Prevalence of Clinical and Subclinical Myocarditis in Competitive Athletes With Recent SARS-CoV-2 Infection: Results From the Big Ten COVID-19 Cardiac Registry.

Importance: Myocarditis is a leading cause of sudden death in competitive athletes. Myocardial inflammation is known to occur with SARS-CoV-2. Different screening approaches for detection of myocarditis have been reported. The Big Ten Conference requires comprehensive cardiac testing including cardiac magnetic resonance (CMR) imaging for all athletes with COVID-19, allowing comparison of screening approaches. Objective: To determine the prevalence of myocarditis in athletes with COVID-19 and compare screening strategies for safe return to play. Design, Setting, and Participants: Big Ten COVID-19 Cardiac Registry principal investigators were surveyed for aggregate observational data from March 1, 2020, through December 15, 2020, on athletes with COVID-19. For athletes with myocarditis, presence of cardiac symptoms and details of cardiac testing were recorded. Myocarditis was categorized as clinical or subclinical based on the presence of cardiac symptoms and CMR findings. Subclinical myocarditis classified as probable or possible myocarditis based on other testing abnormalities. Myocarditis prevalence across universities was determined. The utility of different screening strategies was evaluated. Exposures: SARS-CoV-2 by polymerase chain reaction testing. Main Outcome and Measure: Myocarditis via cardiovascular diagnostic testing. Results: Representing 13 universities, cardiovascular testing was performed in 1597 athletes (964 men [60.4%]). Thirty-seven (including 27 men) were diagnosed with COVID-19 myocarditis (overall 2.3%; range per program, 0%-7.6%); 9 had clinical myocarditis and 28 had subclinical myocarditis. If cardiac testing was based on cardiac symptoms alone, only 5 athletes would have been detected (detected prevalence, 0.31%). Cardiac magnetic resonance imaging for all athletes yielded a 7.4-fold increase in detection of myocarditis (clinical and subclinical). Follow-up CMR imaging performed in 27 (73.0%) demonstrated resolution of T2 elevation in all (100%) and late gadolinium enhancement in 11 (40.7%). Conclusions and Relevance: In this cohort study of 1597 US competitive athletes with CMR screening after COVID-19 infection, 37 athletes (2.3%) were diagnosed with clinical and subclinical myocarditis. Variability was observed in prevalence across universities, and testing protocols were closely tied to the detection of myocarditis. Variable ascertainment and unknown implications of CMR findings underscore the need for standardized timing and interpretation of cardiac testing. These unique CMR imaging data provide a more complete understanding of the prevalence of clinical and subclinical myocarditis in college athletes after COVID-19 infection. The role of CMR in routine screening for athletes safe return to play should be explored further.

Left atrial enlargement and its association with left atrial strain in university athletes participated in 2015 Gwangju Summer Universiade.

AIMS: Intensive and repetitive athletic training may result in cardiac geometric changes, but the determinants of left atrial (LA) enlargement (LAE) has been poorly studied. We investigated incidence and determinants of LAE and its association with LA strains in highly trained university athletes. METHODS AND RESULTS: A total of 1073 athletes (451 females, 22.4 ± 2.4 years old) who were able to measure LA size, volume, and strains during 2015 Gwangju Summer Universiade were enrolled. LAE was defined as the increased LA volume index > 42 mL/m2. LA strains, reservoir, conduit, and contractile were measured by 2D speckle tracking method, and LA reservoir strain < 27.6% was considered as abnormal. LAE was developed in 205 athletes (19.1%). In univariate analysis, male [odds ratio (OR) = 1.679], Caucasian (OR = 1.746), non-African descent (OR = 1.804), body muscle mass (OR = 1.056), body fat mass (OR = 0.962), systolic blood pressure (OR = 1.012), heart rate (OR = 0.980), sports type with cardiovascular (CV) demand (OR = 1.474), training time (OR = 1.011), left ventricular (LV) global longitudinal strain (LVGLS, OR = 0.906), and LV stroke volume (LVSV, OR = 1.044) were significantly associated with LAE. In multivariate logistic regression analysis, heart rate (OR = 0.961) and sports type with CV demand (OR = 1.299), LVGLS (OR = 0.865) and LVSV (OR = 1.013) were independent determinants of LAE. Abnormal LA reservoir strain was noted in 56 athletes (5.2%), and the incidence of abnormal value was not different between two groups; 42 athletes (4.8%) in LAE vs. 14 (6.8%) in no LAE group (P = 0.293). CONCLUSION: LAE was common in university athletes (19.1%) and associated with heart rate, sports type with CV demand, LVGLS, and LVSV. Although LAE was significantly associated with the lower LA reservoir strain, the incidence of abnormal value was very low (5.2%) and indifferent between LAE and no LAE group.

