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 financial and social insurance industry burden on individuals.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 [1]. In a random survey of 99 patients who underwent coronary angiography for chest pain, 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 [2]. Because these patients often show pathological sensitivity, poor compliance with medical advice, and poor control of risk factors, combined with the presence of anxiety and depression with imbalance in cardiac autonomic function and impact on platelet and coagulation function, the incidence of coronary heart disease, cardiovascular events and sudden death increases [3.4.5].
1. Panic attact (PA) and heart disease
Panic disorder (PD) is the most common anxiety disorder in the emergency department of non-psychiatric hospitals. Patients with panic attacks usually do not first seek help from psychiatrists, but mostly think 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 patients still have chest pain, 17% are readmitted for atypical chest pain, and 30% have limited activity [6]. Hurst, a leading American cardiologist, pointed out that “the most common cause of chest pain is not heart disease, but anxiety-related”. In the United States, the false-positive rate of CCU admissions for suspected “coronary heart disease” is around 30%; every year, about 200,000 new cases of negative cardiac catheterization are performed to confirm the cause of chest pain; follow-up results show that 79% of these patients with chest pain who have been excluded from coronary heart disease by cardiac catheterization are still on medications for coronary heart disease. . It can be said that panic attacks are a more expensive disorder for non-psychiatric hospitals than any other psychiatric disorder. It should not be overlooked that in addition to coronary artery disease and angina pectoris, other organic heart diseases also often manifest as panic-like attacks, such as mitral valve prolapse, atrial mucinous tumor, arrhythmia, and congestive heart failure, which should be differentiated to prevent misdiagnosis.
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 the main complaint met the diagnostic criteria for PD in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III R), and 44% of them had previously been diagnosed with coronary artery disease, but 80% of the chest pain at the time of investigation was atypical or non-cardiac chest pain (NCCP), and 75 The incidence of PD was significantly higher in patients with non-coronary chest pain than in patients with coronary disease, and a meta-analysis showed that the incidence of PA was 41-42% in patients with non-coronary chest pain and 8-22% in patients with confirmed coronary chest pain [5]. The former had a longer history of chest pain and a high proportion of atypical chest pain [7.8]. The relative risk of PD was 2.03 (95% CI, 1.41 to 2.92) in patients with non-anginal chest pain and 1.25 (95% CI, 0.87 to 1.80) in patients with coronary artery disease from the emergency room [6].
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 PD combined, and 10% of atypical angina patients have PD combined. 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 [9]. 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 episodes after exertion and relief with nitrates were not good predictors of coronary heart disease. A meta-analysis revealed the following five features that contribute to the diagnosis of simple PD [7].
(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, more likely to focus on pain, conviction that they have heart disease, fear of disease and death, fear of heart disease is a better predictor for patients with NCCP, and patients selectively focus on heart rate and electrocardiographic 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 experience reversible myocardial hypoperfusion during panic attacks [11].Chest pain in patients with PD may be related to myocardial ischemia It may be related to the following three mechanisms [6]: (i) reduced heart rate variability (HRV): PD patients have higher maximum heart rate, faster heart rate during standing, and shorter PR intervals compared to controls. All of these can decrease 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 [12]. reduced HRV predisposes to arrhythmias and sudden death. 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 has a similar electrocardiogram to patients with microvascular angina. (iii) Coronary artery disease: Chronic anxiety may accelerate the development of atherosclerosis, especially in men. Patients with persistent anxiety had significantly thicker intima-media thickness (IMT) in the common carotid artery compared to controls [13]. 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), on the other hand, elevates procoagulant factors (fibrinogen or coagulation factor VII) and reduces fibrinolytic capacity [14]. The Framingham study (20-year follow-up) showed a significantly higher probability of death from myocardial infarction and coronary events in housewives with symptoms of anxiety [15].
2. Depression and cardiovascular disease
Thirteen prospective studies of healthy subjects with a total sample of more than 4000 individuals and a mean follow-up of 10 years showed that depression was an independent risk factor associated with cardiovascular disease prevalence and mortality, with corrected relative risks 4 – 4.5 times higher than normal controls (major depression) and 1.5 C2 times higher [subsyndromic (Subsyndromic) depression], with importance comparable to traditional cardiovascular disease risk factors. 11 prospective studies with a mean 12-month follow-up of approximately 4000 patients with a recent diagnosis of myocardial infarction found a 16 – 20% prevalence of major depression and 17 – 47% prevalence of depressive symptoms in patients with a recent myocardial infarction [16].
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. Hypertension 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 on the correlation between anxiety and hypertension are inconsistent. Clinically, unexplained sudden highs and lows in blood pressure, or when a patient with hypertension who is taking medication with otherwise well-controlled blood pressure 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 aggressively, but there are still a considerable number of physicians in general hospitals who are not clear about the choice of drugs and use them in a confusing manner.
