Psychological cardiovascular pathology is an important area of psychosomatic medicine. Modern psychosomatic medicine attaches great importance to the interaction between the psychological and the physiological. During the onset, development and regression of disease, it is often difficult to distinguish causal relationships between physiological and psychological factors of action. Among the psychological factors, the co-morbidity of psychological disorders and somatic diseases complicates the clinical information and increases the difficulty of diagnosis, while difficulties in communication between doctors and patients arise, thus affecting the compliance of treatment; in turn, somatic diseases have obvious effects on psychological reactions, and somatic diseases affect human perceptions, causing patients’ psychological reactions and aggravating the symptoms and even the prognosis of somatic diseases. Among the psycho-psychiatric factors, depression and anxiety states are a common mental disorder that interact with somatic disorders in patients with cardiovascular disease, further affecting the therapeutic effect of medical treatment and the prognosis of the disease course. Depression, a psychiatric disorder associated with mood disorders, is associated with a large number of depressive symptoms in cardiovascular disease and affects the development and progression of cardiovascular disease (CVD) as a maladaptive social disorder that interacts with psychological behavior. Studies have shown that depression is an independent high-risk factor in the pathophysiological progression of CVD. In recent years some psycho-behavioral changes and depressive states in CVD patients have received increasing attention and focus, and this paper presents a review of the relationship between depression and CVD. 1. Psychiatric disorders associated with CVD According to statistics, the prevalence of psychiatric disorders among patients with chronic somatic diseases is 25%, and the lifetime prevalence of psychiatric disorders is 42%. The recognition rate of depression and anxiety by physicians can reach 72% when the patient is mainly complaining of psychological symptoms, but only 22% when the patient is mainly complaining of physical symptoms. Psychiatric disorders associated with cardiovascular disease include anxiety disorders and depression, the former of which is often highlighted by cardiovascular system symptoms and is the most common patient population in cardiovascular departments; while depression significantly affects the onset, course and prognosis of coronary heart disease. Heavy depression occurs in about 18% of patients with coronary artery disease, of which 16-22% suffer acute myocardial infarction. Therefore, patients with coronary artery disease in particular should be carefully questioned about their medical history, such as physical or psychological trauma, psychosocial problems, excessive stress, extreme fatigue, etc., while patients with chest pain as the main complaint should think about depression. Recent studies have found that a major depressive episode is the strongest predictor of a major cardiac event in patients 12 months after cardiac catheterization intervention, and this event association is independent of cardiac disease severity, left heart function, smoking, and other factors. The three main symptoms of depression are: low mood, depression, and depression; lack of interest and lack of pleasantness; and fatigue and lack of concentration. The core symptoms of depression are lack of motivation, desire, etc., including fatigue, low energy, lack of interest, sluggishness, sense of worthlessness, and sense of uselessness and helplessness. The clinical judgment is made by using the standardized depression diagnosis quantification scale and the scores of Hamilton depression quantification scale and HAMD-24 depression quantification scale, Beck Depression Inventory (BDI) and Zung Self-Rating Scale (SDS), among which, BDI and SDS are easy to operate. The three main symptoms of anxiety disorders are: mental anxiety: nervousness, panic, and fear; motor anxiety: muscle tension, trembling, and restlessness; and vegetative anxiety: palpitations, chest tightness, shortness of breath, and excessive sweating. Clinical judgment is made by Hamilton Anxiety Quantification Scale (HAMA) and HAMD-14 anxiety scale scores. Depression in cardiovascular diseases is often accompanied by anxiety symptoms. 2, depression and coronary heart disease Epidemiological studies have found that there is a close relationship between depression and coronary heart disease, the incidence of depression in patients with coronary heart disease is significantly higher than that in the general population, and the incidence in patients with coronary heart disease, especially unstable angina, can be as high as 14%-47%. The risk of coronary heart disease is also significantly higher in patients with depression than in the rest of the population (relative risk HR 1.5-2.0), and the percentage of cardiac death is 3-4 times higher than in those without depression. Depression significantly reduces patient compliance with treatment, interferes with the recovery process, and significantly increases long-term mortality from coronary heart disease. pratt et al. conducted a baseline survey of 1551 people without heart disease, divided into those with depression (including major depressive episodes and irritable anxiety due to a grieving event in the last 2 weeks) and those without depression. Acute myocardial infarction occurred in 64 cases during 13 years of follow-up. Depression is thus considered an independent risk factor for AMI. wulsin et al. found that depression increases the risk of death from CVD, especially in men. Depression also predisposes to CVD and has a significant impact on its prognosis, and persistent severe depression is a risk factor for cardiovascular events.Abraham et al. found that depression was an independent risk factor for coronary heart disease and overall mortality, and its risk increased with depression score, with a 15% increase in the