University athletes and changes in cardiac geometry: insight from the 2015 Gwangju Summer Universiade.

AIMS: There is a paucity of data regarding the changes of cardiac geometry in highly trained international and multiracial university athletes. We aimed to investigate the incidence of structural cardiac abnormalities and changes of cardiac geometry in highly trained university athletes. METHODS AND RESULTS: Comprehensive echocardiographic studies were performed in 1185 university athletes through the Check-up Your Heart Program during the 2015 Gwangju Summer Universiade. Participants were divided into two groups: normal vs. abnormal left ventricular (LV) geometry (concentric remodelling, concentric hypertrophy, or eccentric hypertrophy). Structural heart diseases associated with sudden cardiac death were not identified, but minor structural cardiac abnormalities were common in university athletes. One hundred and fifty-six athletes (13.2%) had abnormal LV geometry; concentric remodelling (n = 73, 6.2%), concentric hypertrophy (n = 25, 2.1%), and eccentric hypertrophy (n = 58, 4.9%). Abnormal LV geometry was significantly more common in athletes of African descent and in endurance, mixed, or power disciplines. In multivariate logistic regression analysis, athletes of African descent [odds ratio (OR) 2.16, 95% confidence interval (CI) 1.34-3.46; P = 0.001], endurance disciplines (OR 1.79, 95% CI 1.26-2.54; P = 0.001), and training time (OR 1.01, 95% CI 1.00-1.02; P = 0.045) were independent predictors of abnormal LV geometry. CONCLUSION: A large scale cardiovascular screening programme of the 2015 Summer Universiade demonstrated that abnormal LV geometry is not uncommon (13.2%) and concentric remodelling is the most common pattern of LV geometric change in young trained university athletes. Race, type of sport, and training time are significant predictors of abnormal LV geometry. Structural cardiac abnormalities are common in university athletes even though they are minor abnormalities.

Characterization of the brachial artery shear stress following walking exercise.

Habitual exercise provides repeated episodes of elevated vascular shear stress (SS), which may be a mechanism for repair of endothelial dysfunction in disease. Our aim was to determine the brachial artery SS during the 3-hour period following single bouts of low, moderate, and high-intensity walking exercise. In a randomized crossover design, 14 men walked for 45 minutes on a treadmill at 25%, 50% and 75% of VO2peak separated by 2-7 days. Using Doppler ultrasonography, brachial artery SS was assessed immediately after exercise and then hourly for 3 hours. High-intensity walking elicited greater (p<0.05) post-exercise SS compared with low and moderate intensity. In addition, a 3x4 (intensity x time) ANOVA indicated an absence of interaction (p=0.369) and a decline in post-exercise SS over time (p<0.0001) which was abolished after 2 hours. Thus, we found that brachial artery SS is greatest following high-intensity walking and that the rate of decline in SS is similar across all walking intensities.

The flow-mediated dilation response to acute exercise in overweight active and inactive men.

OBJECTIVE: Inflammation has been found to play a role in the etiology of cardiovascular disease as well as provoke endothelial dysfunction. Inflammatory cytokines associated with endothelial function are interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). IL-6 is exercise intensity dependent and has been shown to inhibit TNF-alpha expression directly. The aim of this study was to investigate the interaction of IL-6 and TNF-alpha on endothelial function in response to acute exercise in overweight men exhibiting different physical activity profiles. METHODS AND PROCEDURES: Using a randomized mixed factorial design, 16 overweight men (8 active, maximal exercise capacity (VO(2)peak) = 34.2 +/- 1.7, BMI = 27.4 +/- 0.7 and 8 inactive, VO(2)peak = 30.9 +/- 1.2, BMI = 29.3 +/- 1.0) performed three different intensity acute exercise treatments. Brachial artery flow-mediated dilation (FMD) and subsequent blood samples were taken pre-exercise and 1 h following the cessation of exercise. RESULTS: Independent of exercise intensity, the active group displayed a 24% increase (P = 0.034) in FMD following acute exercise compared to a 32% decrease (P = 0.010) in the inactive group. Elevated (P < 0.001) concentrations of IL-6 following moderate (50% VO(2)) and high (75% VO(2)) intensity acute exercise were observed in both groups; however, concentrations of TNF-alpha were unchanged in response to acute exercise (P = 0.584). DISCUSSION: The FMD response to acute exercise is enhanced in active men who are overweight, whereas inactive men who are overweight exhibit an attenuated response. The interaction of IL-6 and TNF-alpha did not provide insight into the physiological mechanisms associated with the disparity of FMD observed between groups.

