Behavioral Cardiology and Heart Disease
Ellen A. Dornelas
Matthew M. Burg
Historical Perspective and Overview
The earliest appreciation that psychological factors contribute to diseases of the heart can be attributed to Celsus, who is reported to have said, “Fear and anger and any other state of mind may often be apt to excite the pulse.” John Hunter, a leading pioneer of cardiovascular medicine and pathology, acknowledged the links between his outbursts of anger and his anginal attacks, proclaiming, “My life is in the hands of any rascal who chooses to put me in a passion.” He died suddenly in 1793 after participating in a violent argument at a faculty meeting. Sir William Osler later described the circumstances of Hunter’s death: “In silent rage and in the next room he gave a deep groan and fell down dead” (1). Although these reports are anecdotal indications that physicians understood the importance of psychological factors for their cardiac patients, it was two cardiologists, Meyer Friedman and Ray Rosenman, who in 1959 were the first to conduct rigorous scientific studies of these factors and their relationship to CHD. The results of their work drew widespread attention to a clustering of behaviors, including a highly competitive, goal-driven approach to daily activities, aggressive behaviors, a need to perform activities at an unusually high rate of speed, hyperarousal of emotional and physical alertness, and hostile affect, that came to be called the “Type A Behavior Pattern” (2). Although their early studies found an association between this behavior pattern and onset of coronary heart disease (CHD), later studies were unable to replicate this finding. The work of Friedman and Rosenman, however, led to the development of a field, now called Behavioral Cardiology, which applies the theories and principles of the behavioral sciences to the practice of medicine with cardiac patients. The past four decades have seen exponential growth in the understanding that psychological factors are important, both as precipitants and sequelae of cardiac events. Psychosocial factors associated with risk for CHD include stress and emotional elements (e.g., anger, depression), personality traits (e.g., cynicism), social factors (e.g., social support), and lifestyle choices (e.g., tobacco use). This chapter focuses on the role that these factors can play in promoting risk for an acute cardiac event and on recovery from these events.
Psychological Factors and Heart Disease
Stress
Stress has been used ubiquitously to describe both external precipitants and internal reactions that can include emotional, behavioral, cognitive, and physiological responses to environmental triggers. In the section that follows, a heuristic definition is used that defines stress as an external or environmental situation that may tax a person’s coping abilities. In the following section, the relationship between acute and chronic external stressors to CHD is described. Following this section, known psychosocial risk factors (hostility, depression, anxiety, and social support) are described as precipitants and sequelae of cardiac disease.
Acute Stress
Early case series (3,4) describe cardiac arrest or sudden death in response to acute stress such as grief or fear. A recent observational study receiving a great deal of attention in the media reported that sudden emotional stress (e.g., tragic news or news of a close relative or friend’s death) can precipitate severe but reversible left ventricular dysfunction in patients without cardiac disease (5). Epidemiologic studies have shown that sudden death increases in populations suffering emotionally devastating disasters such as earthquake or war (6,7). Toivonen et al. (8) observed proarrhythmic repolarization changes in the ECG of healthy house officers exposed to the sudden stress of an on-call alarm, and an increase in implantable cardioverter
devices shock-treated ventricular arrhythmias was seen in the weeks following the terrorist attacks of 9/11, in both New York City (9) and distant locales (10). In working patients with implantable cardioverter devices, ventricular tachycardia occurs more frequently on the first day of the work week (11).
devices shock-treated ventricular arrhythmias was seen in the weeks following the terrorist attacks of 9/11, in both New York City (9) and distant locales (10). In working patients with implantable cardioverter devices, ventricular tachycardia occurs more frequently on the first day of the work week (11).
Acute stress is also a potent trigger of myocardial ischemia in patients with coronary artery disease (CAD). Holter monitoring studies have found ischemia to be common during periods of low physical exertion but moderate to high mental and emotional stress, with the incidence and duration of these episodes directly related to the intensity of the stress experienced (12,13). Studies in the laboratory with measures of ischemia (left ventricular dysfunction, new regional wall motion abnormality by stress echo, myocardial perfusion defects) have shown that acute mental stress can provoke myocardial ischemia in up to 50% of patients with CAD and the prognostic significance of this “mental stress ischemia” has been demonstrated in several studies (14,15,16). In these studies, patients with ischemia during acute laboratory stress demonstrate 2.4 to 3.0 times increased risk of myocardial infarction (MI) or unstable angina 1 to 4 years later (17,18,19). In addition, the Psychophysiological Investigations of Myocardial Ischemia (PIMI) study investigators (20) reported a 3.0 rate ratio for death over a 5-year follow-up among CAD patients with mental stress ischemia. This was the first study powered to demonstrate an effect for death tied to mental stress ischemia in the lab. Overall, there is consistent evidence that emotional distress, anger, and extreme excitement can trigger acute coronary syndrome (ACS) and sudden cardiac death in susceptible individuals with both immediate (21) and long-lasting impact (20).
Chronic Stress
Chronic stress, assessed as a function of events such as divorce, loss of job, death of a loved one, or catastrophic illness, can play a role in first occurrence of cardiac events. For example, one case control study showed that the cardiac patients reported greater numbers of recent stressful life events than controls (22). In addition, the world-wide INTERHEART study comparing 11,119 first MI patients to 13,648 matched on age and gender controls also showed that stressful life events in the year preceding the index MI were more common in cardiac patients compared to the control group (23).
