Depression is a significant risk factor for coronary heart disease (CHD), independent of traditional risk factors such as hypertension, hyperlipidemia, and diabetes. It increases the risk of developing CHD and worsens its prognosis. Depression is associated with various physiological mechanisms, including inflammatory responses, dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system (ANS) dysfunction, platelet activation, endothelial dysfunction, lipid metabolism disorders, and genetic factors. These mechanisms contribute to the development and progression of CHD. Antidepressant treatment in CHD patients with comorbid depression is controversial, as its effectiveness and safety are still under investigation. Depression also affects treatment adherence in CHD patients, leading to adverse cardiovascular outcomes. The relationship between depression and CHD is complex, involving multiple pathways such as social behavior, type D personality, inflammation, HPA axis dysfunction, ANS dysfunction, platelet activation, endothelial dysfunction, lipid metabolism disorders, and genetics. Depression is associated with increased levels of pro-inflammatory cytokines, which can destabilize atherosclerotic plaques and increase the risk of cardiovascular events. Additionally, depression can lead to changes in neuroendocrine function, activating the HPA axis and sympathetic nervous system, which can increase the risk of CHD. Depression also affects the gut microbiota, which is closely related to the pathogenesis of CHD and depression. The gut microbiota-gut-brain axis plays a role in regulating inflammation, chronic inflammation, and metabolites, which are involved in the development of CHD and depression. Interventions for depression in CHD patients include antidepressant treatment, psychological therapy, exercise therapy, and acupuncture. Antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are commonly used due to their anti-inflammatory, antiplatelet aggregation, and HPA axis activity reduction effects. Traditional Chinese medicine (TCM) is also used, with studies showing that TCM can improve depression symptoms and blood lipid levels in CHD patients. Psychological interventions such as cognitive-behavioral therapy, interpersonal psychotherapy, and problem-solving therapy have shown promise in reducing depressive symptoms and improving treatment compliance. Exercise therapy can also help reduce depression and CHD-related symptoms by modulating inflammatory factors and the parasympathetic nervous system. In conclusion, depression is a significant risk factor for CHD, and its mechanisms are complex and multifaceted. Effective interventions are needed to address the impact of depression on CHD and improve patient outcomes.Depression is a significant risk factor for coronary heart disease (CHD), independent of traditional risk factors such as hypertension, hyperlipidemia, and diabetes. It increases the risk of developing CHD and worsens its prognosis. Depression is associated with various physiological mechanisms, including inflammatory responses, dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system (ANS) dysfunction, platelet activation, endothelial dysfunction, lipid metabolism disorders, and genetic factors. These mechanisms contribute to the development and progression of CHD. Antidepressant treatment in CHD patients with comorbid depression is controversial, as its effectiveness and safety are still under investigation. Depression also affects treatment adherence in CHD patients, leading to adverse cardiovascular outcomes. The relationship between depression and CHD is complex, involving multiple pathways such as social behavior, type D personality, inflammation, HPA axis dysfunction, ANS dysfunction, platelet activation, endothelial dysfunction, lipid metabolism disorders, and genetics. Depression is associated with increased levels of pro-inflammatory cytokines, which can destabilize atherosclerotic plaques and increase the risk of cardiovascular events. Additionally, depression can lead to changes in neuroendocrine function, activating the HPA axis and sympathetic nervous system, which can increase the risk of CHD. Depression also affects the gut microbiota, which is closely related to the pathogenesis of CHD and depression. The gut microbiota-gut-brain axis plays a role in regulating inflammation, chronic inflammation, and metabolites, which are involved in the development of CHD and depression. Interventions for depression in CHD patients include antidepressant treatment, psychological therapy, exercise therapy, and acupuncture. Antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are commonly used due to their anti-inflammatory, antiplatelet aggregation, and HPA axis activity reduction effects. Traditional Chinese medicine (TCM) is also used, with studies showing that TCM can improve depression symptoms and blood lipid levels in CHD patients. Psychological interventions such as cognitive-behavioral therapy, interpersonal psychotherapy, and problem-solving therapy have shown promise in reducing depressive symptoms and improving treatment compliance. Exercise therapy can also help reduce depression and CHD-related symptoms by modulating inflammatory factors and the parasympathetic nervous system. In conclusion, depression is a significant risk factor for CHD, and its mechanisms are complex and multifaceted. Effective interventions are needed to address the impact of depression on CHD and improve patient outcomes.