CLINICAL RESEARCH: ETHNICITY AND CARDIAC CHANGES IN ATHLETES
Relation of Race to Electrocardiographic Patterns in Elite American Football Players
Anthony Magalski, MD, FACC*,*,
Barry J. Maron, MD, FACC ,
Michael L. Main, MD, FACC*,
Marcia McCoy, RN, MSN*,
Angela Florez, BA ,
Kimberly J. Reid, MS*,
Harold W. Epps, MED, ATC, LAT ,
John Bates, MD, FACC|| and
Jon E. Browne, MD¶
* Cardiovascular Consultants PA, Mid-America Heart Institute, Kansas City, Missouri
The Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota
Saint Louis University, St. Louis, Missouri
Kansas City Chiefs Football Club, Inc., Kansas City, Missouri
|| The Care Group, LLC, Indianapolis, Indiana
¶ University of Missouri Kansas City, Kansas City, Missouri.
Manuscript received October 11, 2007;
revised manuscript received December 18, 2007,
accepted January 6, 2008.
* Reprint requests and correspondence: Dr. Anthony Magalski, Associate Professor, University of Missouri Kansas City, Cardiovascular Consultants PA, 4330 Wornall Road, Suite 2000, Kansas City, Missouri 64111. (Email: amagalski{at}cc-pc.com).
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Abstract
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Objectives: The purpose of this study was to establish an electrocardiographic (ECG) profile in a biracial population of highly-trained American football players.
Background: Intense physical training can induce cardiac structural and functional changes ("athlete's heart"), including 12-lead ECG alterations. That race might play a role in determining ECG patterns has been suggested, although not studied in a large athletic population comparing black and white athletes.
Methods: Electrocardiographic analysis of 1,959 elite male athletes attending the National Football League Invitational Camp from 2000 to 2005 was performed. Subjects were classified by race and player position and judged free of structural heart disease.
Results: Abnormal ECG patterns were present in 480 (25%) athletes and were significantly more common among black players (n = 396; 30%) compared with white players (n = 78; 13%) or other races (n = 6; 15%) (p < 0.0001). Distinctly abnormal ECG patterns, suggestive of cardiac disease, were also more common in blacks (n = 76; 6%) than whites (n = 11; 2%) (p = 0.0005). In multivariable analysis, black race was an independent predictor of abnormal ECGs (risk ratio [RR] 2.03, 95% confidence interval [CI] 1.56 to 2.64, p < 0.0001), including patterns judged distinctly abnormal (RR 2.59, 95% CI 1.18 to 5.67, p = 0.02). Abnormal ECGs were also related to player position: most frequent in wide receivers (n = 91; 35%) and least common in quarterbacks (n = 16; 14%) and place kickers (n = 8; 11%). Echocardiograms, obtained in 203 athletes (10%), did not show structural cardiac abnormalities.
Conclusions: Electrocardiographic abnormalities were 2-fold more common in black than in white highly-trained male American football players, with race an independent determinant of ECG pattern. These findings have important implications for pre-participation cardiovascular screening of athletes with ECGs.
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Abbreviations and Acronyms
| | BSA = body surface area | | CI = confidence interval | | ECG = electrocardiogram | | LV = left ventricular | | NFL = National Football League | | RR = risk ratio |
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Physical training can induce cardiac structural and functional changes including left ventricular (LV) cavity enlargement and modest increases in wall thickness and mass, collectively known as "athlete's heart" (1–3). In competitive athletes, it is important to distinguish such normal physiological adaptations to training from pathological conditions such as hypertrophic or dilated cardiomyopathy (4). Mass pre-participation screening can identify or raise the suspicion of cardiovascular abnormalities known to cause sudden death in sports participants (5). Incorporation of the 12-lead electrocardiogram (ECG) into screening programs is practiced in Italy, promoted in Europe (4), and suggested in the U.S. (6). However, there are few systematic data assessing ECG patterns in athletes of different races free of cardiovascular disease. This study assessed ECGs in a large biracial cohort of highly-trained American football players.
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Methods
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Participating subjects.
The study group consisted of collegiate football players (n = 1,959) participating in the annual National Football League (NFL) Invitational Camp (i.e., Scouting Combine) from 2000 to 2005. Each athlete was eligible to attend only once after entering the NFL draft. The primary objective of this event is to assemble medical information. Evaluations include comprehensive history, physical examination, and 12-lead ECG and also echocardiography selectively when clinically appropriate. All study subjects were judged free of structural heart disease. This study was approved by Saint Luke's Hospital Institutional Review Board.
ECGs.
Twelve-lead ECGs were recorded at 25 mm/s in the supine position during quiet respiration and interpreted by 1 investigator (A.M.) blinded to identity, race, and position. The ECGs were classified into subgroups as described by Pelliccia et al. (7) (Table 1).
