Coronary Heart Disease Behavioral Cardiology in Clinical Practice

Steven M Schwartz & Mark W Ketterer. The Health Psychology Handbook: Practical Issues for the Behavioral Medicine Specialist. Editor: Lee M Cohen. Sage Publications. 2003.

Heart disease continues to be the number one killer of men and women in the United States, where myocardial infarctions (MIs) occur at a rate of about 1.5 million per year. For about 30% of these patients, death is sudden and the first “symptom” they experience. Ischemic heart disease or coronary heart disease (CHD) is predicted to remain the leading cause of death worldwide through 2020. Despite these compelling statistics, the survival rate from acute coronary events continues to improve, and more than 1 million people survive acute coronary events annually in the United States. Thus, issues pertaining to psychological functioning, behavioral risk, and quality of life are increasingly relevant as heart patients face more favorable prospects for recovery and rehabilitation. Assessing and treating these patients’ health risk behaviors, such as smoking, obesity, fatty diet, lack of exercise, nonadherence to medical regimen, social isolation, and emotional status (e.g., depression, anger, anxiety) is essential to secondary prevention efforts and is critical for optimal recovery of function and general health.

The modern evolution of behavioral cardiology arguably began during the mid-1970s with the work of Friedman and Rosenman (1974) on “Type A behavior.” Since that time, behavioral scientists and clinicians in collaboration with medical colleagues have considerably expanded and refined our understanding of the relationship among psychological, emotional, psychophysiological, and behavioral factors in the development, maintenance, and exacerbation of CHD. Given the increasing clinical role of behavioral clinicians in managing heart patients, this chapter provides (a) a brief review of the etiology of heart disease, (b) a cognitive-behavioral case conceptualization of CHD, and (c) a pragmatic presentation of the clinical issues for assessing and treating patients with coronary artery disease.

Psychophysiological and Biomedical Aspects of the CHD Patient


Atherosclerosis is defined as the buildup of plaques (e.g., “blockages,” “stenoses,” “lesions,” “occlusions”) typically composed of lipids, complex carbohydrates, and blood products along artery walls. The development of atherosclerosis is multidetermined and progressive unless the condition is vigorously treated. By the time a cohort reaches middle age, half or more will have some amount of atherosclerosis. However, some people reach advanced ages of 80 years or more with little or no clinically significant atherosclerosis. Therefore, although a number of etiological risk factors have been identified, our understanding of the etiology remains incomplete. However, most of the currently accepted risk factors (aside from family history, sex, and age) are modifiable by medication, changes in lifestyle, or both.

When patients have lesions at one site (e.g., coronary arteries), it is highly probable that they will have lesions at other sites (e.g., carotid, femoral, or renal arteries). Blockages that are large enough to threaten blood supply, and thus to threaten oxygen flow to critical areas (e.g., heart, brain, kidney, legs), produce transient ischemia (i.e., reversible oxygen supply/demand deficit) or permanent damage secondary to infarction (i.e., tissue death due to cessation of blood supply). Large plaques (50% or greater blockage) are associated with a higher risk of infarction. Interestingly, although large plaques may threaten adequate blood flow locally, chronic deprivation of an adequate blood supply to the heart can provoke the development of collateral arteries around the occluded sites as a remarkable biological compensatory strategy. These collateral arteries then provide natural bypasses in the event of infarction of the main trunk. Also of note, although large blockages are more likely to produce an infarct, the much higher prevalence of “small” lesions (less than 50% occlusion) means that most MIs (absolute number) actually occur at sites with low-level occlusion.

Atherosclerosis will follow a “stuttering” course marked by periods of growth, stasis, and (sometimes) regression. Plaques may be fibrous and stable, or they may be unstable, containing a pool of dead cells and lipids covered by a thin membrane or cap and eccentric in shape. When this cap ruptures, the contents of the pool are thought to provoke thrombus formation (i.e., clot), sometimes self-resolving (but perhaps provoking angina) and sometimes evolving into a full blockage of the artery (MI). Fully 85% to 90% of infarctions are believed to be caused by this sequence. The cause of plaque instability is thought to be chronic recurring inflammation, perhaps with some causal contribution from genetic factors and/or infection with Chlamydia pneumoniae (Ridker, Hennekens, Buring, & Rifai, 2000; Ross, 1999).

