ABSTRACT
It has been almost two years since the Covid‐19 pandemic hit, with over 5 million deaths globally. It is known that endothelial activation and dysfunction play a crucial role in Covid‐19 pathogenesis. Evidence of widespread endothelial injury is found in advanced cases of Covid‐19, especially in people with cardiovascular comorbidities. However, the effects of Covid‐19 on endothelial function in unique cohorts such as young athletes have been largely unexplored. This study evaluated endothelium function by noninvasive flow‐mediated dilation (FMD) in a sample of 14 college athletes (10M/4F, 18‐23 yrs, BMI, 23.8 ± 1.6 kg/m2) after testing positive for Covid‐19. All athletes had Covid‐19 with mild or no symptoms and did not require hospitalization. The study was performed 24 ± 10 days (13‐44 days) after having Covid‐19 positive tests. We also involved 10 BMI similar healthy young subjects as controls (7M/3F, 20‐25 yrs, BMI, 24.2±2.0 kg/m2). Baseline brachial artery diameters and the largest diameters after post cuff release were measured to calculate FMD. Brachial blood flow mean velocities and diameters were also recorded within 20 seconds after cuff release for calculating the shear rate (8 * mean velocity/ diameter). The baseline brachial artery diameter was significantly larger in the athlete group versus the control group (4.32±0.63 mm vs. 3.54±0.42 mm, p=0.02). The FMD was significantly lower in the athlete group than in the control group (6.49±2.05% vs. 11.05±4.08%, p=0.02). This finding is consistent with the previous reports that FMD was significantly lower in healthy athletes compared with controls. However, FMD adjusted for the ratio of flow‐mediated dilation and shear rate did not show a statistical difference between groups (0.058±0.028 %/s‐1 vs. 0.076±0.056 %/s‐1, p=0.33), even after evaluating baseline diameter as a covariate. Despite the need for extended acute and chronic observations and a healthy athlete control group, our findings suggest endothelial resilience in response to Covid‐19 infection in young athletes, which may explain their mild or asymptomatic status.
ABSTRACT
To date, more than 46 million people in the United States have contracted the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), which causes COVID‐19. Over 700 thousand total cases have been linked to American colleges and universities. Post‐acute sequelae of SARS‐CoV‐2 infection may affect varied systems. It was reported that sympathetic nerve activity following SARS‐CoV‐2 infection was elevated in young individuals. Cardiovascular autonomic function post‐acute SARS‐CoV‐2 infection in other populations such as athletes, however, has not been thoroughly investigated. Collegiate athletes are a unique population given that they might have a high level of physical fitness before the infection. The present study examined 16 collegiate athletes (12 men and 4 women, age: 20±1 yrs, height: 181±10 cm, weight: 81±18 kg) who were evaluated ~2 weeks after testing positive for SARS‐CoV‐2 by polymerase chain reaction assay. These subjects were asymptomatic or with mild/moderate symptoms during infection. None of the subjects had been hospitalized for COVID‐19 and all subjects were asymptomatic at the time of the study. Beat‐by‐beat blood pressure (BP) with Finometer, and heart rate (HR) from ECG were recorded during 10 minutes of supine rest, Valsalva maneuver, slow breathing (6 breaths/min), handgrip exercise, and 10 minutes of standing. BP, HR, heart rate variability (HRV), and cardiac baroreflex sensitivity (CBRS), and venous blood aldosterone and renin levels were analyzed. The vagal tone index from HRV in 3 of 16 athletes was lower than normative values. The responses in BP to Valsalva maneuver during phases IIa (i.e., “early”) and IIb (i.e., “late”) were mildly abnormal in 4 athletes and moderately abnormal in one athlete. The Valsalva ratio was below the normal range in 6 athletes. In response to slow breathing, the respiratory sinus arrhythmia amplitude was below the normal range in 3 athletes. In response to handgrip exercise, one athlete had an atypical response where BP decreased while HR was increased from baseline. Three of the subjects were unable to tolerate an orthostatic challenge for 10 minutes. Four out of 16 athletes had abnormally elevated renin activity and 1 out 16 elevated aldosterone levels. It is important to note that while several athletes had abnormal responses to the various autonomic tests, these abnormalities did not correlate with symptoms seen during the infection. Our data suggest that SARS‐CoV‐2 infection may reduce parasympathetic and increase sympathetic tone and may contribute to the autonomic disfunction associated in a subset of collegiate athletes even after recovering from COVID‐19. This study provides further evidence for potential long‐term cardiovascular autonomic effects of Covid‐19 infection even in healthy young trained athletes. Further studies with a larger patient population as well as suitable healthy control subjects are warranted.
ABSTRACT
COVID-19 is a global pandemic that has had a devastating effect on the health and economy of much of human civilization. While the acute impacts of COVID-19 were the initial focus of concern, it is becoming clear that in the wake of COVID-19, many patients are developing chronic symptoms that have been called Long-COVID. Some of the symptoms and signs include those of postural tachycardia syndrome (POTS). Understanding and managing long-COVID POTS will require a significant infusion of health care resources and a significant additional research investment. In this document from the American Autonomic Society, we outline the scope of the problem, and the resources and research needed to properly address the impact of Long-COVID POTS.