Psychological Factors in Cardiology

Psychological Factors in Cardiology

Coronary Disease

One of the most studied examples of PFAMC is the type A behav-ior pattern and its relationship to coronary artery disease. Type A is a complex set of traits including impatience, hostility, intense achievement drive and time urgency, among others. However, the relationship between type A behavior pattern and coronary disease has come under serious question. Later epidemiological studies have not strongly supported type A behavior pattern as a coronary risk factor, and most angiographic studies have failed to find an association between type A behavior and the extent of coronary artery disease. The possibility that type A behavior pattern is nevertheless an important risk factor should be kept in mind, considering that the evidence for other risk factors (e.g., exercise or cholesterol) has often been ambiguous. Whereas global type A behavior ratings are probably not reliable predic-tors of coronary artery disease outcome, the component behavior of hostility may be although here too there are conflicted studies. Only one large randomized study has been reported, in which men were assigned after myocardial infarction to receive cardiac group counseling with or without type A counseling. The coro-nary artery disease recurrence rate was 7.2% in the group that received type A behavior counseling and 13% in the control sub-jects, with no difference in mortality (Friedman et al., 1986).

Although it has received less media attention than type A, the evidence that depression is a risk factor affecting both the on-set and course of coronary artery disease is stronger than that for type A. The weighting of depression as an independent risk fac-tor in coronary artery disease has had to adjust for its interrela-tionships with other risk factors, especially smoking. Depression in coronary artery disease is associated with increased morbidity and mortality, which cannot be accounted for by other variables including severity of cardiac disease. Frasure-Smith and cowork-ers (1993) reported a fourfold increase in mortality 6 months af-ter myocardial infarction in patients with major depression com-pared with those without depression. In a large epidemiologic study, major depression tripled the relative risk of cardiac mor-tality in those without heart disease, and quadrupled it in those who did have heart disease (Penninx et al., 2001). Depression is also associated with an increased risk for serious arrhythmia. The severity of depressive symptoms has more impact on dis-ability than does the number of stenosed coronary arteries. De-pression also reduces the return to work in patients with coronary artery disease. A recent randomized trial of 1834 post-MI sub-jects who were categorized as depressed and/or socially isolated were treated with antidepressant medication (Taylor et al., 2005). Subjects taking SSRIs were at lower risk of death and recurrent MI compared with untreated subjects.

Although the mechanisms by which depression increases morbidity and mortality in coronary artery disease has not been firmly established, evidence is mounting regarding depression’s adverse effects on heart rate variability, autonomic imbalance and arrhythmia, and platelet activation. In coronary artery dis-ease, depression also reduces functional capacity, amplifies somatic symptoms (especially pain), and reduces motivation and compliance with medication, lifestyle change and cardiac rehabilitation

One specific mechanism by which psychological factors can affect coronary artery disease (CAD) has been demonstrated experimentally. Silent myocardial ischemia (ischemic changes on the electrocardiogram without symptoms of angina) can be precipitated by acute mental stress. Those who experience it are twice as likely to have major cardiac events compared with those who do not. Silent ischemia may be partly a consequence of cog-nitive or defensive traits such as denial, hyposensitivity to so-matic sensation, or systematic misperception of angina. Psycho-logical stress also changes the balance between procoagulation and fibrinolysis. Psychological factors may also affect outcome in CAD via differences in health care received. After myocar-dial infarction, patients with mental disorders are less likely to undergo cardiac catheterization and coronary revascularization than those without mental disorder.

Although the diagnosis and treatment of anxiety in pa-tients with cardiac symptoms have received much attention, there has been less examination of anxiety as a risk factor affect-ing CAD. Increases in myocardial infarction and/or sudden death have been documented in epidemiologic studies of populations undergoing missile attacks, earthquakes and other disasters. A cohort study of 34 000 initially healthy men showed that pho-bic anxiety predicted deaths from CAD, although not nonfatal myocardial infarctions (MI) (Kawachi et al., 1994). Anxiety fol-lowing MI may lead to more frequent readmission for unstable angina and more MI recurrences as well as higher mortality. Anxiety’s adverse effects on CAD outcome may occur via ef-fects on heart rate variability, QT prolongation, or other auto-nomically-mediated phenomena, like the stress-induced silent ischemia described above.

Denial is another common and significant psychological factor in patients with coronary disease. Denial may prevent individuals from acknowledging acute cardiac symptoms and promptly seeking medical care. The length of delay between the onset of symptoms of a myocardial infarction and hospitaliza-tion is a powerful predictor of morbidity and mortality, so denial at the onset of symptoms has an adverse impact on acute coro-nary disease. In contrast, denial during hospitalization may have adaptive value, perhaps even reducing morbidity and mortality.

There are other psychological factors deserving of study. Women with severe marital stress have triple the risk of recur-rent coronary events than those without marital stress. Many studies have also examined maladaptive health behaviors as risk factors in coronary disease, with the effects of smoking better established than those of sedentary lifestyle, obesity, or specific diet. The effects of psychopathology and of smoking on heart disease are easily confounded, as persons with psychiatric dis-orders are overall twice as likely to smoke as others, with the increased risk found with all the major anxiety, mood and psy-chotic disorders.

Arrhythmias

There is evidence that psychological stressors can also play an important role in precipitating serious ventricular arrhythmias. Sudden cardiac death after psychological distress has been reported anecdotally for a long time but is difficult to study sci-entifically. A systematic review of published cases of ventricu-lar fibrillation in patients without known cardiac disease could identify preceding psychological distress in 22% (Viskin and Belhassen, 1990). A recent review of 96 published studies in-vestigating psychosocial risk factors for arrhythmia found that 92% were positive (Hemingway et al., 2001). Whether type A personality traits predict sudden cardiac death after myocardial infarction remains controversial.

Congestive Heart Failure

Depression is especially common in patients with congestive heart failure. In patients hospitalized for congestive heart fail-ure, major depression is independently associated with increased mortality and readmission 3 and 12 months later.

Hypertension

The stress-related physiological response subcategory of PFAMC is particularly relevant to hypertension. There are some data sug-gesting that blood pressure reactivity to stress is a risk factor for the development of hypertension and may influence progression of disease as well. Many studies have examined relationships be-tween personality, coping style, blood pressure reactivity and hy-pertension, but conflicting results and methodological limitations have precluded any consensus conclusions. Findings regarding the effects of stress, anger, hostility, or anxiety on blood pres-sure in normotensive individuals are not necessarily relevant to clinical hypertension. A high level of anxiety at baseline evalu-ation independently predicted twice the risk for development of hypertension in middle-aged men but not in women in one study, but in another study by the same investigators, anxiety did predict hypertension in women (Markovitz et al., 1991). Some epidemiologic studies have found depression and/or anxiety symptoms predictive of later development of hypertension even after controlling for confounding factors. Several measures of occupational stress appear to be independent risk factors for hypertension in the general population. Some of the apparent association between psychological distress and hypertension is chiefly attributable to health risk behaviors (obesity, smoking, alcohol and sedentary lifestyle).

Studies of psychological treatments for hypertension (mainly biofeedback and relaxation techniques) have demon-strated the possibility of modest but clinically significant sus-tained reduction in blood pressure but less effectively than with drug therapy. The major limiting factor in using behavioral treat-ments for hypertension is compliance, because the treatments must be self-administered indefinitely. Behavioral therapies may be helpful as an adjunctive treatment in patients receiving an-tihypertensive drugs; psychological treatment should seldom be given as the sole treatment for hypertension.