Modifiable lifestyle factors and sudden cardiac death: mechanisms, evidence, and prevention strategies
Sudden cardiac death (SCD) accounts for an estimated 4–5 million deaths annually worldwide and remains a major unresolved challenge in cardiovascular medicine. Survival from out-of-hospital cardiac arrest remains below 10% in most regions, and approximately half of SCD events occur as the first clinical manifestation of cardiovascular disease, often in individuals not identified by conventional risk stratification. We conducted a narrative review of the literature in PubMed/MEDLINE, Web of Science, and EMBASE (January 2003 to April 2026), prioritizing prospective cohorts, randomized trials, meta-analyses, and international guidelines. Five major modifiable lifestyle domains are consistently linked to SCD risk: sleep health, physical activity, diet, psychological stress, and tobacco and alcohol use. Sleep duration shows a U-shaped association with cardiovascular mortality, and untreated obstructive sleep apnea may confer substantially elevated risk (subgroup OR 3.87; 95% CI 1.09–13.81), although overall evidence remains heterogeneous. Physical activity also follows a U-shaped pattern, with habitual moderate activity being protective, and brief vigorous incidental activity (∼4 min/day) reducing cardiovascular mortality by 32%–34%, while sedentary behavior and unaccustomed vigorous exertion increase risk. Mediterranean dietary patterns reduce major cardiovascular events by approximately 30%, and psychological stress promotes arrhythmogenesis through neurohormonal activation and adverse remodeling. These exposures converge on four key mechanisms: autonomic dysfunction, systemic inflammation, structural and electrophysiological remodeling, and metabolic-hormonal dysregulation. Integrating lifestyle-based interventions into routine cardiovascular risk assessment offers a low-cost and scalable strategy for primary prevention. Emerging digital health technologies, including AI-enhanced electrocardiography and consumer-grade wearables, provide complementary opportunities for individualized risk prediction and population-level monitoring, particularly in resource-limited settings where conventional device-based prevention remains limited. Given the observational nature of most included evidence and the heterogeneity of SCD definitions across studies, the mechanistic and clinical inferences presented here should be regarded as hypothesis-generating, motivating prospective and where feasible interventional research rather than immediate practice change.