Longitudinal Aortic Root Dilatation in Collegiate American‐Style Football Athletes

Abstract

Background

Clinically relevant aortic dilatation (>40 mm) and increased cardiovascular risk are common among retired professional American‐style football athletes. Among younger athletes, the effect of American‐style football participation on aortic size is incompletely understood. We sought to determine changes in aortic root (AR) size and associated cardiovascular phenotypes across the collegiate career.

Methods and Results

This was a multicenter, longitudinal repeated‐measures observational cohort study of athletes across 3 years of elite collegiate American‐style football participation. A total of 247 athletes (119 [48%] Black, 126 [51%] White, 2 [1%] Latino; 91 [37%] linemen, 156 [63%] non‐linemen) were enrolled as freshmen and studied at pre‐ and postseason year 1, postseason year 2 (N=140 athletes), and postseason year 3 (N=82 athletes). AR size was measured with transthoracic echocardiography. AR diameter increased over the study period from 31.7 (95% CI, 31.4–32.0) to 33.5 mm (95% CI, 33.1–33.8; P<0.001). No athlete developed an AR ≥40 mm. Athletes also demonstrated increased weight (cumulative mean Δ, 5.0 [95% CI, 4.1–6.0] kg, P<0.001), systolic blood pressure (cumulative mean Δ, 10.6 [95% CI, 8.0–13.2] mm Hg, P<0.001), pulse wave velocity (cumulative mean Δ, 0.43 [95% CI, 0.31–0.56] m/s, P<0.001), and left ventricular mass index (cumulative mean Δ, 21.2 [95% CI, 19.2–23.3] g/m², P<0.001), and decreased E′ velocity (cumulative mean Δ, −2.4 [95%CI, −2.9 to −1.9] cm/s, P<0.001). Adjusting for height, player position, systolic blood pressure, and diastolic blood pressure, higher weight (β=0.030, P=0.003), pulse wave velocity (β=0.215, P=0.02), and left ventricular mass index (β=0.032, P<0.001) and lower E′ (β=−0.082, P=0.001) were associated with increased AR diameter.

Conclusions

Over the collegiate American‐style football career, athletes demonstrate progressive AR dilatation associated with cardiac and vascular functional impairment. Future studies delineating aortic outcomes are necessary to determine whether AR dilation is indicative of maladaptive vascular remodeling in this population.

Nonstandard Abbreviations and Acronyms

AR

aortic root

ASF

American‐style football

PWV

pulse wave velocity

Clinical Perspective.

What Is New?

• Aortic root enlargement occurs with American‐style football participation.

• This aortic enlargement is associated with multiple maladaptive measures of cardiovascular health including arterial stiffening, increased body weight, and decreased diastolic function.

What Are the Clinical Implications?

• American‐style football athletes with clinically relevant aortic dilatation (>40 mm) warrant more frequent clinical monitoring and additional evaluation for underlying cardiovascular risk factors.

Clinically significant aortic dilatation predicts acute aortic events in the general population. ¹ However, recent cross‐sectional data suggest a higher than expected prevalence of clinically significant aortic dilatation (defined as >40 mm in diameter) among healthy aging athletes. ² , ³ The clinical significance of these observations is uncertain and among youthful athletes, the effect of sport participation on aortic root (AR) size is also poorly understood. ⁴ , ⁵ , ⁶ Although prior cross‐sectional data have shown AR size is slightly larger in young athletes, ⁵ , ⁶ , ⁷ , ⁸ there is a dearth of longitudinal data characterizing the impact of sport participation on aortic dimensions.

Among retired professional American‐style football (ASF) athletes, a recent study reported a 30% prevalence of clinically significant aortic dilatation. ³ Although clinical outcomes detailing the prevalence of acute aortic syndromes are lacking in this population, it is well established that retired ASF athletes, particularly those who had increased playing‐time body‐mass index or who were linemen position players, experience increased cardiovascular disease mortality compared with the general population. ⁹ , ¹⁰ Early markers of cardiovascular risk are also common in young, collegiate ASF athletes with increased incident hypertension ¹¹ , ¹² and the development of a maladaptive cardiovascular phenotype characterized by relative arterial stiffening, reduced diastolic function, and concentric left ventricular (LV) hypertrophy. ¹³ , ¹⁴ , ¹⁵ , ¹⁶ Whether active ASF participation also leads to changes in aortic size has not previously been analyzed.