Precisely what triggers a rupture remains a matter of debate (Allen & Scheidt, 1996), although it has been hypothesized that elevated emotional states may be one triggering mechanism secondary to emotion-aggravated contractility of the heart, blood pressure changes, increased blood viscosity, vasoconstriction, and/or localized vasospasm. Thrombogenesis is certainly encouraged by various psychobio-chemicophysical events, including via stress reactivity pathways. For example, elevated circulating catecholamines and platelet aggregation are associated with states of acute fear or anger (Markovitz, 1998). Heart rates and diastolic and systolic blood pressures rise, sometimes precipitously, in response to even mild transient and contrived stressors in the laboratory (Goldberg et al., 1996; Ketterer, Freedland, et al., 2000). Daily life stress is typically more meaningful and chronic, provoking more intense and prolonged emotional burden on patients. This has been measured with in vivo monitoring studies (e.g., Polk, Kamarck, & Shiffman, 2002).

Note that even when accounting for all of the factors in epidemiological studies, only about half of cases of ischemic heart disease can be explained (Farmer & Gotto, 1997). Although most infarctions are probably the result of unstable plaque rupture, 2% to 10% of all infarctions in the human heart occur in the absence of any atherosclerosis, and another 5% to 10% occur in a part of the coronary vascular tree without plaque. Thus, acute thrombus formation can occur independent of plaque rupture. It is now believed that the occurrence of a MI requires something beyond atherosclerosis.

Depending on location (which determines the amount of heart muscle affected by cessation of blood flow) and the presence of collateral circulation and/or anatomical variants in the coronary vascular tree, the size and significance of an infarction can vary widely. MIs considered large will generally decrease the heart’s pumping function (i.e., ejection fraction [EF]). A normal EF (i.e., the proportion of blood ejected from the left ventricle during systole) will average about 66% in the heart of a healthy adult but includes values above 50%. Unless the patient engages in strenuous physical activity, EFs above 40% may be undetectable by the patient. EFs below 40% define heart failure, and this generally affects routine physical function (i.e., dyspnea, fatigue, and/or dependent edema). With EFs below 20%, the patient may be considered for a transplant.


Angina pectoris refers to transient chest pain or discomfort resulting from ischemia of heart muscle. The discomfort occurs secondary to an oxygen supply/demand deficit. Hence, strenuous physical activity that increases the heart’s workload is a common trigger. Most commonly experienced as chest “discomfort” (e.g., pain, pressure, fullness, squeezing), angina sometimes manifests as arm pain, jaw pain, lower back pain, headache, nausea/vomiting/upset stomach, cognitive confusion, dyspnea (i.e., shortness of breath), dizziness, syncope/near syncope, and/or weakness. Stable angina has well-delineated triggers (typically physical exertion and sometimes stress) and responds well to nitrates. Unstable angina is far less predictable and is often accompanied by severe and prolonged pain. The presence of unstable angina is clinically considered an acute coronary event requiring emergent care because it may be caused by plaque rupture.

Angina is generally presumed to result from ischemia, but this “causal” relationship is less than perfect (e.g., Krantz et al., 1994). Importantly, the symptoms of angina are shared by a wide range of other conditions, including acute emotional states, psychiatric disorders, and other medical conditions, making differential diagnosis difficult at times (Richter, 1992; Schwartz, Trask, & Ketterer, 1999). Most episodes of ischemia captured on Holter monitoring in both laboratory testing and in vivo settings are not associated with chest pain/pressure or other symptoms, typically referred to as silent myocardial ischemia. (A Holter monitor is a small portable device that collects electrocardiogram [ECG] data on a continuous basis during daily life.) Furthermore, most episodes of chest pain are not associated with ischemia as measured by surface ECG (“atypical” or “noncardiac” chest pain). In fact, recurrent emergency room visits by cardiac patients for chest discomfort without evidence of ischemia/infarction are quite common.

Angina is strongly associated with depression/anxiety, and cognitive-behavioral treatment of emotional distress has been found to reduce episodes of angina and ischemia (Blumenthal et al., 1997; Ketterer, Fitzgerald, et al., 2000; Lewin, 1997). Pain intolerance secondary to depression/anxiety, or ischemia/angina provocation secondary to fear/anger, increases chest discomfort (Ketterer, Fitzgerald, et al., 2000; Ketterer et al., 1998; Schwartz et al., 1999), and chest discomfort provokes treatment seeking and aggressive diagnostic/treatment decisions by physicians. Thus, if not directly affecting disease progression, emotional distress will still affect quality of life, illness behavior, and disease management in adverse ways.

