead ECG appears to be associated with only a small proportion of abnormal findings requiring additional testing (such as inverted T waves, increased R/S wave voltages suggestive for LV hypertrophy, major conduction disorders), i.e. about 5% of a large, unselected population of 32 652 individuals. We believe, therefore, that a critical reassessment of the current customary clinical practice is needed for preparticipation screening. In particular, this change seems appropriate for elite athletes, a selected cohort of top-level competitors who have financial resources for a more comprehensive screening process.     

ECG diagnostics in competitive athletes. Current implications for preparticipation screening

In young competitive athletes sudden cardiac death frequently occurs as a tragic first manifestation of clinically inapparent underlying structural or electrical cardiac disorders. An increased risk may be reflected by typical electrocardiogram (ECG) alterations preceding symptoms but a correct interpretation is often challenging due to a high prevalence of training-related ECG alterations in competitive athletes mimicking such disorders. Misinterpretation may thus result in either unnecessary disqualification from competitive sports or continuation despite an increased risk or extensive diagnostic work-ups yielding additional equivocal findings. However, as observed in large athlete cohorts in recent years a variety of ECG alterations, such as isolated increased QRS voltage, early repolarization, sinus bradycardia, first degree AV block or incomplete right bundle branch block, represent common variants of ECGs of athletes reflecting physiological and training-related cardiac adaptations. These alterations do not usually require further diagnostic evaluation. In contrast, alterations such as repolarization abnormalities, complete bundle branch block, prolonged QT intervals or pathological Q waves, are strongly suggestive of underlying disorders and require further evaluation even in asymptomatic athletes. Thus, the ECG plays a pivotal role in the prevention of sudden cardiac death in competitive athletes. The present article summarizes current recommendations for the interpretation of athlete ECGs regarding the differentiation between physiological or pathological cardiac adaptation.