We therefore sought to investigate whether ASF participation leads to AR dilatation, defined in this study as any longitudinal increase in AR diameter. We hypothesized that ASF athletes would demonstrate progressive AR dilatation over the course of collegiate ASF participation and that AR dilatation would be associated with previously described maladaptive ASF cardiovascular phenotypes. ¹⁵ To address this hypothesis, we performed a multicenter, longitudinal repeated measures observational cohort study of collegiate ASF athletes with rigorous cardiovascular phenotyping over the course of the competitive collegiate ASF career.

METHODS

College ASF athletes ≥18 years old were recruited from National Collegiate Athletic Association Division‐I programs at Georgia Institute of Technology (Atlanta, GA) and Furman University (Greenville, SC) and studied between 2014 and 2019. Clinical characteristics, anthropometric measurements, transthoracic echocardiography, and vascular applanation tonometry were prospectively and longitudinally captured for all study participants over this time period. The Emory Institutional Review Board approved all aspects of this study and all participants provided written informed consent. Analytic methods are available upon reasonable request to the corresponding author. Due to potential for subject identification, data are not available for public use.

Study Population

ASF athletes were initially recruited as freshmen each year of the study in parallel with the academic calendar. Participants were then followed prospectively throughout their college career and during the study period. For the freshman season, athletes were studied at 2 time points that included the preseason (baseline) and the immediate conclusion of the season (postseason year 1), approximately 5 to 6 months later. For the sophomore season, athletes were studied at just 1 time point (postseason year 2), approximately 1 year after postseason year 1, and for the junior season, athletes were again studied at just 1 time point (postseason year 3), approximately 1 year after postseason year 2 (Figure 1). Two time points for freshman ASF athletes were included because of the significant cardiovascular plasticity previously demonstrated among first‐year college athletes in response to athletic training. ¹⁴ Because ASF athletes at the participating institutions engage in consistent levels of ASF training throughout the calendar year after the freshman season, only annual postseason study time points were captured beyond the first year (postseason years 2 and 3). Athletes with known hypertension on pharmacotherapy were excluded. Athletes with suspected genetic aortopathy, including those with bicuspid aortic valves, and those who did not complete the first competitive ASF season were also excluded.

Figure 1. Subject enrollment and prospective follow‐up.

Subjects were required to abstain from exercise for >24 hours before data collection. Clinical data including age (years), height (centimeters), current medication use, family history of cardiovascular disease or sudden death, and self‐reported race and ethnicity were collected at baseline. Player position was classified as either lineman or non‐lineman as previously proposed. ¹⁷ All athletes were subject to performance‐enhancing drug testing protocols as per National Collegiate Athletic Association guidelines (generally 1–2 times per season). Weight (kilograms), systolic blood pressure (mm Hg), and diastolic blood pressure (mm Hg) were collected at all time points. Blood pressure was measured after ≥15 minutes of rest using a manual aneroid sphygmomanometer and an appropriately sized cuff and recorded as the average of 3 measurements.

Two‐Dimensional Transthoracic Echocardiography

Transthoracic echocardiography was performed using a commercially available system (Vivid‐I; GE Healthcare, Milwaukee, WI) at all study time points. Two‐dimensional and tissue‐Doppler imaging from standard parasternal and apical positions were performed by experienced sonographers, who were consistent throughout the years of this study. Frame rates were individualized per study for optimal image quality between 60 and 100 Hz. All information was stored digitally, and blinded, poststudy offline data analysis (EchoPAC version 7; GE Healthcare) was performed by study investigators (J.V.T., J.H.K.). Definitions of normality for cardiac structure and function were adopted from the most recent guidelines. ¹⁸ LV mass was measured using the area‐length method (accounts for LV morphology in both the short and long axis) and indexed to body surface area, and LV ejection fraction was calculated using the modified biplane technique. ¹⁸ Comprehensive assessment of cardiac diastolic function using tissue‐Doppler imaging was performed, and tissue velocities (E′, A′, and S′) were measured from color‐coded images at the lateral and septal mitral annulus. E′ was then reported as the average value of the septal and lateral annular measurements. AR diameter was measured in the standard parasternal long‐axis view at end‐diastole using the leading edge to leading edge method ¹⁹ Absolute AR diameter, rather than AR diameter indexed to body size is reported because AR size plateaus at the extremes of body size. ²⁰ Not only is this applicable to ASF athletes, but additional and deliberate weight gain is also a hallmark of competitive ASF training. ²¹

AR Measurement Variability

For quality consistency and assurance, AR diameter was measured in 48 randomly selected echocardiographic studies (12 from each study time point) by a separate study investigator (B.R.W.) who was blinded to all previous measurements. Pearson correlation analysis yielded an r=0.91 (P<0.001). A paired t test used to assess discrepancies among observations revealed no significant variability among observers (mean difference 0.06 mm, P=0.7). Bland–Altman analysis resulted in a mean bias of 0.06 mm (95% CI, −0.25 to 0.37) with upper and lower limits of agreement 2.17 and −2.05, respectively.