Benzodiazepines (such as alprazolam, lorazepam, clonazepam, etc.) can effectively relieve anxiety, reduce the frequency of panic attacks, improve sleep, and also reduce the dosage of nitroglycerin in angina pectoris in patients with combined coronary artery disease [6]. However, because of the risk of causing cognitive impairment, pharmacogenic depression and postural hypotension, especially in the elderly, they should be applied in small doses, preferably for no more than 4 to 8 weeks. Traditional tricyclic antidepressants have the advantage of positive efficacy and cheapness, but they are not recommended as first-line drugs because of their more pronounced cardiovascular and cholinergic side effects and lower tolerability and safety. Newer antidepressants, such as 5-hydroxytryptamine reuptake inhibitors (SSRI) and 5-hydroxytryptamine and norepinephrine reuptake inhibitors (SNRI), have been widely used in clinical practice because of their good clinical efficacy in anxiety and depression and their greatly reduced adverse effects compared with cyclic antidepressants. In addition to being indicated for depression, sertraline, fluoxetine, paroxetine, and citalopram in SSRIs are also approved by the FDA for the treatment of panic disorder. Because cardiovascular patients are generally older, have many risk factors, and often combine multiple diseases, requiring several or even a dozen drugs to be taken simultaneously, the safety of drugs has become one of the common concerns of doctors and patients.The SADHAT randomized double-blind placebo-controlled study, which included subjects taking as many as 11 types of medications, showed that sertraline had a significant effect on heart rate, blood pressure, and left ejection fraction in patients with acute myocardial infarction and unstable angina. , blood pressure, left heart ejection fraction, PR interval, and QT interval were not significantly different from placebo, cardiovascular events were reduced compared to the placebo group, and non-cardiovascular events were similar to the placebo group, showing better tolerability and safety with recommended doses of 50-100 mg/day [21]. Also, the SADHAT study showed that sertraline (and its active metabolites) in plasma can exert antiplatelet properties at therapeutic concentrations and improve heart rate variability after myocardial infarction.
In summary, patients with cardiovascular disease are at high risk for anxiety and depression, and once combined, the prognosis of cardiovascular patients will be severely compromised. Early and correct identification of anxiety-depression and selection of safe and effective drugs 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.
REFERENCES
1, Todaro JF, Shen BJ, Niaura R, et al. Effect of negative emotions on frequency of coronary heart disease (The Normative Aging Study). Am J Cardiol, 2003, 92(8):901~906.
2. He JH, Guo LF, Wu ZS, et al. A study on the preoperative psychological state of coronary angiography in patients with chest pain. Chinese Journal of Cardiovascular Diseases, 2005, 33(9):823.
3, Fleet RP, Beitman BD. Cardiovascular death from panic diaorder: a critical review of the literature. J Psychosom Res, 1999, 44(1):71-88.
4, Doerfler LA, Paraskos JA. Post-traumatic stress disorder in patients with coronary artery disease: screening and management implications. Can J Cardiol, 2005, 21(8): 5. Fleet RP, Dupuis G, Marchand A, et al. Panic disorder in emergency department chest pain patients: prevalence, comorbidity, suicidal ideation, and physician recognition. Am J Med, 1996, 101(4):371-380. 6. David K. Panic & Plaques: Panic Disorder & Coronary Artery Disease in Patients with Chest Pain. J Am Board Family Practice. 2004. 7, Jeff CH, Mark HP. Predicting Panic Disorder among Patients with Chest Pain: A analysis of the literature. psychosmatics, 2003, 44:222-236. 8, Dammen T, Arnesen H, Ekeberg O, et al. Psychological factors, pain attribution and medical morbidity in chest-pain patients with and without coronary artery disease. Gen Hosp Psychiatry, 2004, 26(6):463-469. 9, Stollman NH, Bierman PS, Ribeiro A, et al. CO2 provocation of panic: symptomatic and manometric evaluation in patients with noncardiac chest pain. Am J Gastroenterol, 1997:92:839-842. 10, Stephen JB, David MC, Murray DE, et al. “Stress” and coronary heart disease: psychosocial risk factors. national Heart Foundation of Australia position statement update. mja, 2003, 178:272-276. 11, Lambert , Bernard B, Nancy FS. Myocardial Perfusion Study of Panic Attacks in Patients with Coronary Artery Disease. Am J Cardiology, 2005, 96(8):1064-1068. 12, Lavoie KL, Fleet RP, Laurin C, et al. Heart rate variability in coronary artery disease patients with and without panic disorder. Psychiatry Res, 2004, 128 (3):289-299. 13, Sabrina P, Mahmoud Z, Pierre D, et al. Sustained Anxiety and 4-year Progression of Carotid Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 2001, 21:136-? 14, Roland VK, Paul JM, Claudia F, et al. Effects of Psychological Stress and Psychiatric Disorders on Blood Coagulation and Fibrinolysis. A Biobehavioral Pathway to Coronary Artery Disease? Psychosomatic Medicine, 2001, 63:531~544. 15, Kubzansky LD, Davidson KW, Rozanski A. The clinical impact of negative psychological states: expanding the spectrum of risk for coronary artery disease. Psychosom Med, 2005, 67 16, Jiang et al, Depression and Heart Disease Review; CNS Drugs, 2002 17, Laghrissi-Thode F, et al. Biol Psychiatry 1997;42:290C295 18, FRasure-Smith N, et al. JAMA 1993;270:1819-1825. 19, Frasure-Smith N, et al. Circulation 1995;91:999-1005. 20, JAMA. 2003;290:2138-2148. 21, Wei J, Jonathan RTD. Antidepressant therapy in patients with ischemic heart disease. Am Heart J, 2005, 150(5):871~881