Covassin, Naima

Background Disruption in rest‐activity rhythm (RAR) is an emerging risk factor for cardiovascular disease (CVD) and mortality, but the strength of evidence is unclear. Therefore, we conducted a systematic review and meta‐analysis to assess associations between RAR characteristics and cardiovascular disease incidence or prevalence, cardiovascular mortality, and all‐cause mortality. Methods A systematic search was conducted in PubMed, Web of Science, Cochrane Library, and Embase for cohort or cross‐sectional studies published up to August 2025. The exposure variables were nonparametric RAR parameters, including interdaily stability (describing day‐to‐day stability of the RAR), intradaily variability (a measure of RAR fragmentation), and relative amplitude (indicating robustness or strength of the RAR). The primary outcomes were cardiovascular mortality and all‐cause mortality. The secondary outcomes included cardiovascular disease prevalence and incidence. Results Seven studies involving 109 365 participants were included. Pooled results showed that higher intradaily variability was associated with a significantly increased risk of all‐cause mortality (hazard ratio [HR], 1.05 [95% CI, 1.02–1.09]) and cardiovascular disease prevalence (odds ratio, 1.73 [95% CI, 1.21–2.47]). Lower relative amplitude was significantly associated with higher cardiovascular mortality (HR, 1.50 [95% CI, 1.13–1.98]) and all‐cause mortality (HR, 1.46 [95% CI, 1.27–1.68]). Interdaily stability showed no significant associations with any outcome. Conclusions Measures of disrupted rest‐activity rhythms were associated with increased cardiovascular mortality, and all‐cause mortality. These findings support using RAR metrics as early, noninvasive risk indicators. Future work should investigate whether appropriately timed physical activity and sleep, as well as other interventions targeting RAR can mitigate cardiovascular risk.

Abstract Background The implications of poor sleep for cardiovascular disease risk are increasingly recognised. Although previous research has focused on clinical sleep disorders, emerging evidence highlights the relevance of subclinical sleep aspects for cardiovascular health. Sleep midpoint, an index of sleep timing and a proxy of circadian phase, has been shown to be associated with markers of cardiometabolic risk, including obesity, in the general population. Purpose We aimed to assess whether sleep midpoint was related to body composition measures in patients with coronary heart disease enrolled in cardiac rehabilitation (CR). Methods Study participants were recruited from the patient population referred to our CR center for acute coronary syndrome or coronary revascularisation. Shift work was exclusionary. Participants underwent sleep testing prior to entering the CR program, including completion of one week of wrist actigraphy and sleep log. Using actigraphy-derived sleep metrics, sleep midpoint was calculated as the middle time (hh:mm) between bedtime and wake up time for each individual night, and averaged across the monitoring week. Based on the median sleep midpoint of the sample, participants were categorised as having early (before 2:42) or late (after 2:42) sleep midpoint. Body composition and regional fat distribution were determined by whole-body dual-energy absorptiometry (DEXA). Between-group characteristics were compared using independent t-test, Mann-Whitney U test and Chi-square statistics as appropriate. Linear regression was used to test the association between sleep midpoint and body fat measures. Results Thirty-one participants (26 males, 64.7±12.5 years) completed both actigraphy and DEXA assessments. Demographics, lifestyle, and clinical characteristics were similar between patients with early sleep midpoint (n=15; sleep midpoint, hh:mm: 2:00, range 0:57 to 2:41) and patients with late sleep midpoint (n=16; sleep midpoint 3:18, range 2:42 to 4:17). Despite comparable body mass index between groups (p=0.21), patients with late sleep midpoint had significantly higher total body fat percentage (p=0.017), android fat percentage (p=0.015), and gynoid fat percentage (p=0.045). Late sleep midpoint remained significantly associated with adiposity measures in age- and sex-adjusted analysis (total body fat percentage, beta = 0.371, 95% CI 0.063 to 0.68; android fat percentage, beta = 0.394, 95% CI 0.078 to 0.71; gynoid fat percentage, beta = 0.301, 95% CI 0.007 to 0.596). Conclusions Late sleep midpoint was associated with excess adiposity in patients with coronary heart disease enrolled in CR. These findings support the predictive value of sleep timing for cardiometabolic risk and emphasise the importance of objective sleep assessment for secondary prevention.

