The growing burden of coronary artery disease (CAD) has led to a deeper exploration of the pathophysiologic mechanisms underlying the disease process with the hope of finding novel treatments to reduce CAD morbidity and mortality. Sleep is a normal physiologic phenomenon essential for maintaining homeostasis. Disruption in sleep physiology has been linked to the activation of pro-inflammatory cytokines that may predispose to a greater risk of CAD. Several studies have evaluated the etiologic relationship between sleep deficiency and CAD. In this review, we attempt to highlight the key mechanisms proposed to play a role in the association of sleep with the pathophysiology of CAD, the findings and limitations of the pertinent studies, and possible future direction for evaluating and leveraging the relationship between sleep and CAD to develop new therapeutics.
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http://dx.doi.org/10.1016/j.pcad.2024.10.002 | DOI Listing |
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