Because angina is the major driving force behind medical system use, treatment of emotional distress may reduce this use (Black, Allison, Williams, Rummans, & Gau, 1998; Davidson, 2000; Frasure-Smith & Lesperance, 1998). Recently, Schwartz and colleagues (1999) proposed a spectrum approach to chest pain management (e.g., pain and palpitations) that includes presentations consistent with pain/anxiety, Syndrome X/nonischemic chest pain, Prinzmetal’s angina, and angina pectoris. Because psychological and behavioral problems are similar in angina and other forms of chest discomfort regardless of the underlying cause, disease management strategies should be multidisciplinary. The rise of “chest pain” clinics for nonemergent chest pain attests to greater recognition of this overlapping and complex problem.


The heart contracts and relaxes in a highly orchestrated fashion or rhythm to efficiently move blood from the venous compartment (deoxygenated blood) to the arterial compartment (oxygenated blood). This is a two-phase process in which the heart fills during the relaxation phase (diastole) and then the heart forcefully empties during the contraction phase (systole). This orchestration is electrochemical in nature and is maintained by a specialized cluster of cells collectively called the sinoatrial node or natural pacemaker. Disruption of this sequencing is referred to as an arrhythmia. Arrhythmias can range from benign to malignant. Of particular clinical significance are sustained ventricular tachycardia and ventricular fibrillation, the presumed causal culprits in sudden cardiac death. Note that the ventricular portion of the heart is the primary pumping chamber for the brain and general body. There are a number of factors (e.g., drugs, disease, infarction, emotional distress) that can produce abnormal rhythms, many of which can be serious or even life threatening. In severe instances, blood flow may slow sufficiently to cause acute brain failure (syncope). When the heart has been thrown into inefficient sequencing of its contractions, cardioversion (transthoracic electrical shock) is used to achieve a normal sinus rhythm.

Patients at high risk for future life-threatening arrhythmias will likely receive antiar-rhythmic medications that regulate heartbeat, pacemakers, and (in severe cases) implantable cardioverter defibrillators. This latter device, like the pacemaker, is placed inside the body and can function as an “onboard” crash cart that greatly improves both sudden cardiac death and all-cause mortality relative to medication management alone (Gilkson & Friedman, 2001). However, there is growing evidence that the device itself can produce problems of behavioral or psychological maladjustment in a significant subgroup of patients (for an excellent review, see Sears, Todaro, Lewis, Sotile, & Conti, 1999).

Behavioral clinicians are particularly familiar with the sinus tachycardias most characteristic of panic attacks and other acute anxiety and mood states. Importantly, clinicians must be aware that patients can and do develop anxious presentations from more dangerous heart rhythms as well (Schwartz et al., 2002). Also, there is considerable evidence that the subjective symptom of palpitation correlates poorly with underlying cardiac rhythm (Barsky, 2001; Barsky, Cleary, Barnett, Christiansen, & Ruskin, 1994), as was described previously for chest pain. Although it is generally acknowledged that panic spectrum disorders can and do masquerade as cardiac problems, the reverse is also true. To illustrate the complexity among anxiety, palpitations, and cardiac rhythm, Lessmeier and colleagues (1997) found that 67% of patients presenting for treatment of paroxysmal supraventricular tachycardia (PSVT) met criteria for panic and that PSVT went unrecognized in 55% of the patients even after an initial medical evaluation. Equally striking, 86% of patients displayed resolution of anxiety symptoms with antiarrhythmic therapy.


This chapter has already alluded to the notion that the heart can develop compensatory strategies in the presence of heart dysfunction/disease (e.g., development of collateral arteries as a natural bypass). Hemodynamics is the study of the forces involved in the movement of blood through the circulatory system. It is through the study of these processes that one can understand the physical and functional changes that occur in the diseased heart as it attempts to maintain homeostasis in the body. A simplified version of the process is as follows. As the EF of the heart declines in heart failure, or with infarct-related heart muscle damage, the heart begins to struggle to push blood out into the body, creating a variety of physical changes in the heart’s structure over time. This process, referred to as remodeling, can be characterized by heart enlargement, thickening of the heart walls, and leaking heart valves that regurgitate blood as the heart becomes more inefficient. This inefficiency is manifest in wall motion abnormalities. Wall motion abnormalities can be visualized by blood pool radionuclide imaging (technetium sestamibi) or on echocar-diogram. Localized perfusion defects can be visualized by uptake of radioactively labeled glucose (technetium pyrophosphate or thallium). This type of diagnostic testing is thought to reflect impairment of blood flow to an area of heart muscle. This impairment can be reversible when the patient is not being stressed, or it is “fixed” (present when the patient is both at rest and stressed), implying permanent tissue death (“infarction”). Likewise, certain patterns on the ECG (ST segment depression) reflect ischemia or infarction. Table 15.1 presents some of the common cardiac diagnostic and treatment procedures.