Augmented cardiovascular responses to spontaneous nocturnal arousals were previously shown in chronic short-sleeping adults, without known sex differences. Sustained 4-h sleep restriction produced a sex-dependent alteration in heart rate responses to arousals and resulted in a prolonged reduction in postarousal pulse transit time in females only. These findings yield the first sex-specific characterization of nocturnal cardiovascular responses to spontaneous arousals following sleep restriction, and may place females at greater sleep truncation-related cardiovascular disease risk.

Background: Sleep regularity is emerging as an independent determinant of health. Multiple studies suggest a link between increased variability in sleep duration and timing and adverse cardiovascular, metabolic, and cognitive outcomes. There is, however, a lack of data on the implications of sleep regularity for aerobic capacity and physical endurance, particularly in patients with established cardiovascular disease. This study seeks to investigate the influence of irregularity in sleep duration on functional capacity in patients with coronary artery disease (CAD) undergoing cardiac rehabilitation (CR). Methods: We recruited a sample of patients with CAD who were referred to CR at Mayo Clinic Rochester. Participants completed a 6-minute walk test (6MWT) upon enrollment into CR. 6MWT variables included distance walked (meters), predicted distance walked (percentage) and estimated metabolic equivalents (METs). 24-hour objective sleep quality and quantity were assessed over a 7-day period by wrist actigraphy. Average standard deviation (SD) of sleep duration was used to define sleep regularity, with SD >60 minutes indicating irregular sleep. Chi-square test, independent samples t-test, and linear regression were used for statistical analysis. Results: Twenty-eight participants with valid actigraphy and 6MWT were included in this analysis (eight females; mean age 67.4 ± 11.6 years; body mass index 31.1 ± 5.8 kg/m 2 ). The average total sleep time was 7.1 ± 1.2 hours, and 10 participants (35.7%) exhibited sleep duration SD >60 minutes. Demographic, clinical and sleep characteristics were comparable between the regular and irregular sleep groups. Compared to patients with regular sleep, those with irregular sleep had poorer 6MWT, with shorter distance walked (406.2 ± 81.2 meters vs 338.8 ± 80.7 meters; p = 0.045), lower % of predicted distance walked (87.1 ± 18.7% vs 69.2 ± 11.4%; p = 0.011), and lower METS (2.99 ± 0.36 vs 2.63 ± 0.38; p = 0.022). Irregular sleep remained significantly associated with performance at the 6MWT after taking into account age and sex, with patients walking 14.4 meters fewer with every 10-minute increase in sleep variability (95% CI -28.1, -0.7; p 0.041). Conclusions: Increased day-to-day fluctuation in sleep duration is associated with reduced exercise capacity in patients with CAD undergoing CR. These findings add to the mounting body of evidence linking irregular sleep patterns to heightened cardiovascular risk, and support the integration of sleep monitoring in the CR practice to enhance risk stratification and outcome prediction. Funding Source: Sleep Number Corp. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Abstract Background Obstructive sleep apnea (OSA) is a risk factor for hypertension and some evidence suggests this risk may not be mitigated with positive airway pressure. Low-intensity statin therapy can modestly reduce blood pressure (BP). In this exploratory analysis, we examined if six months of high-intensity statin therapy could lower resting or ambulatory BP in patients with OSA. Methods 39 patients with OSA (13F, age = 49 ± 9yrs, body mass index = 32.9 ± 4.2kg/m2, apnea-hypopnea index = 22.2 ± 12.4 events/hour) were randomized to high-intensity atorvastatin or placebo. BP was assessed using seated, “office” measurements and in 20-minute intervals over 24 consecutive hours at three timepoints (baseline, three- and six-months post-randomization). Participants maintained a diary denoting sleep and wake times for analysis. Changes (Δ) in BP from baseline were assessed and adjusted for adherence to participants’ intervention (atorvastatin or placebo) as well as to their treatment for OSA (yes or no). Results There were no between-group differences in baseline BP variables (P = .09-.96). At three months, the changes in resting (P = .74-.87), 24 hour mean (P = .54-.96), daytime (P = .70-.96), nor nighttime (P = .74-.96) BP did not differ between groups. Similarly, the changes in resting (P = .23-.92), 24 hour mean (P = .51-.82), daytime (P = .17-.78), and nighttime (P = .51-1.00) BP did not differ between groups following six months of their respective intervention. Conclusions Our data suggest that high-intensity atorvastatin does not lower resting or ambulatory BP in patients with OSA relative to a placebo. Thus, it does not appear that atorvastatin is a viable adjunct intervention for BP reduction in patients with OSA. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT03308578.

Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder, characterized by recurrent upper airway obstruction during sleep, resulting in intermittent hypoxia, increased sympathetic activation, and sleep deficiency. Over the past 2 decades, there has been a robust body of evidence to support a strong link between OSA and cardiometabolic diseases. Obesity is an important risk factor for OSA. Observational studies indicate that OSA is a strong risk factor for the development of hypertension and diabetes. Moreover, clinical and experimental studies support a causal role of OSA in hypertension and impairments in glucose metabolism, beyond excess weight. Notably, OSA is particularly underdiagnosed and undertreated in women, which may heighten the cardiometabolic risk. OSA is often overlooked during pregnancy and has been linked to adverse cardiometabolic outcomes in observational studies. In randomized clinical trials, treatment of OSA with continuous positive airway pressure reduces blood pressure in individuals with hypertension, but the beneficial effects of continuous positive airway pressure on glycemic outcomes are less convincing. Inconsistent cardiometabolic response to OSA treatment can be partly explained by failure to consider heterogeneity in OSA and variable continuous positive airway pressure adherence among diverse populations. In this review, we summarize the relationships between OSA and cardiometabolic conditions with a particular focus on obesity, hypertension, and diabetes. We review the current knowledge on the heterogeneity in OSA and discuss potential underlying mechanisms for impairments in blood pressure and glucose metabolism in OSA. We also provide a clinical perspective for OSA management considering current research gaps and emerging approaches for the prevention and treatment of cardiometabolic disease.

Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia, with its incidence rising due to aging populations, obesity, and advancements in diagnostic modalities. The interplay between sleep disorders and AF is increasingly recognized, with obstructive sleep apnea (OSA) serving as a well-established risk factor. However, emerging evidence implicates additional sleep disturbances—including central sleep apnea, insomnia, and restless legs syndrome—in AF pathogenesis and progression. Despite compelling observational data, interventional studies evaluating the impact of sleep disorder treatment on AF outcomes have yielded mixed results. Although continuous positive airway pressure therapy in patients with OSA mitigates AF recurrence, randomized controlled trials have yet to confirm a definitive causal benefit. This review synthesizes epidemiological, mechanistic, and interventional data linking sleep disorders to AF.

