Trends Cardiovasc Med. 2025 Oct 17:S1050-1738(25)00139-2. doi: 10.1016/j.tcm.2025.10.004. Online ahead of print.
ABSTRACT
The background for this review includes negative emotions-including anger, sadness, and chronic stress-that are biologically active contributors to atherothrombosis but remain under-integrated in prevention. The objective is to synthesize epidemiologic, mechanistic, and interventional evidence linking emotional dysregulation to the pathogenesis and acute expression of ASCVD, and to contextualize effect sizes alongside traditional risk factors. The methods include a narrative review of large cohorts and case-crossover studies, neural and immunologic mechanisms (amygdala-bone marrow-arterial axis), and trials of β-blockers, SSRIs, cognitive behavioral therapy (CBT), mindfulness, and endothelial function responses to provoked emotions. We found that depressive symptoms and trait anger confer ∼30-50% higher incident MI risk; intense anger outbursts transiently raise MI risk up to ∼8-9 ×, and bereavement up to ∼20 × within 24 hours. Stress-evoked amygdalar activity predicts myelopoiesis, arterial inflammation, and events. Mechanisms include HPA axis activation, IL-6/NLRP3 signaling, eNOS uncoupling, and catecholamine-driven platelet activation. Interventions such as β-blockers, SSRIs, CBT, and mindfulness improve vascular/inflammatory markers and may reduce event susceptibility. We conclude that emotions are causal drivers of atherothrombosis and acute coronary events. Incorporating emotion metrics, inflammatory biomarkers, and targeted behavioral/pharmacologic strategies into preventive cardiology can close residual risk gaps.
PMID:41110616 | DOI:10.1016/j.tcm.2025.10.004
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