Vascular Applanation Tonometry

Arterial stiffness was measured at all time points using high‐fidelity applanation tonometry (SphygmoCor; Atcor Medical, Sydney, Australia), which records sequential high‐quality pressure waveforms at peripheral pulse sites. The primary measure of arterial function was the carotid–femoral pulse wave velocity (PWV), the gold‐standard index of arterial stiffness, ²² measured as previously described. ¹³

Statistical Analysis

Baseline continuous variables are presented as the mean±SD, and categorical variables as percentages. Separate linear mixed‐effects models were constructed to evaluate for longitudinal changes in clinical and cardiovascular measurements, with time being the categorical (baseline, year 1, 2, and 3) independent variable adjusting for player position (non‐lineman or lineman). The predicted marginal means with 95% CIs for the clinical and cardiovascular measurements were reported for each time point. Type III tests of fixed effects were used to evaluate the overall change in each selected variable over the study period. To assess for factors associated with AR diameter, a linear mixed‐effects model was constructed with independent variables including height, player position, weight, systolic blood pressure, diastolic blood pressure, PWV, E′, and LV mass index. All measurements at all available time points for subjects were included in this model. Participant specific random intercepts were incorporated to account for within‐participant correlations. Analyses were performed with SAS software (version 9.4; SAS Institute, Cary, NC). A P value of ≤0.05 was considered significant.

RESULTS

Baseline Characteristics

Between 2014 and 2019, 272 collegiate freshman ASF athletes were serially enrolled in this study. 2 athletes were then excluded, 1 due to the presence of bicuspid aortic valve with associated aortopathy and 1 athlete due to clinically significant aortic dilatation and family history of Marfan syndrome. The final analysis included 247 athletes who completed at least 1 competitive ASF season. Due to the rolling nature of study enrollment aligned with the collegiate academic calendar, 247 were analyzed at baseline and postseason year 1, 140 were analyzed at postseason year 2, and 82 were analyzed at postseason year 3 (Figure 1). At baseline (preseason year 1), the final study cohort was composed of N=119 Black athletes (48%), N=126 White athletes (51%), and N=2 athletes of Latino self‐identified race and ethnicity (1%). N=91 (37%) were linemen and N=156 (63%) non‐linemen (Table 1). There was no significant change in the proportion of linemen versus non‐linemen across the study time points with subject attrition (P=0.45).

Table 1.

Baseline Characteristics

Characteristic	N=247 Athletes
Age, y	18±0.4
Race and ethnicity	119 (48%) Black
	126 (51%) White
	2 (1%) Latino
Player position	91 (37%) Linemen
	156 (63%) Non‐linemen
Height, cm	185±6
Weight, kg	100.2±19.1
Systolic blood pressure, mm Hg	128±12
Diastolic blood pressure, mm Hg	76±10

Longitudinal Changes in Cardiovascular Phenotypes and AR Diameter

Longitudinal changes in cardiovascular phenotypes for all study participants are summarized in Table 2. Adjusting for player position, athletes demonstrated increased weight (cumulative mean Δ, 5.0 [95% CI, 4.1–6.0] kg, P<0.001), systolic blood pressure (cumulative mean Δ, 10.6 [95% CI, 8.0–13.2] mm Hg, P<0.001), and PWV (cumulative mean Δ, 0.43 [95% CI, 0.31–0.56] m/s, P<0.001) from baseline to postseason year 3. Athletes also demonstrated cardiac changes including increased LV mass index (cumulative mean Δ, 21.2 [95% CI, 19.2–23.3] g/m², P<0.001) and decreased E′ (cumulative mean Δ, −2.4 [95% CI, −2.9 to −1.9] cm/s, P<0.001). AR diameter increased over the 3‐year study period (cumulative mean Δ, 1.8 [95% CI, 1.5–2.0] mm, P<0.001) from 31.7 (95% CI, 31.4–32.0) to 33.5 mm (95% CI, 33.1–33.8). In considering just the N=82 who completed 3 full years of collegiate ASF, AR diameter also significantly increased from 31.7 mm (95% CI, 31.1–32.2) to 33.5 mm (95% CI, 33.0–34.1; P<0.001) (Figure 2). In considering differences in the change in AR size by player position (linemen versus non‐linemen), there was no interaction between player position and AR size across study time points (P=0.53). Finally, no athlete started with or developed an AR ≥40 mm during the study period or demonstrated any significant aortic regurgitation at any time point.

