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Comprehensive Cardiovascular Care and Evaluation of the Elite Athlete
Historical Perspective
The elite athlete has enjoyed a celebrated status within our culture since ancient times. The Olympic Games solidified that status as early as 776 BC, and it was amplified by Pheidippedes, who was a legendary Greek Olympic champion in 500 BC. Ten years later when the Persians arrived at the plains of Marathon and threatened to conquer Athens, Pheidippedes was dispatched from Athens to recruit the assistance of the Spartans. While remembered most for his 26-mile run from Marathon to Athens to announce the Greek victory, this run was only part of a remarkable triathlon of events for this remarkable Greek athlete. He began the first leg of his journey with a 145-mile run over mountains and plains that included swimming across the aquatic obstacles on his way to reach Sparta in only 2 days and without sleep. The second leg included travel by boat from Sparta to Marathon, where he joined in the victorious battle against the Persians. Only then did he embark upon his now infamous run back to Athens, where he proclaimed victory before dying suddenly in front of his fellow Greek citizens. The remarkable athletic accomplishments of Pheidippedes emphatically etched the Marathon run into sports modernity and deeply engraved the tragic event of athletic sudden death (SD) into our cultural consciousness. The Oxford poet and scholar A. E. Housman captured the effect of sudden athletic death in the poem “To an Athlete Dying Young” (1896):
The time you won your town the race We chaired you through the market place
The metaphor of the winning athlete on the shoulders of the townspeople is an image we have all witnessed in some form many times. With the unexpected death of the athlete, Housman brings the same metaphor full circle from celebration to sadness with athlete's coffin resting upon the shoulders of those same townspeople:
Shoulder-high we bring you home, And set you at your threshold down, Townsman of a stiller town.
Estimates of the incidence of athletic SD reassure us that this is a rare event. The consequences of athletic SD, however, resound far beyond the individuals directly affected. The advent of continuous media coverage through television, radio, and the internet that is now further augmented by social media has created instant access to any adverse event involving a previously healthy and seemingly invincible athlete. Accordingly, a tragic athletic SD immediately affects family, friends, fellow athletes, students, coaches and administrators, and that effect can rapidly ripple into the minds of sports fans anywhere in the world. The sudden deaths on the soccer pitch of Marc Vivien Foe in 2003 (a Cameroon national player with hypertrophic cardiomyopathy) and Fabrice Muamba in 2012 (a player for Bolton in the English Premier league) illustrate the magnitude of the amplification of modern information. Disturbing videos of both events are widely available on the internet and have been viewed by millions of fans around the world.
The SD of Hank Gathers in 1990 had a seminal impact upon the landscape of sports cardiology in the United States. Gathers played Division I college basketball for Loyola Marymount on a team that had realistic aspirations for a national championship. The previous season, he had become the second player in NCAA history to lead the nation in scoring and rebounding. Gathers fainted on the court, and both sustained and nonsustained ventricular arrhythmias were documented most likely as a result of underlying myocarditis. With the extraordinary success of this team from a small university, there was tremendous pressure for Gathers to continue to play. He ultimately returned to play later in the season and died tragically on the court during a tournament game. This case illustrates the entwined complexity inherent to any cardiovascular diagnosis in an elite athlete. Gathers was admittedly noncompliant with his propranolol. The reluctance to disqualify him under the circumstances was profound. The emotional cost to Gather's family, friends, teammates, and the Loyola Marymount community at large is beyond measure. There was also a profound financial impact, with judgments and settlements against the physician and the university. Now that we are more than 25 years removed from this event, it is reasonable to assume that Loyola Marymount is still suffering beneath the dark cloud of this occurrence. Death during competition would intercede as “the most unwelcome spectator” (Jim Murray, The Los Angeles Times ) for other notable athletes as well, including Tom Simpson, an English cyclist who died on Mont Ventoux in the 1967 Tour de France (likely from amphetamines); Flo Hyman, an Olympic volleyball player who died of aortic dissection from the Marfan syndrome four years before Gathers; basketball players Pete Maravich (anomalous coronary artery), Reggie Lewis, and Jason Collier; Sergei Grinkov (ice-skating), Jiri Fischer (hockey), Thomas Herrion (football), and Fran Crippen (swimming). In addition to elite athletes with national and international notoriety, SD has also had a profound impact in communities around the world coping with unexpected deaths of athletes of all ages and levels of ability. The amplification of athletic SD into our cultural consciousness has stimulated considerable research and medical practice interest into the causes of SD in athletes, potential preventive measures inclusive of screening, and the development of care and management guidelines for athletes with known cardiovascular abnormalities. In practice, the prevention of SD represents only a part of the comprehensive cardiovascular care of the elite athlete. In this chapter, we will discuss the current state of practice, controversy with regard to screening, and the detection and management of cardiovascular disorders, with particular emphasis on the normal physiologic cardiovascular remodeling that can occur with elite levels of training.