Somali Americans, originating from East Africa, are a fast-growing minority in the United States. Emerging data suggest Somali individuals exhibit increased cardiovascular (CV) risk compared to non-Hispanic White adults. Previous data from our laboratory demonstrated elevated ambulatory arterial stiffness in Somali Americans, as derived from 24-hour blood pressure monitoring. We sought to confirm these vascular stiffness findings via gold-standard applanation tonometry and examine potential sex differences, given that females of African ancestry are at elevated risk of CV disease (CVD). We therefore examined aortic hemodynamics and carotid-femoral pulse wave velocity in male and female Somali Americans. We hypothesized that female Somali Americans would present with greater aortic wave reflection and arterial stiffness compared to males. We further examined the accuracy of prediction of aortic wave reflection from a predominantly White population, when applied to the Somali American population. We utilized applanation tonometry to quantify arterial stiffness in 24 female (age: 27±10 years, BMI: 27±6 kg/m 2 ) and 19 male (age: 22±6 years, BMI: 27±5 kg/m 2 ) Somali Americans without CVD. Each participant arrived in the laboratory at Mayo Clinic, fasted for at least three hours, and did not consume caffeine or exercise for at least 12 hours prior to testing. After 15 minutes of supine rest, duplicate recordings of aortic blood pressure and augmentation index (AIx) were obtained via pulse wave analysis. Similarly, aortic stiffness was quantified via duplicate carotid-femoral pulse wave velocity recordings. Statistical analysis included independent samples t-tests to test for sex differences in aortic hemodynamics, and paired samples t-tests to determine differences between estimated and obtained AIx (α≤0.05). Aortic systolic arterial pressure (111±11 vs. 108±7 mmHg, p=0.295) was similar between female and male Somali Americans. Aortic diastolic arterial pressure (75±7 vs. 67±7 mmHg, p<0.001) and heart rate (67±9 vs. 57±7 beats/min, p<0.001) were higher in female Somali adults. Similarly, AIx (28±14 vs. 19±12%, p=0.045) and AIx normalized to 75 heart beats/minute (24±13 vs. 10±13%, p=0.001) were higher in female Somali Americans. Carotid-femoral pulse wave velocity (5.4±0.9 vs. 5.5±0.8 m/s, p=0.661) was similar between sexes. Estimated AIx (corrected for sex, age, height, and resting heart rate) was markedly lower than observed AIx in both female (13±7 vs. 28±14%, p<0.001) and male (6±5 vs. 19±12%, p<0.001) Somali Americans. These findings, obtained in young, healthy Somali adults are suggestive of elevated CVD risk, evident at an early age. These data are particularly concerning regarding vascular dysfunction in Somali females and suggest that prediction models for arterial stiffness should factor in race to optimize performance. Future work into mechanisms underlying vascular dysfunction in Somali Americans is warranted. Sleep Number Grant to Mayo Clinic and by NIH R01-HL160619, R01-HL169320, T32-DK007013, K12 AR084222, and AHA 24POST1241616. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Abstract Introduction Cardiovascular disease (CVD) remains the leading cause of death in the United States. We previously showed a high prevalence of obstructive sleep apnea (OSA) among former National Football League (NFL) players. Further, we hypothesized that post-career OSA impacts CVD risk among retired professional athletes, even though these former NFL players are often near peak physical fitness for a significant portion of their lifespan. The Living Heart Foundation Heart-Obesity-Prevention-Education Group aimed to provide an in-depth health assessment for CVD risk factors among former NFL players to examine the role of OSA on blood pressure (BP) and echocardiographic measurements. Methods Forty-three former NFL players completed an at-home sleep study and outpatient health assessment to determine CVD risk including office BP and transthoracic echocardiogram (TTE) measurements. Seated BP readings were made in triplicate, TTE measurements, including ejection fraction, left atrial size, left ventricular size and thickness, and ascending aortic diameter, were obtained in 17 former NFL players without OSA (age: 46±10 years, BMI: 32±5 kg/m2, apnea-hypopnea index: 3±1 events/hour) and 26 with OSA (age: 51±9 years, BMI: 33±5 kg/m2, apnea-hypopnea index: 17±12 events/hour). Independent sample t-tests were utilized to determine differences in blood pressure and TTE measurements between OSA and non-OSA groups (α=0.05). Results Systolic BP was similar in non-OSA vs. OSA groups (131±12 vs. 135±16 mmHg, p=0.443), while diastolic BP was higher in former NFL players with OSA (78±8 vs. 86±9 mmHg, p=0.007). Ejection fraction, left atrial size, left ventricular size, and left ventricular thickness were similar between groups (p&gt;0.05 for all). However, ascending aortic diameter was modestly larger in former NFL players with OSA (3.3±0.19 vs. 3.5±0.40 cm, p=0.048). Conclusion These findings suggest OSA may be a primary driver of increased BP and increased aortic diameter in former NFL players, and impact cardiac structural health, suggesting augmented CVD risk in former NFL players. Future work is warranted to investigate impact of race and player position on OSA-mediated CVD risk in retired NFL players. Support (if any) NFL Players Association, NIH T32-DK007013, and the American Heart Association (24POST1241616)