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
Importance: Diseases of despair (ie, mortality or morbidity from suicidality, drug abuse, and alcoholism) were first characterized as increasing in rural White working-class populations in midlife with low educational attainment and associated with long-term economic decline. Excess mortality now appears to be associated with working-class citizens across demographic and geographic boundaries, but no known qualitative studies have engaged residents of rural and urban locales with high prevalence of diseases of despair to learn their perspectives. Objective: To explore perceptions about despair-related illness and potential intervention strategies among diverse community members residing in discrete rural and urban hotspots. Design, Setting, and Participants: In this qualitative study, high-prevalence hotspots for diseases of despair were identified from health insurance claims data in Central Pennsylvania. Four focus groups were conducted with 60 community members in organizations and coalitions from 3 census block group hotspot clusters in the health system between September 2019 and January 2020. Focus groups explored awareness and beliefs about causation and potential intervention strategies. Main Outcomes and Measures: A descriptive phenomenological approach was applied to thematic analysis, and a preliminary conceptual model was constructed to describe how various factors may be associated with perpetuating despair and with public health. Results: In total, 60 adult community members participated in 4 focus groups (44 women, 16 men; 40 White non-Hispanic, 17 Black, and 3 Hispanic/Latino members). Three focus groups with 43 members were held in rural areas with high prevalence of diseases of despair, and 1 focus group with 17 members in a high-prevalence urban area. Four themes emerged with respect to awareness and believed causation of despair-related illness, and participants identified common associated factors, including financial distress, lack of critical infrastructure and social services, deteriorating sense of community, and family fragmentation. Intervention strategies focused around 2 themes: (1) building resilience to despair through better community and organizational coordination and peer support at the local level and (2) encouraging broader state investments in social services and infrastructure to mitigate despair-related illness. Conclusions and Relevance: In this qualitative study, rural and urban community members identified common factors associated with diseases of despair, highlighting the association between long-term political and economic decline and public health and a need for both community- and state-level solutions to address despair. Health care systems participating in addressing community health needs may improve processes to screen for despair (eg, social history taking) and codesign primary, secondary, and tertiary interventions aimed at addressing factors associated with distress. Such actions have taken on greater urgency with the COVID-19 pandemic.