Reproducibility of the flow-mediated dilation response to acute exercise in overweight men.

Flow-mediated dilation (FMD) has been established as a reliable noninvasive measurement of endothelial function. The reproducibility of FMD under resting conditions has previously been reported; however, the reproducibility of FMD in response to exercise remains to be investigated. On two separate days, we determined if flow-mediated dilation is reproducible in response to acute exercise in nine overweight men. Following pre-exercise FMD measurements, subjects were asked to walk on a treadmill for 45 min at 50% of their VO(2)peak. Subsequently, FMD was measured immediately, and every hour for 3 h thereafter. Reproducibility of FMD following exercise was assessed utilizing: (1) a two-way analysis of variance (ANOVA), (2) Intraclass correlation coefficients (ICC), (3) Pearson correlations (r), and (4) coefficient of variation (CV %) and coefficient of variation prime (CV') for FMD at each time-period. Four acceptable reproducibility assessments were required to confirm FMD reproducibility in response to acute exercise. No differences (F(1,8) = .01; p = 0.942) in FMD were observed between trials collapsing for time. All the ICC(FMD) fell within the reproducible criterion set and are as follows: pre-exercise 0.602, immediately post 0.840, 1 h post 0.632, 2 h post 0.724 and 3 h post 0.631. The correlation and the average CV% for FMD between trials was 0.579% and 25.2%, respectively. The FMD response to an acute bout of moderate treadmill exercise appears to be as reproducible as FMD measured during resting conditions. The findings of the present study support the use of FMD as an outcome variable in response to acute exercise.

The effect of acute exercise on endothelial function following a high-fat meal.

The transient impairment of endothelial function following a high-fat meal is well established. Brachial artery flow-mediated dilation (FMD) decreases between 2 and 6 h post ingestion. Whether this impairment can be reduced with acute aerobic exercise has not been investigated. The purpose of this study was to investigate if a single sustained aerobic exercise session can counteract the postprandial attenuation in brachial artery FMD associated with the ingestion of a high-fat meal. Eight apparently healthy adults (five men, three women), age 25.5 +/- 0.8 years, performed three treatment conditions in a counter-balanced design: (1) low-fat meal alone (LFM), (2) high-fat meal alone (HFM), and (3) one session of aerobic exercise presented 2 h after ingesting a high-fat meal (HFM-EX). The examination of brachial artery FMD was performed at baseline and 4 h following the ingestion of the meal for each treatment condition. A 3 x 2 (treatment x time) repeated measures ANOVA exhibited a significant interaction (P = 0.019). Preprandial FMDs were similar (P = 0.863) among all three treatment conditions. The FMDs following the LFM (7.18 +/- 1.31%) and HFM-EX (8.72 +/- 0.94%) were significantly higher (P = 0.001) than the FMD following the HFM (4.29 +/- 1.64%). FMD was significantly elevated above preprandial values following the HFM-EX (5.61 +/- 1.54 to 8.72 +/- 0.94%, P = 0.005) but was unchanged following the LFM (6.17 +/- 0.94 to 7.18 +/- 1.31%, P = 0.317) and the HFM (5.73 +/- 1.23 to 4.29 +/- 1.64%, P = 0.160). These findings suggest that a single aerobic exercise session cannot only counteract the postprandial endothelial dysfunction induced by the ingestion of a high-fat meal, but also increase brachial artery FMD in apparently healthy adults.

Accumulation of physical activity leads to a greater blood pressure reduction than a single continuous session, in prehypertension.

