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Sleep deprivation represents a growing global public health concern, driven by the widespread use of digital devices and by socio-environmental changes that increasingly disrupt the alignment between biological and social rhythms. Reduced sleep duration, quality, and regularity are associated with an increased cardiovascular and cardiometabolic risk, identifying sleep as a modifiable determinant of health. This review examines the principal pathophysiological mechanisms linking sleep deprivation to cardiovascular disease, with particular emphasis on autonomic dysregulation, endothelial dysfunction, systemic inflammatory activation, and neuroendocrine-metabolic alterations, through which insufficient sleep promotes hypertension, insulin resistance, visceral obesity, type 2 diabetes, and atherosclerosis. An emerging role is attributed to circadian misalignment, a condition associated with increased cardiometabolic risk independently of sleep duration alone. Compensatory mechanisms such as weekend sleep recovery and daytime napping appear to exert partial protective effects under specific conditions but cannot be considered equivalent to regular sleep. Overall, current evidence suggests that sleep duration, quality, continuity, and circadian synchronization should be regarded as essential components of clinical assessment and cardiovascular prevention, highlighting the need for further prospective research into therapeutic and preventive strategies aimed at improving sleep health.