The work environment has most often been used to study chronic stress as it relates to CAD (24). In this research, job strain, defined as the confluence of high job demands and low job control, has been associated with increased CVD prevalence (25). Greater numbers of work-related stressors are also associated with increased risk for cardiac mortality (26). Overall, the data suggest that chronic stressors influence the development and progression of CAD. Job strain has been the most often studied model of chronic stress and lack of control (e.g., the perception of little power to impact on decision making) is thought to be the most pathogenic component of work-related stress (27). Although environmental stressors have an independent effect on CHD, it is the combination of external stressors and internal psychological factors, such as those described below, that exert the greatest degree of influence on the development and course of CHD.
Hostility and Anger
Hostility is a multidimensional psychological construct that involves three primary factors: cynicism/mistrust (cognitions), anger/contempt (emotions), and verbal/physical aggression (behaviors) (28). Anger is an affective experience, ranging from mild irritation or annoyance, to full-blown rage (29). As described, a relationship between anger/hostility and CHD has been proposed throughout the centuries, with Rosenman and Friedman in the 1950s launching scientific investigations into the Type A Behavior Pattern. They found this behavior pattern to incur a greater than twofold increased risk of developing ischemic heart disease, controlling for traditional risk factors, in an initially healthy sample (30). A detailed analysis of this data (31) revealed the relative importance of the hostility and anger components as predictors of CHD onset. Hostility is also associated with a 1.9-fold increased risk of death (32), up to a 14.6-fold increased risk of cardiac events among patients with CAD (33), and a 2.5-fold increased risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA) (34). Highly hostile patients also demonstrate more rapid progression of carotid atherosclerosis (35) and are more likely to evidence myocardial ischemia during mental stress testing (36,37). The experience of moderate to extreme anger is associated with a 2.5-fold increased risk of MI for up to 2 hours after anger provocation (38); the induction of anger in the laboratory, either by structured interview (36) or by recall of a previous anger-provoking incident (39,40), can provoke myocardial ischemia in patients with CHD. Thus, hostility has come to be thought of as the most pathogenic aspect of the type A behavior pattern. This line of research has led to new developments in the understanding of how other negative emotions, particularly depression, are related to CHD.
Depression
Depression refers to both a diagnostic entity (e.g., major depressive disorder) and a clustering of symptoms with psychological (e.g., feelings of sadness), behavioral (e.g., difficulty functioning in ordinary role activities), and somatic (e.g., sleep problems) characteristics. Symptoms of depression are seen in up to 65% of patients after MI, with between 16% and 22% evidencing major depression (41,42,43) and up to one third developing depression over 12 months (44). For these patients, depression follows a chronic relapsing course, particularly if a full remission is not realized (44). Life-time history of depression increases risk for cardiac-related morbidity and mortality (45,46,47). In patients with chronic CAD, a diagnosis of major depression incurs a twofold risk of ACS (41), and depression after acute MI incurs a greater than fourfold risk of 6-month mortality, and ongoing mortality risk for 5 years (44,48,49). Depression after MI also increases the risk for reinfarction, particularly for patients with post-MI ventricular arrhythmias (50). This effect of depression is independent of CAD severity, left ventricular dysfunction, or history of MI. In addition, this effect is seen for both diagnostic depression (41) and subsyndromal depression (e.g., score ≥10 on the Beck Depression Inventory) (42,44,49). Depression prior to or after coronary artery bypass grafting (50) also incurs a threefold risk for CAD progression over 6 months (51) and a fourfold risk of cardiovascular death over 2 years (51), independent of a range of medical comorbidities, behavioral health risks, or surgical complications.
Anxiety
Anxiety is a clustering of symptoms that include psychological (uncontrollable worry) and somatic (acute physiologic arousal) features. Between 15% and 30% of post-ACS patients experience symptoms of anxiety (52). Although normative, higher symptom levels at the time of hospitalization for ACS are related to poorer subsequent psychological and psychiatric outcomes (53,54). Panic attacks, characterized by palpitations, sweating, dyspnea, chest pain, and feelings of losing control or going crazy, are common manifestations of anxiety disorders.
The prevalence of panic disorder in cardiac populations ranges from 10% to 15% (55) and 30% to 50% of patients with recurrent chest pain and normal coronary arteries meet criteria for panic disorder (56).
The prevalence of panic disorder in cardiac populations ranges from 10% to 15% (55) and 30% to 50% of patients with recurrent chest pain and normal coronary arteries meet criteria for panic disorder (56).
Studies of initially healthy populations have linked anxiety to ACS incidence (57,58). In addition, the few studies concerning post-ACS anxiety and prognosis demonstrate almost fivefold independent risk of in-hospital cardiac complications or death (59), 2.5-fold independent risk for 1-year recurrent MI (60), and 8-year, 4.7-fold independent risk of a cardiac event for patients with both high anxiety and social inhibition (61). Although these studies are clearly suggestive, they rely mostly on self-report of symptoms and have been accomplished with small numbers of post-MI patients. There is a well-established relationship between depression, hostility, and heart disease, but there is a need for additional research to determine the impact of anxiety on CHD prognosis.
Social Support
Social support is an important predictor of initial ACS incidence and subsequent mortality. In addition, high levels of support can buffer the impact of the ACS event. Lack of social support in combination with high levels of stress was associated with a more than fourfold increased mortality risk among patients in the Beta Blocker Trial (62). Subsequent studies have linked the presence, degree, and quality of intimate social ties—including marital status, whether the person lives alone or with others, and the availability of various sources of emotional support—to mortality in patients after ACS (63,64,65,66). Indices of social network size, frequency of social activity, group membership, and perceived support have also been found to predict survival (67,68,69,70) controlling for sociodemographic and disease severity indices.
A number of explanations have been offered for the beneficial effects of social support on cardiovascular disease (71
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