Medical Home of the Elite Athlete
It is imperative that the elite athlete begin with a medical home composed of a multidisciplinary team, ideally led by a primary care sports medicine provider. Athletic trainers are a vital part of this medical home as well, and bring a rapidly evolving expertise involving the overall health and wellness of the athlete. Trainers are keenly aware of the importance of cardiovascular health and are now familiar with a wide array of useful technology and equipment including blood pressure cuffs, stethoscopes, automatic external defibrillators (AEDs), and electrocardiogram (ECG) machines. In addition, smartphone technology has greatly enhanced the ability of the sports trainer to assess their athletes in real time. Trainers at some Division 1 programs now use a digital application that provides immediate rhythm analysis for symptomatic athletes. It is very helpful when trainers can accompany athletes to subspecialty encounters, because they can reliably relay important information onto the practice and playing field and report back on the development of any important signs, symptoms, or physical findings that may place the athlete at risk.
There is increasing recognition that the medical home of an elite athlete should ideally include a dedicated cardiovascular specialist, with their scope of practice and depth of involvement depending on the specific needs of the individual. These cardiovascular specialists, often referred to as sports cardiologists, may be tasked with oversight of preparticipation screening as well as the evaluation and management of athletes with suspected or previously diagnosed cardiovascular disease. Given this evolving role of cardiovascular specialists in the care of elite athletes, both the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) have dedicated resources to define specific skills and core competencies to guide the practice of sports cardiologists.
Preparticipation Screening
The initial history and physical exam performed by the primary care sports medicine provider now includes the fourth edition of the Preparticipation Physical Evaluation (PPE-4) and has evolved to include a somewhat more reliable detection process for familial cardiovascular abnormalities that might increase the risk of SD and were adopted by the American Heart Association consensus panel for preparticipation cardiovascular screening. However, the state of the current initial athlete evaluation suffers from significant limitations. There is a wide variation from state to state with regard to the type of provider performing the PPE-4 and the content of the PPE-4. In addition, the PPE-4 relies on self-reporting by the athletes themselves, which is inherently prone to error. Furthermore, the PPE-4 has been demonstrated to have poor sensitivity for the detection of cardiovascular disorders. Indeed, in a retrospective look at SD in athletes who had participated in preparticipation screening, only 3% were thought to have potential cardiovascular abnormalities, and none were restricted from participation. Following the PPE-4, referral of an athlete for more advanced cardiovascular care or evaluation occurs as a result of an abnormal physical finding, a family history of premature sudden death, or the development of new symptoms that elicit concern. Many of the most dangerous cardiovascular conditions that could threaten the athlete often are asymptomatic and have no physical finding that would trigger a referral. This includes conditions such as hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), congenital Long QT and Brugada syndromes, Wolff-Parkinson-White (WPW), and the anomalous coronary artery. The absence of a positive family history for SD can be falsely reassuring in the autosomal dominant familial conditions (HCM, ARVC, Long QT, the Marfan syndrome), because up to 25% to 33% of affected individuals will have new spontaneous mutations with no previously affected family members. Accordingly, the current state of evaluation of the elite athlete in the United States is unlikely to detect most threatening cardiovascular conditions. Furthermore, the normal physiologic adaptations of hypertrophy of the left ventricle to rigorous isometric training (often referred to as the “athlete's heart”) can very closely mimic HCM, which is the most prevalent and dangerous cardiovascular disease in young athletes. In addition, physiologic changes in left and right ventricular cavity size and systolic function can be difficult to distinguish from forms of dilated cardiomyopathy and ARVC. Perhaps nowhere in medicine does normalcy mimic disease as it does in this circumstance. As a result, further screening or evaluation of elite athletes requires a sophisticated and programmatic approach that is designed to avoid the pitfall of potentially life-changing false-positive results that will be the inherent weakness in the evaluation of large populations of athletes with a low prevalence of disease. Because of these inherent complexities, expert consensus in the United States, including the American College of Cardiology and American Heart Association (ACC/AHA), has not recommended routine evaluation of the athlete beyond the PPE-4. While this recommendation is well wrought and reasonable, evidence is lacking regarding the efficacy of the PPE-4 in prevention of morbidity and mortality in athletes. In addition, this differs from other expert guidelines, including the ESC and the International Olympic Committee (IOC), which recommend the addition of ECG screening in order to improve the sensitivity of preparticipation screening. Current practice in the United States varies in regard to the inclusion of diagnostic screening tools beyond the PPE-4. As an example, more than one third of National Collegiate Athletic Association (NCAA) Division-1 athletes undergo additional screening with either an ECG or echocardiogram.