BACKGROUND: Despite limited research, the accumulation of physical activity has been recommended for the treatment of prehypertension. OBJECTIVES: To compare the duration and magnitude of blood pressure reduction after accumulated physical activity with that after a single session of continuous physical activity, and to investigate sympathetic modulation as a possible mechanism for the reduction in blood pressure after each acute session. METHODS: Prehypertensive adults (n = 21) participated in a randomized crossover design. Ambulatory blood pressure and heart rate variability (Holter monitoring) were measured for 12 h after accumulated physical activity (4 x 10-min walks (1/h for 4 h) at 50% of VO2peak), continuous physical activity (40-min walk at 50% of VO2peak) and control treatments. Blood pressure and heart rate variability after each activity treatment were compared with the respective periods from the control treatment. Heart rate variability was correlated with reduction in blood pressure. RESULTS: Systolic blood pressure (SBP) was reduced for 11 h after accumulated physical activity (P < 0.01), and for 7 h after continuous physical activity (P < 0.05). Diastolic blood pressure (DBP) was reduced for 10 h after accumulated physical activity (P < 0.05) and for 7 h after continuous physical activity (P < 0.05). With accumulated physical activity, the differences in normalized low-frequency (r = 0.517, P < 0.01) and high-frequency (r = -0.503, P < 0.05) power were correlated with reduction in SBP and the differences in normalized low-frequency (r = 0.745, P < 0.001), high-frequency (r = -0.738, P < 0.001) powers, and low frequency: high frequency ratio (r = 0.756, P < 0.001) were correlated with reduction in DBP. With continuous physical activity, the difference in low frequency: high frequency ratio (r = 0.543, P < 0.05) was correlated with reduction in DBP. CONCLUSION: The accumulation of physical activity appears to be more effective than a single continuous session in the management of prehypertension. Sympathetic modulation was associated with reduced blood pressure after each session.

Variability of flow-mediated dilation measurements with repetitive reactive hyperemia.

To capture the response of an acute intervention, multiple post intervention measurements of flow-mediated dilation (FMD) must be performed. The effect of repetitive reactive hyperemia on endothelial function and the measurement of FMD are unknown. The purpose of this investigation was (1) to examine the effect of repetitive reactive hyperemia on brachial artery FMD and (2) to determine whether brachial artery FMD is stable during a 2-h morning period. We investigated FMD in 20 apparently healthy college students on three randomized treatment days every 30 min (T30), 60 min (T60), and 120 min (T120) throughout a 2-h morning period (08.00 h to 10.00 h). An ANOVA (p > 0.05) and ICC (> 0.40) were both needed to confirm no difference among repetitive reactive hyperemia treatments. In response to repetitive reactive hyperemia, there was no difference (p = 0.307; ICC > 0.40) within the first and last FMD measurements of each treatment condition or between treatment conditions (p = 0.344; ICC > 0.40). FMD was similar (p = 0.348) throughout the 2-h morning period. In conclusion, repetitive reactive hyperemia over a 2-h period has no effect on FMD measurements in apparently healthy college students. In addition, this study found no time trends for FMD measurements during the 2-h morning period to allow for pre/post intervention FMD measurements.

A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation.

The measurement of brachial artery vasodilation in response to a hyperaemic stimulus has been used extensively to assess changes in endothelial function. However, whether or not similar changes occur in response to an active hyperaemic stimulus is unknown. The purpose of the present study was to compare brachial artery vasodilation in response to an active compared with a reactive hyperaemic stimulus following a known perturbation of endothelial function. Eight apparently healthy adults were assigned to four treatment conditions in a counter-balanced design: (i) low-fat meal with active hyperaemic stimulus (LFM-A), (ii) high-fat meal with active hyperaemic stimulus (HFM-A), (iii) low-fat meal with reactive hyperaemic stimulus (LFM-R), and (iv) high-fat meal with reactive hyperaemic stimulus (HFM-R). Meals were ingested at 08:00 hours on each treatment day. Brachial artery vasodilation was assessed via ultrasound 4 h after ingestion of each meal. The active hyperaemic stimulus was induced by 5 min of rhythmic handgrip exercise, whereas reactive hyperaemia was induced by 5 min of forearm occlusion. Brachial artery vasodilation was expressed as the percentage change in diameter from baseline to post-active/reactive hyperaemia. Using a 2x2 repeated measures ANOVA, a significant stimulusxmeal interaction (P=0.025) was found. Simple main effects revealed no difference (P=0.541) in brachial artery vasodilation between LFM-A (5.75+/-1.64%) and HFM-A (6.39+/-1.45%); however, a significant decrease (P=0.014) in brachial artery vasodilation was found in the HFM-R (4.29+/-1.64%) compared with the LFM-R (7.18+/-1.13%) treatment. In conclusion, the measurement of brachial artery vasodilation in response to active hyperaemia did not detect a change in endothelial function following a single perturbation meal, whereas reactive hyperaemia did.