Table 2.

Longitudinal Changes in Clinical and Cardiovascular Measurements

Characteristic	Baseline (N=247)	Year 1 postseason (N=247)	Year 2 postseason (N=140)	Year 3 postseason (N=82)	P value
Weight, kg	100.7 (99.2–102.2)	102.4 (100.9–103.9)	103.9 (102.3–105.4)	105.7 (104.1–107.4)	<0.001
Systolic BP, mm Hg	128.5 (126.9–130.1)	133.0 (131.4–134.6)	133.9 (131.9–135.9)	139.1 (136.6–141.6)	<0.001
Diastolic BP, mm Hg	76.0 (74.7–77.2)	76.3 (75.1–77.6)	77.6 (76.0–79.2)	78.3 (76.3–80.3)	0.12
LV mass, g	204.0 (200.2–207.8)	231.1 (227.3–234.9)	241.8 (237.3–246.2)	258.9 (253.6–264.1)	<0.001
LV mass/body surface area, g/m2	89.8 (88.4–91.2)	101.0 (99.6–102.3)	104.5 (102.8–106.2)	111.0 (109.0–113.1)	<0.001
LV internal diameter at end‐diastole, mm	52.2 (51.6–52.7)	53.2 (52.6–53.7)	53.6 (53.0–54.2)	54.2 (53.6–54.9)	<0.001
Mean wall thickness, mm	9.0 (8.9–9.1)	10.0 (9.9–10.1)	10.3 (10.2–10.5)	10.8 (10.7–11.0)	<0.001
Relative wall thickness	0.35 (0.34–0.36)	0.38 (0.37–0.39)	0.39 (0.39–0.40)	0.40 (0.39–0.41)	<0.001
LV ejection fraction, %	61.4 (60.8–62.0)	60.1 (59.5–60.8)	60.4 (59.6–61.3)	60.0 (58.9–61.0)	0.01
E′, cm/s	16.3 (16.0–16.6)	15.2 (14.9–15.5)	14.6 (14.2–15.0)	13.9 (13.4–14.4)	<0.001
Pulse wave velocity, m/s	5.0 (4.9–5.1)	5.2 (5.1–5.3)	5.4 (5.3–5.5)	5.4 (5.3–5.5)	<0.001
Aortic root diameter, mm	31.7 (31.4–32.0)	32.4 (32.1–32.7)	33.0 (32.6–33.3)	33.5 (33.1–33.8)	<0.001

Mean wall thickness: [interventricular septum+posterior wall]/2. E′, average of early diastolic septal and lateral tissue‐Doppler velocities. Relative wall thickness: mean wall thickness/LVIDD. Mean (95% CI), adjusted for player position. BP indicates blood pressure; and LV, left ventricular.

Figure 2. Longitudinal aortic root diameters among athletes present at all time points.

Aortic root size increased over the study period. Violin plot interpretation: the heavy dashed line represents the median aortic root size. The lighter dashed lines represent the interquartile range, and the width represents distribution of aortic root size.

Factors Associated With AR Diameter

In univariate analysis including all measurements per variable at all available time points for subjects (Table 3), height (β=0.108, P<0.001), lineman player position (β=1.57, P<0.001), and higher weight (β=0.056, P<0.001), systolic blood pressure (β=0.028, P<0.001), diastolic blood pressure (β=0.011, P=0.047), PWV (β=0.624, P<0.001), and LV mass index (β=0.045, P<0.001) were associated with larger AR diameter. In addition, lower E′ (β=−0.189, P<0.001) was associated with larger AR diameter. In multivariable mixed‐effects linear regression analysis including all measurements at all available time points for subjects, higher weight (β=0.030, P=0.003), PWV (β=0.215, P=0.02), and LV mass index (β=0.032, P<0.001), and lower E′ (β=−0.082, P=0.001) were associated with increased AR diameter (Table 3).

Table 3.