Current recommendations have created an unanticipated consequence in the field of sports cardiology. There is a paucity of well trained and knowledgeable cardiovascular providers familiar with the nuances of the normal physiologic adaptations to elite training and how to differentiate normalcy from disease. Encounters with elite athletes are uncommon for most practicing cardiologists. Accordingly, athletes who undergo more extensive testing and evaluation by inexperienced providers are commonly sidelined unnecessarily, subjected to over testing, relegated to the emotional consequences of concern for survival, and temporary or permanent disqualification from sports altogether. The incorporation of cardiovascular care into the medical home of the athlete must be done very carefully with knowledgeable providers dedicated to understanding the complex world of the athlete.
Cardiovascular Adaptations and Remodeling Associated With Rigorous Athletic Training
The earliest recognition of the physiologic changes commonly referred to as the “athlete's heart” were astutely described in 1899 by a Swedish physician who detected cardiac enlargement in elite Nordic skiers utilizing remarkably accurate skills of auscultation and percussion. That same year, these findings were reinforced in a study of Harvard University rowers. It is not surprising that the earliest descriptions of cardiac enlargement were made in Nordic skiers and elite rowers, because these disciplines include extreme combinations of endurance training (isotonic, dynamic, aerobic) and strength training (isometric, static, anaerobic) that lead to more striking combinations of both left ventricular (LV) cavity dilation and hypertrophy. A few years later, Paul Dudley White would strengthen the legacy of sports cardiology in Boston by observing pulses in endurance-trained runners participating in the Boston Marathon and would later describe bradycardia associated with this level of endurance training. The evolution of more sophisticated technology would allow for the complex assessment of the electrophysiologic and structural cardiovascular adaptations to varying degrees and types of athletic training. Accordingly, any cardiovascular evaluation of an athlete inclusive of electrocardiography or any form of cardiovascular imaging must be undertaken with in-depth knowledge of the training-specific changes in cardiac structure and function. Pure endurance training involves prolonged activities with sustained increases in cardiac output without significant elevation in mean arterial pressure. This type of volume load can lead to dilation of all four chambers of the heart and to some degree the great vessels as well. Strength-training subjects the heart to more brief but dramatic increases in mean arterial pressure that in turn leads to an increase in myocardial muscle hypertrophy. Marathon running is a good example of pure endurance training, and weight lifting is an example of pure strength training. Most sports, however, will have varying degrees of both types of training that will also vary with the approach of the individual athlete. Therefore the heart of any athlete may manifest changes across a broad spectrum of physiologic adaptation.
Structural Adaptations to Rigorous Training
Left Ventricle
The effects of training on the LV are routinely detected on the ECG and increases in voltage have been documented for decades. Endurance training that also incorporates increasing degrees of isometric/strength training (cycling, rowing, cross country skiing, canoeing) are more likely to demonstrate these manifestations on the resting ECG. Transthoracic echocardiography (TTE) has been used extensively to document the spectrum of LV cavity dilation and increase in LV wall thickness/left ventricular hypertrophy (LVH) associated with rigorous training. LV cavity size across a large variety of sports is larger than sedentary controls and ranges from 43 to 70 mm (mean 55 mm) in men and 38 to 66 mm (mean 48 mm) in women. LV wall thickness is generally less than 13 mm in elite athletes, but larger increases in wall thickness (1.3 to 1.5 mm) that stray into the “gray zone” with hypertrophic cardiomyopathy are more commonly seen in older elite athletes (rowers) who train with large degrees of static and dynamic exercise. LV systolic function as measured by TTE is usually normal in elite athletes. It is important to recognize, however, that LV systolic function can be low normal to mildly depressed (mimicking mild forms of dilated cardiomyopathy), as shown in some of the fittest athletes in the world participating in the Tour de France. These adaptive changes in cavity dimension, wall thickness, and the associated increase in LV mass have also been demonstrated in magnetic resonance imaging (MRI) studies and have been recently reviewed in depth. LV diastolic function is usually normal in elite athletes and can be improved with endurance training, leading to more robust early diastolic filling. Less is known about the effects of strength training on diastolic function, but there is evidence that diastolic function may be impaired, which could be an untoward long-term effect of hypertrophy that warrants further study.