risk of coronary heart disease for every 5-point increase.Barefoot et al. investigated 1250 patients with coronary artery disease, rated depression on the Self-Rated Depression Scale (SDS), and were followed for 19.4 years for prognostic mortality, showing that SDS scores were associated with increased death from cardiac events and total mortality at follow-up, after correction for severity of original disease and treatment. Mortality from cardiac events and various diseases was 69% and 78% higher in those with moderate and severe depression than in those without depression, respectively. The risk of cardiac event death at 5-10 years and at 10 years was 84% and 72% higher in those with moderate and severe depression than in those without depression, respectively. The mechanism of interaction between depression and coronary artery disease may be that elevated blood levels of catecholamines in patients with heart disease and high blood levels of norepinephrine in depressed patients make the two synergistic, thus exacerbating the disease. Increased inflammatory markers such as leukocytes, C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor (TNF) in depressed patients lead to an inflammatory response that develops into coronary heart disease. ladwig et al. found that in a healthy population, depressed mood increased CRP levels and that the combination of high-sensitivity C-reactive protein (hCRP) in those with depressed mood predicted future coronary heart disease events (HR2.91). Recent studies have found that depression affects the prognosis of coronary heart disease through two main mechanisms: biobehavioral and pathophysiological mechanisms. Such patients have an increased risk of developing metabolic syndrome, which promotes the development of coronary heart disease. Depression can lead to hypothalamic-pituitary-adrenal axis dysfunction, which increases glucocortical levels in patients and further causes trunk obesity, hypertriglyceridemia, hypercholesterolemia, hypertension, and increased heart rate. In addition, depressed individuals under stressful conditions have enhanced intraplatelet calcium ion mobility, significantly higher calcium ion concentration, reduced adenylate activating enzyme activity, protein kinase cell activation, increased platelet surface glycoprotein IIb/IIIa receptor expression, enhanced platelet aggregation, and platelet release of thromboxane A2 and platelet factor IV, which contribute to coronary artery constriction, thrombus formation, and increased myocardial ischemia and can In a study by Ladwig et al, a 7-year follow-up of 6239 individuals (45-74 years old) free of coronary heart disease, stroke and neoplasm found a critical correlation between depression and obesity [HR1.73; P=0.06], with a synergistic effect of both in multiple risk factors for coronary heart disease. Those with obesity and depressed mood had an increased risk of coronary heart disease (HR2.32), leading to an increased relative risk of CHD events (HR1.84).Laforet et al. demonstrated that depressed patients had higher fibrinolytic enzyme activator inhibitor (PAI-1) activity (P=0.006) than non-depressed individuals, after correcting for clinical status (with or without CHD). Smoking, hypertension, high cholesterol concentrations, body mass index (BMI), and PAI-1 activity remained high in depressed patients (P=0.03). Carney found that those with depressed mood were more likely to feel angina pectoris with the same degree of myocardial ischemia. The mechanism may be related to changes in ß-endorphin regulation and downregulation of 5-hydroxytryptamine (5-HT) receptor levels. The results of scoring and testing found that resting-state plasma ß-endorphin levels were significantly higher in angina patients with higher depression scores and lower during activity, so it is speculated that angina occurrence may be related to a delayed or absent ß-endorphin response. Huang Zuo et al. found that the incidence of depression in patients with coronary artery disease in China was lower than that in Western countries, which may be related to differences in cultural background, emotional expression, and rhythm of life. Correlation analysis was done with coronary angiography results with Leaman score of coronary artery lesion degree and depression self-rating scale score, and there was no correlation between them. This indicates that there is no correlation between depressive symptoms and the degree of coronary artery lesions in our patients with coronary artery disease. It was suggested that the poor prognosis, heavy symptoms and significantly increased mortality in patients with coronary artery disease with depressive symptoms may be related to increased platelet activity, reduced heart rate variability, poor patient compliance with treatment and aggravated atherosclerotic lesions in depressed patients. In addition, depression may have an impact on the prognosis of patients with diabetes mellitus (DM).Bruce et al. investigated 1273 patients with type 2 DM and found that 31.5% of those with depression had a longer duration of DM, more cardiovascular risk factors, coronary heart disease, cerebrovascular disease, and microvascular complications of DM than those without depression, and had higher all-cause mortality and cardiac mortality at follow-up than those without depression. Higher all-cause mortality and cardiac mortality at follow-up. The study concluded that although depression is not an independent risk factor for all-cause mortality and cardiac mortality in DM, it has an impact on the prognosis of patients with DM, especially for macrovascular and microvascular disease. 