Factors Associated With Aortic Root Size

Characteristic	Univariate		Multivariable
	β (95% CI)	P value	β (95% CI)	P value
Height, m	0.108 (0.062 to 0.154)	<0.001	0.030 (−0.025 to 0.084)	0.3
Player position	1.57 (0.97 to 2.17)	<0.001	0.021 (−0.812 to 0.853)	0.9
Weight, kg	0.056 (0.043 to 0.069)	<0.001	0.030 (0.011 to 0.050)	0.003*
Systolic BP, mm Hg	0.028 (0.019 to 0.037)	<0.001	0.007 (−0.002 to 0.017)	0.1
Diastolic BP, mm Hg	0.011 (0.00 to 0.023)	0.047	−0.003 (−0.015 to 0.008)	0.5
Pulse wave velocity, m/s	0.624 (0.439 to 0.809)	<0.001	0.215 (0.029 to 0.402)	0.02*
E′, cm/s	−0.189 (−0.238 to −0.139)	<0.001	−0.082 (−0.132 to −0.032)	0.001*
Left ventricular mass/body surface area, g/m2	0.045 (0.037 to 0.053)	<0.001	0.032 (0.023 to 0.041)	<0.001*

BP indicates blood pressure.

^*These values are statistically significant with P<0.05.

DISCUSSION

To our knowledge, this is the first prospective and longitudinal analysis of AR size, inclusive of other cardiovascular structural and functional measures, in a young, athletic population. Key findings are summarized as follows. First, progressive AR enlargement occurs throughout the entirety of collegiate ASF participation. Second, increased AR size is associated with established ASF‐related maladaptive cardiovascular phenotypes including vascular stiffening ¹³ and reduced diastolic function. ¹⁴ , ¹⁵ Taken together, mild AR dilatation appears to have a causal relationship with collegiate ASF participation and may represent an additional maladaptive cardiovascular phenotypes observed in this athletic population.

Data ascertaining the effect of sport participation on aortic size in young athletes are limited and come primarily from cross‐sectional and case–control studies. ⁵ , ⁶ , ²³ , ²⁴ In a meta‐analysis from Iskandar and Thompson, aortic diameter was largest at the level of the sinuses of Valsalva and 3.2 mm larger in athletes versus nonathletes. ⁵ In the largest cross‐sectional cohort study analyzing AR size in multisport Italian athletes (N=2317), Pelliccia and colleagues observed clinically significant AR dilatation was rare. In a secondary analysis in this study, a control cohort of mixed‐sport athletes (N=115, 62% male) was followed periodically and male athletes demonstrated just 0.7 mm (P<0.01) AR growth over 9±4 years of continuous training. Results from the present study add to our understanding of the effect of sport participation on the aorta. Rigorous and standardized serial imaging assessments over multiple years demonstrate progressive AR dilatation in ASF athletes. Moreover, in contrast to data from Pelliccia, our results suggest there may be strength sport specificity in the context of AR enlargement. Importantly, our findings were repeated measures and aligned with seasonal training versus cross‐sectional, which could be subject to numerous unknown confounders.

Our findings are best interpreted, first, in the context of aortic data taken from retired National Football League athletes. It is well established that retired professional ASF athletes, particularly those with obese playing time body mass index, carry increased cardiovascular risk later in life. ⁹ , ¹⁰ , ²⁵ Intriguingly, in a cohort of 206 retired ASF players, 30% demonstrated clinically significant aortic dilatation and significantly increased ascending aortic size compared with a matched cohort from the Dallas Heart Study‐2. ³ Whether aneurysmal dilatation of the aorta contributes to increased cardiovascular mortality in retired ASF athletes is uncertain. Moreover, whether early AR enlargement, as observed in the present study, predicts later‐life aortic enlargement is also unknown. As such, caution is warranted when applying our data to observations taken from retired ASF athletes. Second, it is also well established that young collegiate ASF athletes manifest early traditional cardiovascular risk, particularly hypertension ¹¹ , ¹⁴ , ²⁶ and may develop a maladaptive cardiovascular phenotype ¹⁵ consisting of relative arterial stiffening, ¹³ reduced diastolic function, ¹⁴ , ¹⁵ ventricular‐arterial uncoupling, ²⁶ and concentric left ventricular hypertrophy. ¹¹ , ¹⁵ , ¹⁶ Progressive AR dilatation, associated with increased weight, arterial stiffening, and reduced diastolic function further suggests AR enlargement observed in ASF athletes may also be a maladaptive consequence related to traditional early cardiovascular risk. Finally, although AR dilatation is also common in Masters endurance athletes, ² endurance athletes generally possess lower cardiovascular risk profiles. ²⁷ At present, it is unknown whether youthful endurance athletes develop longitudinal aortic enlargement.

