Every time an athlete dies on the field there is renewed interest in the controversial topic of preparticipation screening. One key limitation in the field is that there is little or no good data about what constitutes a healthy heart in athletes. Now a new study published in JAMA Cardiology provides an extraordinarily detailed look at the hearts of professional basketball players.
David Engel (Columbia University) and colleagues analyzed comprehensive echocardiographic data from 526 NBA players obtained during mandatory league testing. Many experts suspect that basketball players, due to their size and, perhaps, ethnicity, may be at higher risk for sudden cardiac death than the general population or athletes in other sports.
The main immediate value of this cross-sectional study is to provide a reliable and detailed “snapshot” of the NBA athletes at one point in time. The study now provides for the first time a “frame of reference,” said Engel in an interview. “We can now see the upper limits of normal.”
One important but not unexpected finding of this study is that the left ventricle (LV) was significantly larger in athletes than in the general population. Importantly, however, the “LV size was proportional to body size.” About a quarter of the players had left ventricular hypertrophy (LVH), which is often described as “athlete’s heart” in this population and is not thought to be linked to a big increase in risk. “The results of our study reinforce the concept that scaling LV size to body size is vitally important in the cardiac evaluation of basketball players,” wrote the authors. “We now have a much stronger frame of reference for health care providers to distinguish normal from abnormal” hypertrophic cardiomyopathy, Engel told me.
Perhaps the most important and surprising finding of the study was that, unlike the left ventricle, the size of the aorta did not increase proportionally, “despite the immense body size of these athletes.” In fact, the authors reported, aortic root size did not differ from athletes in other sports. Less than 5% of the NBA players had an aortic root that was 40 mm or greater. This finding supports current ACC/AHA recommendations to follow with serial imaging all athletes who have aortic root diameters above 41 mm, since an enlarged aorta may be a sign of Marfan syndrome, which has been the underlying cause of death in some prominent cases of sudden cardiac death in athletes.
Screening Recommendations and Controversies
Engel said he supported current recommendations for preparticipation screening based on a basic 14 element history and physical. He does not support either routine ECG or echocardiography unless specifically indicated by the initial exam for student athletes. Routine echocardiography would be extremely expensive and would present additional problems, since it requires a fair amount of expertise for proper interpretation. Both ECG and echocardiography would certainly lead to more false positive and false negative diagnoses, he said.
Barry Maron (Minneapolis Heart Institute) is the world’s leading authority on screening and SCD. He raises troubling and difficult questions about the field. For instance, he asks, why do we screen only athletes? There is no evidence that athletes are at significantly higher risk, but the issue is rarely raised because “they don’t get in the newspapers, they don’t die on the athletic field in front of everybody.”
Maron also pointed out that sport-related concussions are an important public health issue that hasn’t provoked the same kind of immediate emotional response.
Another often neglected perspective, Maron has written, is that suicide and drug overdoses pose a much greater risk to students than SCD. Denmark, for instance, saved lives by not screening athletes and instead used the money to prevent these and other more common causes of death in young people.
What About Long QT Syndrome?
One dangerous but very rare condition is Long QT syndrome. A recent Washington Post story featured a 13-year-old boy who was banned from sports when he was found to have Long QT syndrome after an ECG during a routine screening program. But, notes Engel, the article does not present a compelling case for more widespread use of ECG screening. “Without a known family history of long QT syndrome or preceding symptoms that would raise concern of an arrhythmogenic disorder, detection of this syndrome on a pre-participation history and physical is effectively impossible.”
Asked to comment on the article, Maron said that “it has always been and will continue to be an emotional issue. These single cases always drive the media… because they are dramatic stories.”
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