Echocardiography.
Two-dimensional echocardiography was performed with Hewlett Packard Sonos 2500 and 5500 instruments (Andover, Massachusetts). Images were obtained in multiple cross-sectional planes with standard transducer positions. Cardiac dimensions were measured according to American Society of Echocardiography recommendations (8). Parameters of LV filling were obtained with pulsed Doppler echocardiography.
Echocardiograms were obtained selectively in 203 athletes (10%), including 33 with distinctly abnormal ECGs. Athletes were selected for echocardiography by virtue of clinical suspicion of cardiovascular disease on the basis of ECG pattern, heart murmur, or family history. Echocardiograms were interpreted without knowledge of player identity or ECG.
Statistical analyses.
Variables were assessed with chi-square or Fisher exact tests for categorical variables expressed as proportions and the Student t test or analysis of variance for continuous variables expressed as mean ± SD. Dunnett's multiple comparison adjustment was used to adjust p values for player position. Independent association of race, player position, body surface area (BSA), and age with abnormal ECG was assessed with multivariable modified Poisson regression models. Dichotomous outcomes were analyzed with logistic or modified Poisson regression models to obtain odds ratios, which were used to estimate adjusted relative risk (9). Covariates in the multivariable model included race, player position, BSA, and age. Statistical significance was defined as a 2-sided p value <0.05. Analyses were performed with SAS 9.1 (SAS Institute, Inc., Cary, North Carolina) and R 2.1.1 (R Foundation for Statistical Computing, Vienna, Austria).
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Results
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Demographic data.
The mean age of study subjects was 23 ± 0.9 years (range 20 to 29 years); all were male (Table 2). By race, 1,321 (67%) were black, 598 (31%) white, and 40 (2%) of other races. The BSA was 2.4 ± 0.3 m2. Abnormal ECGs were identified in 480 (25%) athletes, of which 88 (5%) were regarded as distinctly abnormal and 392 (20%) mildly abnormal (see Fig. 1
for representative examples).
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Figure 1 Diversity of Abnormal 12-Lead ECG Patterns in 5 Black Athletes
Diversity of abnormal 12-lead electrocardiographic (ECG) patterns in 5 black athletes characterized by (A) ST-segment depression in inferior leads, J-point elevation in right precordial leads, and diffuse T-wave inversions in a 21-year-old lineman; (B) deep symmetric T-wave inversions in V1 to V3 in a 21-year-old defensive back; (C) J-point elevation in right precordial leads, deep symmetric T-wave inversions in V3 to V6, and inferior T-wave inversions in a 22-year-old defensive back; (D) marked increased voltage (>40 mm in V4) in a 21-year-old wide receiver; and (E) markedly increased voltage (>40 mm in V4), J-point elevation in V2 to V3, and T-wave inversion in V2 to V4 in a 21-year-old wide receiver.
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Race and ECG.
Abnormal ECGs were significantly more common among black players (n = 396; 30%), compared with whites (n = 78; 13%) or other races (n = 6; 15%; p < 0.0001) (Fig. 2). The ECG patterns classified as distinctly abnormal and most suggestive of cardiac disease were also more common in black athletes (n = 76; 6%) than in whites (n = 11; 2%) or other races (n = 1; 3%; p = 0.0005) (Fig. 2).
Specific ECG patterns also showed a relation to race. T-wave inversion and increased R- or S-wave voltages  35 mm, usually in precordial leads, were also significantly more common in black players (Fig. 3). All 7 athletes with 1 distinctly abnormal ECG finding were black.
Player position.
Significant associations between player position and abnormal ECG were evident (p < 0.0001) (Table 3). Abnormal ECGs were most common in wide receivers (n = 91; 35%), defensive backs (n = 100; 30%), and running backs (n = 62; 29%) and least common in quarterbacks (n = 16; 14%) and place kickers (n = 8; 11%). Black players who were defensive backs, linebackers, offensive linemen, and quarterbacks more commonly had abnormal ECGs compared with whites at the same positions (p < 0.05) (Fig. 4).
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Figure 4 Abnormal ECG With Respect to Race and Player Position
*p < 0.05 for comparisons by race; only 1 black athlete at this position (electrocardiogram [ECG] was abnormal). DB = defensive back; DL = defensive lineman; LB = linebacker; OL = offensive lineman; PK = place kicker; QB = quarterback; RB = running back; TE = tight end; WR = wide receiver.
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Echocardiograms.