Cognitive-Behavioral Case Conceptualization of CHD

Understanding the factors that contribute to both acute and chronic aspects of CHD would be incomplete without consideration of the psychological, emotional, and behavioral characteristics of the patient or the patient population. The clinical study of these unique risk factors and their modification is at the very “heart” of behavioral cardiology. Given what is currently supported by the evidentiary literature, a general cognitive-behavioral conceptualization of cardiovascular disease development and rehabilitation can be constructed on the following assumptions:

  • Many of the biological processes that underlie cardiovascular disease develop over time out of health risk behaviors and lifestyles. These risk factors for CHD are relevant to disease development, maintenance, and exacerbation and also contribute to related and complicating conditions such as emphysema, type 2 diabetes, pulmonary hypertension, and heart failure.
  • Lifestyle and behavioral risks are generally immediately and highly gratifying. The powerful reward value of these risk behaviors causes them to become habitualized as a consequence of frequent and persistent practice, thereby making them particularly resistant to intervention. For example, a pack-a-day smoker receives 70,000 infusions of nicotine during the course of a year; that is a number of “hits” unparalleled by any other recreational drug.
  • The negative, debilitating health consequences of these behaviors typically develop slowly over time, allowing the person to accommodate to many of the symptoms of physiological degradation and reduced function.
  • The individual’s cognitive and emotional status mediates lifestyle risk factors and also contributes more directly to disease development, maintenance, and exacerbation through the autonomic nervous system’s stress reactivity pathways associated with fight/flight and psychoneuroimmunological pathways.
  • The biological, psychological, and behavioral factors noted previously, as well as environmental factors, influence one another in a bidirectional or reciprocal fashion.

Table 15.1 Common Cardiac Diagnostic and Treatment Procedures

ECG: Monitors the electrical activity in the heart to past or present heart attack, the location of the heart affected, and the rhythm of the heart; can be used with or without exercise (treadmill testing) and in vivo with Holter monitoring (continuous monitoring) or event monitoring (event-specific recordings)
Echocardiogram: Ultrasound evaluation of the heart allowing for an imaging of the working heart to be captured, including chambers, valves, and heart muscle walls; can also be done in conjunction with exercise or use of a medication (e.g., Dobutamine) that increases heart rate
Invasive procedure that is performed by inserting a catheter (tube-like device) into an artery (typically in the groin) and advancing through the arterial system into the heart, with the catheter able to measure pressures inside the heart chambers and, when equipped with a camera, able to take video of the heart in action
transluminal coronary
angioplasty (PTCA)/
directional coronary
atherectomy (DCA):
Advancing a catheter up to a blockage in a critical artery and reducing the occlusion by expanding a small balloon or using a plaque-cutting device, with stents (stainless steel mesh tubes) sometimes being put into place to prevent re-occlusion
Coronary artery
bypass graft:
Surgical procedure that takes blood vessels from another part of the body (typically in the legs or chest) and then stitches them around the blocked coronary artery

Assessment of the CHD Patient


Identification and triaging of emotionally distressed patients from cardiac settings often requires the use of an objective, psychometrically sound questionnaire to aid clinical staff in recognizing distress. There are a number of well-validated self-report measures for assessing CHD patients, and most focus on emotional status, functionality, and/or quality of life. Table 15.2 lists some of the commonly used tools and the underlying constructs they purport to measure. Any of the psychometric instruments validated as prospective predictors of cardiac outcomes could be used, but they are clearly redundant in terms of their predictive utility (Ketterer et al., 2002). Because of brevity, nonstigmatizing content, and ease of administration and scoring (many CHD patients will become frustrated with lengthy questionnaires or test batteries), the Hospital Anxiety and Depression Scale (HADS). with a cutoff of 13 or greater, is recommended (Herrman, 1997). The chapter authors suspect that screening will eventually require an instrument designed for completion by a significant other so as to circumvent denial (Ketterer et al., 1996, 1998, 2002), but this remains to be proven in prospective studies.

