Intimate Partner Violence and Cardiovascular Disease Risk: A Systematic Review of Biological Stress-Response Mechanisms

Objective Intimate partner violence (IPV) is increasingly recognized as a social determinant of cardiovascular disease (CVD), yet the specific biological mechanisms underlying this relationship remain poorly defined. This systematic review synthesizes evidence on biological stress-response mechanisms through which IPV exposure may contribute to CVD risk. Methods Using systematic review methods informed by the Cochrane Handbook, a systematic search was conducted across PubMed, APA PsycINFO, APA PsycNet, Web of Science, and Google Scholar. Eligible studies were peer-reviewed, quantitative investigations that assessed IPV victimization and objectively measured biological markers associated with CVD risk. Methodological quality was appraised using the NHLBI Quality Assessment Tool. Results Sixteen studies met inclusion criteria. Across studies, IPV exposure was associated with HPA axis dysregulation (flattened cortisol slopes, elevated evening cortisol, blunted awakening responses), preliminary evidence of altered autonomic reactivity during emotional arousal, context-dependent inflammatory responses (TNF-α elevation, adiposity-linked CRP increases, endothelial activation), and markers of accelerated cellular aging and oxidative stress (shorter telomeres, elevated 8-isoprostanes, reduced antioxidant capacity). While findings were largely consistent across biomarkers, most studies were cross-sectional, modest in sample size, and limited to women in high-income countries. Conclusions IPV exposure is associated with dysregulation across multiple biological stress-response systems that are well-established precursors to CVD. These findings underscore the importance of considering IPV as a contributor to CVD risk. Expanding research to diverse populations and life-course stages, as well as incorporating longitudinal, mechanistic designs, is essential for clarifying how IPV may shape cardiovascular health.