Right Ventricle
Sustained increases in cardiac output have a similar effect on the right ventricle (RV) as compared with the LV, particularly with regard to cavity dilation. Older M-mode and 2-D TTE studies in endurance-trained athletes showed symmetrical dilation in both the RV and the LV. Due to the unique geometry of the RV, echocardiography has struggled to assess RV size and function, and cardiac MRI has greatly enhanced our ability to evaluate the RV. More recent MRI studies in elite endurance athletes have reinforced the balanced dilation of the RV and LV demonstrating increases in LV and RV mass, LV and RV diastolic volumes, and LV and RV stroke volumes. Abnormalities in systolic function in endurance athletes can also be abnormal and generally seen in athletes with more extensive RV dilation. The impact of strength training on the RV is less clear but likely to be a topic of future clarification utilizing TTE and cardiac MRI.
Atria
As expected, increased right and left atrial volumes and sizes are also seen in endurance athletes with more numerous studies evaluating the left atrium. A large volume of data supports the physiologic effects of sustained endurance volume loading on all four cardiac chambers, including the atria. In the largest Italian series, 20% of athletes had left atrial dimensions of >40 mm measured by TTE, and supraventricular arrhythmias were not common in this group.
Great Arteries and Veins
The great arteries and veins are subject to the physiologic effects of endurance training. The aorta is of particular interest with regard to strength training, as extraordinary increases in both systolic and diastolic blood pressure (480/350 mm Hg!) have been documented in weight lifters. Studies have documented somewhat inconsistent aortic root dilation with regard to specific types of sports and training regimens. Strength-trained athletes have been shown to have larger dimensions of the aorta measured by TTE at the aortic annulus, the sinuses of Valsalva, sinotubular junction, and proximal aortic root when compared with controls, and this effect increased with the duration of training. Aortic root size was greater in taller athletes and typically measured between 3.0 and 4.0 cm, and only rarely measured greater than 4.0 cm. While aortic regurgitation was found in none of the controls, 9% of the strength-trained athletes had mild ( n = 5) or moderate ( n = 4) aortic regurgitation. Another large trial supported these findings comparing strength-trained with endurance-trained athletes. In a large trial of a wide range of sports in Italy, the largest measurements were found in endurance-trained athletes, particularly in the disciplines of cycling and swimming. This apparent inconsistency may be attributed the sustained combination of isometric and isotonic exercise associated with these sports. In totality, it is important to note that while athletic training in various disciplines may lead to increase in aortic root dimensions, these increases have not been shown to approach diameters typically concerning for pathologic dilatation. In this light, a meta-analysis investigating aortic root dimensions in athletes versus nonathlete controls found that elite athletes have a minor, and likely clinically insignificant, increase in aortic root dimensions. The authors rightfully noted that marked aortic root dilatation likely represents a pathologic process rather than an adaptation to exercise.
The effects of training are also seen on a wide range of great vessels in endurance athletes and taller athletes, including larger caliber carotids, branch pulmonary arteries, superior and inferior vena cavae, and abdominal aorta as shown in cyclists, long-distance runners, and volleyball players. It has been our observation in endurance-trained athletes that the inferior vena cava is routinely larger than normal, and that published estimates of RA pressure based upon vena cava size and inspiratory collapse do not apply to the elite athlete.
The Athlete's Electrocardiogram and Electrophysiologic Adaptations to Rigorous Training
Training-induced alterations in cardiac structure and autonomic regulation are reflected on the ECG of the athlete in many ways, and the resting ECG will have a range of well-documented variations as compared with normal controls in most cases. Common training-related findings on the athlete's ECG include sinus bradycardia, first degree atrioventricular (AV) block, incomplete right bundle branch block (RBBB), early repolarization, and voltage criteria for LVH ( Fig. 12.1 ). Electrophysiologic aberrations, like their structural counterparts, are more common in endurance sports that include a significant amount of strength training as well (cycling, rowing, canoeing, and cross-country skiing).
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