Table 15.2 Self-Report Measures for the Cardiac Patient

  • Hospital Anxiety and Depression Scale
  • Symptom Checklist-90-Revised (Brief Symptom Inventory)
  • Beck Depression Inventory
  • State-Trait Anxiety Inventory
  • Crown-Crisp
  • Cook-Medly Hostility Scale
  • Ketterer Stress Symptom Frequency Checklist
  • Millon Behavioral Health Inventory
  • Toronto Alexithymia Scale
  • SF36
  • Seattle Angina Questionnaire
  • Minnesota Living With Heart Failure Questionnaire
  • Cardiac Anxiety Questionnaire

Clinical Interviewing (Functional Analysis)

Evaluation should, as always, include a thorough psychosocial history, mental status exam, and review of cardiovascular risk factors (Table 15.3 lists the domains to consider in an initial evaluation). Importantly, this evaluation should include identification of barriers to change as well as cardiovascular risk factors. Behavioral assessment models have long been used in the functional analysis of problem behaviors (Barrios, 1988), including illness behavior (Schwartz, Gramling, & Mancini, 1994). Because the modifiable risk factors for CHD are deeply embedded in the psychology and behavior of the patient, approaching the initial assessment of the patient can be greatly facilitated by using a functional-analytic framework. The Stimulus-Organismic-Response-Consequence (SORC) model (Goldfried & Sprafkin, 1976) is one of several common models and is used here for illustration purposes.

The Stimulus (patient triggers or hot buttons). The stimulus portion of the SORC model refers to the triggers or cues that evoke health risk behavior. Stimulus control variables relate to cardiovascular risk in a number of ways. Overt behaviors such as substance abuse (e.g., nicotine, alcohol, cocaine), lack of exercise, and acute emotional reactions can have a broad range of environmental and cognitive triggers. For example, it is not unusual for the mere presence of a critical supervisor to trigger acute autonomic arousal and concomitant emotional distress (e.g., anxiety, anger, irritation, worry), even when there is no current overt conflict. Therefore, it is imperative to identify the patient’s triggers (or buttons), noting that patients may vary greatly in their understanding of or insight into the functional relationships between triggers and emotional or behavioral responses.

Organismic Variables. Organismic variables are the dispositional characteristics of the patient (e.g., genetic, physiological, temperamental, experiential) that are peculiar to the individual. The familial aspects of cardiovascular disease reflect both genetic factors and early learning experiences. Of particular interest may be the early modeling of cardiovascular risk behaviors such as smoking, angry acting out, and a maladaptive emphasis on competition and/or achievement at the expense of other important aspects of development.

Table 15.3 An Evaluation Checklist for CHD Patients

  • Frequency and triggers for chest pain
  • Disease-specific worries (often grief over disease-imposed role changes or limitations)
  • Disease-specific knowledge (what the patient knows about his or her condition and recovery)
  • Physical activity level (including activities such as walking and gardening)
  • Smoking (e.g., number of cigarettes per day, smoking history in years)
  • Eating habits (e.g., high-risk foods with high fat content, salt, sugar; eating behaviors such as binging, rapid eating, stress/emotional eating)
  • Alcohol intake (e.g., number of drinks per day/week, drinking history, CAGE questions)
  • Interpersonal conflicts (particularly focusing on work and marital relationships)
  • Job stress (e.g., deadlines, responsibilities)
  • Sleep habits (e.g., apnea, insomnia, restless leg syndrome)
  • Emotional status (e.g., depression, grief, anxiety, anger/hostility, alexithymia)
  • Comorbid medical conditions (e.g., diabetes, heart failure, chronic obstructive pulmonary disease)

The Response. The response describes the target risk behavior itself (e.g., eating a fatty meal). The response can also be operationalized as a nonbehavior (i.e., failure to act) such as an inability or unwillingness to engage in regular exercise. In addition, behavioral risk includes not only overt acts or failures to act but also covert behaviors such as certain cognitions. Table 15.4 lists some of the common maladaptive cognitions to assess in the CHD patient.

Consequences. There are several factors that affect the power of a consequence to shape behavior. Many of the risk behaviors seen in the CHD patient are highly overlearned, habitualized, and/or otherwise resistant to change. Understanding the ways in which these behaviors are reinforced or maintained is critical to the secondary prevention process. Timing is particularly important in health risk behavior. As a general rule, temporal proximity of behavior and consequence will wield greater influence over the behavior. As noted previously, many risk behaviors provide immediate gratification. In particular, it is important to view the CHD patient’s actions as maintained by relief from negative affective states.

