Patients with cardiovascular disease are at high risk for psychiatric disorders such as anxiety and depression, and numerous epidemiological studies have confirmed that anxiety and depression disorders significantly influence the course of cardiovascular disease, clinical manifestations and recurrence of vascular events, leading to reduced social functioning and overall quality of life. At the same time, it not only raises the consumption of medical resources, but also increases the burden on individuals financially and on the social insurance industry.Todaro et al. reported a linear positive correlation between anxiety and depression and the incidence of coronary heart disease in older men in the United States. The authors once randomly surveyed 99 patients who underwent coronary angiography for chest pain, of whom 53.5% had normal or near-normal angiographic findings, 44.6% had anxiety symptoms, and 17.8% had depressive symptoms. Coronary angiography confirmed 37% of patients with combined anxiety symptoms and 13% of patients with depressive symptoms. Because these patients often show pathological sensitivity, poor compliance with medical advice, and poor control of risk factors, combined with the imbalance of cardiac autonomic function when anxiety and depression appear, and affect platelet and coagulation function, make the incidence of coronary heart disease, cardiovascular events and sudden death increase.
1, panic attacks and heart disease
Panic disorder is the most common anxiety disorder in the emergency department of non-psychiatric hospitals. Patients with panic attacks usually do not first turn to a psychiatrist; most believe they have a heart attack and visit the emergency room or cardiology department again and again during panic attacks, repeatedly undergoing various cutting-edge tests related to heart disease. Even when patients are told that their coronary angiogram results are normal, 60% of them still have chest pain, 17% are readmitted for atypical chest pain, and 30% have limited activity. Hurst, a leading American cardiologist, noted that “the most common cause of chest pain is not heart disease, but is related to anxiety”.
Chest pain is a common symptom of both PD and coronary artery disease.
Fleet et al. reported that approximately 25% of patients with chest pain as a primary complaint met the diagnostic criteria for PD in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-IIIR), and 44% of these patients were previously diagnosed with coronary artery disease, but 80% of the chest pain on the occasion of the survey was atypical or noncardiogenic chest pain, and 75% of patients were discharged with an NCCP diagnosis.PD in non-coronary artery disease The incidence of PD was significantly higher in patients with chest pain than in patients with coronary artery disease. A meta-analysis showed that the incidence of PA was 41% to 42% in patients with non-coronary chest pain and 8% to 22% in patients with chest pain diagnosed with coronary artery disease. The former had a longer history of chest pain and a high proportion of atypical chest pain. The relative risk of PD was 2.03 (95% CI, 1.41 to 2.92) for patients with non-anginal chest pain and 1.25 (95% CI, 0.87 to 1.80) for patients with coronary artery disease from the emergency room.
The more urgent and dangerous patients in clinical practice are those with both acute myocardial ischemia and panic disorder, and identifying whether the source of chest pain is a panic attack or angina or myocardial infarction is an important but difficult matter. On the one hand, 4 to 65% of typical angina patients have combined PD, and 10% of atypical angina patients have combined PD. on the other hand, only 64% of patients with heart disease have chest pain, and many patients with coronary artery disease have atypical chest pain, and only 74% of severe coronary artery disease have angina occurring. Usually chest pain in coronary artery disease is characterized as occurring after exertion, pressure, and located in the retrosternal or precordial region; whereas chest pain in anxiety or PD is non-exertional, dyspeptic (food-related) or neurotic, occurs at night, and is located in the chest wall (contour), right hand, or extremities. However, the pattern of attacks after exertion and remission with nitrates were not good predictors of coronary heart disease.
The meta-analysis revealed the following five features that contribute to the diagnosis of simple PD.
(1) absence of coronary artery disease ;
(2) atypical nature of chest pain;
(3) women, especially those with a previous history of anxiety disorders;
(4) Younger age;
(5) higher anxiety self-rating values.
Patients with PD are emotionally sensitive and more likely to be concerned about pain, convinced they have heart disease, and fear disease and death. Fear of heart disease is a better predictor for patients with NCCP, and patients selectively focus on heart rate and ECG changes. Although PD is more common in patients without coronary artery disease, a significant proportion of patients have comorbid coronary artery disease. Lambert et al. used a CO2 excitation test to induce panic attacks in patients and performed SPECT nuclear scans of their myocardium and found that patients with coronary artery disease combined with PD were more likely to have reversible myocardial hypoperfusion during panic attacks.
Chest pain in PD patients may be related to myocardial ischemia by three possible mechanisms.
1. reduced heart rate variability (HRV).
