IMPACT OF SLEEP DISORDERS ON CARDIOVASCULAR HEALTH: MECHANISMS AND INTERVENTIONS

Abstract

This study investigates the impact of sleep disorders, specifically sleep deprivation and obstructive sleep apnea (OSA), on cardiovascular health through a combination of in vivo, in vitro, and biochemical analyses. Using a rat model, we subjected experimental groups to sleep deprivation (72 hours) and intermittent hypoxia to mimic OSA. The results revealed significant cardiovascular dysfunction in both experimental groups, including elevated systolic and diastolic blood pressure, reduced heart rate, and myocardial remodeling characterized by fibrosis and hypertrophy. Biochemical assays demonstrated increased levels of oxidative stress markers, such as malondialdehyde (MDA), and reduced antioxidant enzyme activities (SOD and GPX) in the sleep-deprived and OSA rats, highlighting the role of oxidative damage in cardiovascular impairment. Gene expression analysis revealed elevated pro-inflammatory cytokines (TNF-α, IL-6) and pro-apoptotic markers (BAX), with decreased anti-apoptotic BCL-2 expression, indicating a significant inflammatory and apoptotic response in myocardial tissue. In vitro laboratory tests which exposed human endothelial cells (HUVECs) as well as cardiomyocytes to simulated sleep disruption demonstrated both diminished cell health and increased inflammatory mediator production.  Ốxidative stress together with inflammation and mortality rates confirm that sleep disturbances lead to adverse cardiovascular outcomes.  The research establishes that treatments targeting these channels will hold the key to lowering cardiovascular risks which result from sleep disturbances.  Studies should examine treatment strategies to reduce heart consequences of sleep disturbances while investigating the molecular origin of these sleep problems more accurately.