The effect of differences in sport‐specific hemodynamics, dynamic versus static exercise, on AR size is unclear. ASF training is generally characterized by a higher volume of isometric/static exercise, particularly for the lineman player position. ²¹ Conceptually, the hemodynamic pressure challenge inherent to static training could lead to aortic enlargement. ⁸ , ²⁸ Indeed, multiple measures of increased arterial stiffening have been reported in young strength‐trained athletes, ²⁸ , ²⁹ , ³⁰ and in the present study we note that AR size is associated with PWV, a measure of central aortic stiffening. However, in other cross‐sectional aortic analyses of athletes, AR size may be larger in endurance‐trained versus strength‐trained athletes. ⁵ , ⁷ , ²⁴ As such, strength training may be representative of just 1 contributor to ASF‐associated AR dilatation, but in a more complex and multifactorial process. Other ASF‐specific contributing risk factors could include rapid deliberate weight gain, ²¹ hypertension ¹² or hypertensive response to exercise, and frequent nonsteroidal anti‐inflammatory drug use. ³¹ Although elite collegiate ASF athletes also typically accrue years of prior ASF exposure in high school, previous data suggest that the temporal acceleration of maladaptive cardiovascular phenotypes occurs after the transition from high school to collegiate ASF. ¹⁴

There are important clinical implications taken from these data. First, the presence of early traditional cardiovascular risk associated with changes in cardiovascular phenotypes continues to emphasize the critical need to focus on early preventive efforts, which include counseling, education, and pharmacotherapy when clinically indicated, in young ASF athletes. Second, for ASF athletes with bicuspid aortic valves or incidentally discovered clinically significant AR dilatation, additional clinical adjudication should be pursued in consideration of BP pharmacotherapy or sports eligibility. Maximum effort exercise testing for delineation of exercise BP changes should be considered. Importantly, our results do not support strength training restrictions or competitive sport disqualification for these athletes as none of the athletes in our cohort developed AR >40 mm. ³² Athletes with clinically significant aortic dilatation do warrant more frequent surveillance imaging and clinical follow‐up for elevated blood pressures as well as further investigation for other underlying cardiovascular risk factors. Determination of the appropriate exercise prescription and sports eligibility should ultimately be guided by an athlete‐centered shared decision‐making approach. ³³ Future studies are warranted to determine long‐term aortic outcomes in competitive ASF athletes with clinically significant aortic dilatation.

We acknowledge several limitations to this study. First, AR diameter was measured with echocardiography, which can inaccurately measure maximal vessel diameter and be subject to interobserver variability. ³⁴ However, the repeated‐measures design of this study mitigates this limitation. Analysis of aortic size was also limited to AR measurement, although this is typically the most studied aortic dimension and may be more relevant to future acute aortic events. ³⁵ Second, although collegiate ASF training incorporates intense isometric training regimens, we did not quantify exercise load or perform exercise testing to evaluate exercise blood pressure, both of which may theoretically affect AR size. Third, we were unable to evaluate athletes who were lost to attrition and ceased competitive ASF training. This represents a key future research direction to define the cardiovascular changes that may occur with ASF detraining. Fourth, ASF culture includes many unique factors that may influence cardiovascular risk including deliberate weight gain and a high prevalence of nonsteroidal anti‐inflammatory drug use, thus limiting generalizability to other non‐ASF athletes. ²¹ , ³¹ Finally, no women were included in this study as National Collegiate Athletic Association ASF athletes are generally all male and we did not include a nonathlete control population.

CONCLUSIONS

ASF athletes develop progressive AR dilatation over the course of the collegiate career. AR dilatation is associated with increased weight, vascular stiffening, and relative reductions in diastolic function, suggesting that increases in AR size may represent a maladaptive structural alteration in young ASF athletes. Future studies are warranted to determine long‐term aortic outcomes in competitive ASF athletes with clinically relevant AR or aortic dilatation.

Sources of Funding

This work was entirely supported by National Institutes of Health/National Heart, Lung, and Blood Institute research grant K23 HL128795 (to Dr Kim). Dr Tso was supported by the Abraham J. & Phyllis Katz Foundation.

Disclosures

Dr Kim receives compensation serving in his role as team cardiologist for the Atlanta Falcons. Dr Baggish receives compensation serving in his role as team cardiologist for the New England Patriots. The remainder of the authors report no financial disclosures.