Compared with controls, PD patients have a higher maximum heart rate, a faster heart rate during standing, and a shorter PR interval. All of these can reduce HRV, leading to increased myocardial oxygen consumption and ischemia. HRV is used to detect autonomic control of heart rate, and reduced HRV indicates reduced autonomic control. Compared with patients with PD alone or coronary artery disease alone, patients with coronary artery disease combined with PD exhibit lower sympathetic modulation under routine daily living conditions. reduced HRV predisposes to arrhythmias and sudden death.
2. microvascular angina.
During panic attacks patients hyperventilate, sympathetic tone increases, blood levels of catecholamines rise, peripheral resistance increases, and small arteries within the myocardium spasm, leading to microvascular angina. About 50% of female non-coronary chest pain patients have microvascular dysfunction unrelated to cardiovascular risk factors, 40% of patients with microvascular angina have panic attacks, and PD and microvascular angina patients have similar electrocardiograms.
3. Coronary artery disease.
Chronic anxiety may accelerate the onset of atherosclerosis, especially in men. Patients with persistent anxiety had significantly thicker intima-media thickness (IMT) in the common carotid artery compared to controls. In addition, anxiety is associated with a hypercoagulable state. In healthy individuals, acute anxiety states activate both coagulation and fibrinolytic systems, whereas in patients with atherosclerosis and impaired endothelial function, the procoagulant response induced by acute anxiety may outweigh fibrinolytic mechanisms leading to a hypercoagulable state. Chronic psychosocial stress (work stress or low socioeconomic status) increases procoagulant factors (fibrinogen or coagulation factor VII) and decreases fibrinolysis. the Framingham study (20-year follow-up) showed that housewives with anxiety symptoms had a significantly higher probability of death from myocardial infarction and coronary events.
2. Depression and cardiovascular disease
Thirteen prospective studies of healthy individuals with a total sample of more than 4,000 and a mean follow-up of 10 years showed that depression is an independent risk factor associated with cardiovascular disease prevalence and mortality that is comparable in importance to traditional cardiovascular disease risk factors. 11 prospective studies of approximately 4,000 patients with a recent diagnosis of myocardial infarction were conducted with a mean follow-up of 12 months. follow-up, found a 16-20% prevalence of major depression and a 17-47% incidence of depressive symptoms in patients with recent myocardial infarction. Depression can affect the prognosis of cardiovascular disease and increase the incidence of cardiovascular events. One study reported that acute myocardial infarction patients with comorbid depression had 3.1 and 3.6 times higher mortality at 6 and 18 months after the disease than infarction patients without depression, respectively [18.19].
The mechanism may be related to the following factors.
(1) depression increases platelet activity or aggregation. Studies have shown that cardiovascular patients suffering from depression have significantly increased platelet factor 4 (PF4) and β-thromboglobulin (βCTG) than controls and cardiovascular patients alone without comorbid depression [17].
(2) Depression alters the autonomic rhythm of the heart and reduces the variability of heart rate.
(3) Depressed patients have decreased adherence to treatment and recommendations regarding lifestyle changes.
3. Hypertensive disease and anxiety
Prospective studies have shown that time urgency and hostility are highly correlated with the incidence of hypertension after 5 years [20], but the findings of the correlation between anxiety and hypertension are inconsistent. Clinically, unexplained sudden highs and lows in blood pressure, or when an otherwise well-controlled blood pressure after taking medication in patients with hypertension becomes difficult to control and no proper cause can be found, are often associated with mood disorders. Taking a medical history, the patient mostly has a combination of sleep disorders and can often ask about negative life events that cause psychological conflicts.
4. Treatment and safety of cardiovascular disease combined with anxiety and depression
Because anxiety and depression can have a serious impact on the occurrence and prognosis of cardiovascular disease, thus bringing a heavy burden to the patient’s work, life and social economy, there is now a basic consensus that cardiovascular disease combined with anxiety and depression should be treated actively, but there are still a considerable number of doctors in general hospitals who are not clear about the choice of drugs and the use is rather confusing. Benzodiazepines (e.g., alprazolam, lorazepam, clonazepam, etc.) can effectively relieve anxiety, reduce the frequency of panic attacks, improve sleep, and also reduce the dosage of nitroglycerin in patients with combined coronary artery disease. However, because of the risk of causing cognitive impairment, pharmacogenic depression and postural hypotension.
In summary, patients with cardiovascular disease are at high risk for anxiety and depression, and once combined with anxiety and depression, the prognosis of cardiovascular patients will be seriously affected. Early and correct identification of anxiety-depression and selection of safe and effective medications are important measures in the treatment of cardiovascular disease and are no less important than antiplatelet and statin drugs, calling for more attention to anxiety-depression in cardiovascular patients and making it part of the rehabilitation and secondary prevention of cardiovascular disease.