3, depression and HRV and arrhythmia Autonomic abnormalities are another way in which depression affects coronary artery disease, manifested by increased sympathetic nervous system activity, decreased vagal tone, decreased heart rate variability, increased blood pressure, and coronary artery spasm. increases reflect increased parasympathetic activity, while decreases reflect increased sympathetic activity. The latter can lower the threshold of ventricular activity and induce fatal ventricular arrhythmias. The mechanism of HRV reduction is not clear, but it may be due to the stimulation of cardiac receptors by myocardial ischemia, hypoxia, and changes in the morphology of the ventricular wall, resulting in reduced HRV due to increased sympathetic tone, suppressed vagal activity, and decreased sensitivity of the sinoatrial node to neurohumoral regulation. Carney et al. found that depressed patients with Holter-confirmed coronary artery disease had a significantly lower HRV compared to those without depressed coronary artery disease (90±35ms Vs 117±26ms, P<0.01). Autonomic function of the heart has an important role in the regulation of blood pressure and heart rate variability. The alteration of autonomic function can affect coronary endothelial function, causing coronary endothelial injury, coronary spasm, reduced myocardial blood supply and oxygenation, and worsening angina symptoms. At the same time, depressed people have a lower threshold for different stimulus perception and are more sensitive to their own somatic symptoms. The discomfort caused by arrhythmias such as premature beats can be easily detected, thus causing panic and anxiety and aggravating depressive symptoms, forming a vicious circle and increasing the difficulty of treatment. Through the increased secretion of adrenaline, activation of cardiac ß receptors, the autoregulation of Purkinje fibers increases, repolarization dispersion increases, and the threshold of ventricular ectopic excitation decreases, eventually leading to the occurrence of ventricular arrhythmias. 4. contradictions and problems of current research Some recent studies on depression and cardiovascular disease have not shown consistent results. dickens et al. found no correlation between depression before and 12 months after MI and cardiac death at 8-year follow-up. factors predicting cardiac death included age, previous angina/infarction, Killip classification, and use of B-blockers. The relationship between depression and death after MI is thus considered complex, and it has been demonstrated that depression and inflammation are independent predictors of the development of severe CVD in patients with CHD, and that elevated inflammatory factors are associated with depression in healthy populations without CHD. However, Whooley et al. did not show elevated levels of inflammatory factors such as white blood cell count, CRP, fibrinogen, and interleukin-6 (IL-6) in 984 patients with CHD, but rather decreased them. Inflammation could not explain the association of severe CVD occurrence in CHD patients with depression. 5. Treatment of cardiovascular depression The treatment of depression in cardiovascular disease is important and has very serious consequences if neglected. Therapeutic interventions can be made through three types of approaches, namely psychosocial interventions, exercise therapy, and antidepressant medication. Psychotherapy is one of the important methods of depression treatment. Its aim is to reduce the psychological stress of patients and thus improve the prognosis. Patients have a high incidence of depression at the beginning of hospitalization, and psychological interventions should be performed as early as possible. A comprehensive assessment of the patient's condition, including symptoms of discomfort, degree of self-care, understanding of the disease, psycho-emotional reactions, and social support, is needed to enhance nurse-patient communication. For patients with coronary artery disease, especially those with acute myocardial infarction, active and reasonable psychological interventions can significantly improve patients' immediate and long-term prognosis. Psychological interventions include behavioral therapy, interpersonal therapy, and cognitive therapy, which are professionally demanding and require collaboration between psychological or psychiatric professionals and cardiologists. Exercise therapy is an effective treatment for depressed patients with coronary artery disease, both to improve depressive symptoms and to effectively control risk factors for coronary artery disease (e.g., hypertension, hyperlipidemia, insulin resistance, autonomic dysfunction da etc.). Reasonable exercise therapy can reduce cardiac mortality by 31% in such patients. Antidepressant medication is the effective treatment of choice for most depressed patients. Current antidepressants mainly include: tricyclic antidepressants (promethazine), selective 5-hydroxytryptamine reuptake inhibitors (SSRIs such as Prozac, Zoloft, Xarelto), monoamine oxidase inhibitors, benzodiazepines (alprazolam), etc. Studies have shown that antidepressants can significantly reduce the risk of death and reinfarction in patients with myocardial infarction, thereby improving prognosis. However, the coexistence of coronary artery disease and depression increases the difficulty of treating depression. Antidepressant treatment should be chosen from antidepressants that are less toxic to the heart to reduce the risk of aggravating coronary artery disease. Traditional tricyclic antidepressants have similar effects as IA class antiarrhythmic drugs, which may cause postural hypotension, prolonged cardiac conduction and early cardiotoxicity, as well as more anticholinergic effects such as drowsiness, dry mouth and constipation, and even aggravate myocardial ischemia, and should be used with caution especially for elderly patients. Currently selective 5-hydroxytryptamine reuptake inhibitors have no significant effect on NE receptors and dopamine receptors, have a better cardiovascular system safety, and can better control depressive symptoms, and have been used as the drug of choice for the treatment of coronary artery disease with depression. In conclusion, cardiovascular disease combined with depression seriously affects the health and life of patients, and we medical practitioners should pay attention to this type of disease, and medical staff and social health system also need to create a comprehensive and effective diagnosis and treatment defense system for these patients.