Of 203 athletes with echocardiograms, 197 (97%) were judged within normal limits for trained athletes (1–3). Ventricular septal thickness was 7 to 12 mm (mean 10 ± 1 mm), LV end-diastolic cavity dimension was 40 to 64 mm (mean 54 ± 4 mm), and ejection fraction was 50% to 75% (mean 60 ± 5%). The other 6 athletes (3%) had septal thicknesses within the ambiguous zone of 13 to 14 mm, which were judged unlikely to represent hypertrophic cardiomyopathy in these highly-trained athletes in the absence of other echocardiographic abnormalities and with normal Doppler inflow velocities (3).
Among 88 athletes with distinctly abnormal ECGs, 33 (38%) had echocardiograms, including only 1 with borderline septal thickness of 14 mm. Systolic anterior motion of the mitral valve (or any other feature of hypertrophic cardiomyopathy), mitral valve prolapse, and evidence of coronary anomalies of wrong sinus origin were absent in each of the 203 athletes.
Univariate/multivariable analyses.
Unadjusted predictors of abnormal ECGs appear in Table 3. Compared with white players, blacks were significantly more likely to have abnormal ECGs (risk ratio [RR] 2.30, 95% confidence interval [CI] 1.84 to 2.87, p < 0.0001), whereas athletes with a larger BSA were less likely to have abnormal ECGs (RR 0.93, 95% CI 0.90 to 0.96, p < 0.0001). After adjustment for all other variables in multivariable analysis, black race was the only independent predictor of an abnormal ECG (RR 2.03, 95% CI 1.56 to 2.64, p < 0.0001), including patterns regarded as most abnormal (RR 2.59, 95% CI 1.18 to 5.67, p = 0.02) (Table 4).
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Discussion
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We evaluated the prevalence of ECG abnormalities in a large biracial population of healthy elite American football players. Diverse ECG abnormalities were present in 25%, including 5% that were characterized as distinctly abnormal with patterns likely to raise clinical suspicion of structural heart disease.
We also found that race was associated with different frequencies of abnormal ECGs. First, a significantly higher proportion of abnormal ECG patterns were present in black compared with white athletes (by >2:1). Second, multivariable analysis showed black race to be an independent predictor of both mildly and markedly abnormal ECGs, even after differences in ECG pattern by player position were taken into account. Specific ECG abnormalities most common in black athletes included increased precordial voltages and diffuse T-wave inversion.
These findings are consistent with historical assertions that ECG patterns might differ between healthy black and white subjects. In the early 1950s, J-point and ST-segment elevation in the right precordial leads was regarded as characteristic of young black male individuals without heart disease (10–12). More recently, several studies have demonstrated a higher prevalence of ECG abnormalities in young black men (13) or athletes (14) without systemic hypertension or cardiac disease.
Xie et al. (13) reported substantial differences in prevalence of LV hypertrophy by ECG in young healthy black (16 of 1,000) compared with white men (2.4 of 1,000). Likewise, in a healthy, middle-age, biracial population, Vitelli et al. (15) reported ECG abnormalities in 8% of black compared with 5% of white men. Finally, in a study population similar to ours, Choo et al. (14) found ST-T abnormalities more commonly in black compared with white football players. These prior observations and the present findings indicate that race is an important independent predictor of abnormal ECG patterns.
These observations have important implications for pre-participation screening strategies in populations of competitive athletes (5). For example, European investigators (4) and the International Olympic Committee (16) have recommended screening programs routinely incorporating 12-lead ECGs, a process employed in Italy over the last 25 years (17). Electrocardiograms are now commonly obtained in U.S. professional athletes (18), particularly those in football and basketball. Therefore, such ECG-based screening programs and those proposed for U.S. high school and college-age athletes (6) could expose black athletes to false positive screening, in which abnormal ECGs unnecessarily raise the suspicion of cardiac disease.
Prevalence of abnormal ECGs differed among the various positions played in professional football, even though all participants were highly-trained athletes involved in competitive sports for much of their lives. For example, abnormal ECGs were more common at positions requiring sprinting and similar bursts of physical activity associated with abrupt elevations in heart rate (i.e., wide receivers, running backs, and defensive backs) but less common at positions with lower levels of exertion (e.g., linemen and place kickers). However, player position was not a strong multivariable determinant of ECG patterns.
Echocardiographic data available in a relatively small subset of athletes offer a measure of substantiation that altered ECG patterns reported here are not manifestations of cardiac disease, and differences identified between ECGs obtained in white and black athletes are based predominantly on race.
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Conclusions
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In conclusion, ECG abnormalities were present in 25% of highly-trained professional football players and were 2-fold more common in black compared with white athletes. Furthermore, black race proved to be the only multivariable predictor of an abnormal ECG. These data have important implications for cardiovascular screening programs routinely incorporating ECGs, suggesting the potential for a high rate of false positive results in black athletes.
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Acknowledgments
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The authors would like to thank Joseph Murphy for editorial assistance.
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Footnotes
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This work was funded by a grant from the National Football League Charities.
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References
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Abstract
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