Emotional Status

There are several emotional domains that have consistently proven themselves to have robust relationships to cardiac outcome and/or are relevant to individual work with the CHD patient (for an excellent review, see Rozanski, Blumenthal, & Kaplan, 1999). Assessment of depression/dysphoria, anger/hostility, stress, anxiety, and alexithymia is essential in a thorough evaluation of the CHD patient. It is important to note that many patients may present with subclinical levels of emotional distress (relative to cutoffs for traditional psychiatric patients), and these levels may still be clinically significant, related to important clinical outcomes, and worthy of treatment even if they do not meet formal DSM (Diagnostic and Statistical Manual of Mental Disorders, fourth edition [American Psychiatric Association, 1994]) diagnostic criteria. In many cases, patients will “somatize” their distress (i.e., report only the physical symptoms and deny or minimize the affective/cognitive symptoms). Therefore, emphasizing the concrete benefits of improved sleep or energy, or of reduced chest pain, can help the patient to accept treatment.

Table 15.4 Common Cognitive Errors in CHD Patients

  • Chronic and excessive worry or anger about uncontrollable events (e.g., “catastrophizing” finances of retirement, allowing kids to sink or swim, confronting boss) is a chronic stressor for many patients. In many cases, patients have difficulty in discriminating the degree of control present in any stressful situation.
  • Inaccurate understanding of “normal” is common, particularly among Type A or assertiveness-impaired patients. Unrealistic expectations regarding their own behavior or others’ behavior can cause chronic aggravation or feelings of being unloved (commonly accompanied by the “shoulds” or a set of rigidly held obligations or responsibilities).
  • “Anyone would react as I did” is probably a variant of the misunderstanding of “normal” and can be assessed using the “Rule of 100” test.a
  • Malevolent attributions are present in many cases. Often, patients will make attributions regarding the motives and intentions of others as malevolent (e.g., a car cuts them off on the highway, thereby provoking rage because the other driver was “obviously” stupid, irresponsible, and/or dangerous).
  • Surreptitious arrogance in interpersonal interactions is often characterized by overt politeness but dismissal of others’ desires/opinions and devaluation of their feelings.
  • Inability to trust is frequently present and may have its origins in malevolent attributions or deeper insecurities that patients might not acknowledge or even be aware of fully.
  • Catastrophizing lateness/“unproductive” time is part of the time urgency characteristic of the Type A personality. Often, patients will have a profound intolerance for “downtime.” Various forms of self-pacing exercises requiring the patient to go slower are helpful.
  • Confusing “right” with “harmful” might also be called the “just world hypothesis,” in which patients will get very angry over perceived injustices, slights, or inequities. They believe that if they can “prove” their case, the world would have to come into compliance. In fact, it often does not matter whether one is right or not, and anger will still kill. Is this worth dying for?
  • Importance of “things” over persons, that is, what is regretted on deathbeds is time not spent with family/friends rather than time not spent at the office.
a. The clinician should ask himself or herself, “If 100 people were in this situation, what proportion would react in this way?” Thus, the clinician’s sense of normative behavior can be used to gauge how “normal” the patient’s reaction is.

Obtaining two or three adjectives for affect, and then obtaining concrete examples where these imply chronic conflict, for each significant other (e.g., parent, sibling, spouse/lover, child, boss) facilitates efforts toward mapping the patient’s psychosocial stressors. This can also provide some clues as to how the patient construes and responds to others and as to the success of these coping patterns. Of particular importance are overlearned/automatized coping responses (which are presumably learned early in life and are often outside the patient’s awareness) and whether they succeed at merely reducing distress but not stress (maladaptive) or at reducing both distress and stress (adaptive). Testing the patient’s history against the “Rule of Three” may be a useful exercise. If the patient has made the same mistake three times or more (e.g., getting fired, marrying an abusive alcoholic), it is highly likely that this is a deeply ingrained pattern that the patient does not perceive regarding himself or herself. It should become a goal of treatment to raise the patient’s awareness of this pattern, define a face-saving way of construing the pattern, and then develop more adaptive alternative responses. For example, instead of framing the problem as “I’m an angry guy,” it may be more acceptable and constructive to frame it as “I care too much and have too high a set of expectations, and therefore I get frustrated a lot.”

Depression. There are now numerous published reports linking depression and depressive symptoms to adverse cardiac outcomes (e.g., Booth-Kewley & Friedman, 1987; Carney, Freedland, Eisen, Rich, & Jaffe, 1995; Cassem & Hackett, 1973; Frasure-Smith, Lesperance, & Talajic, 1993). Based on this evidence, depression should now be considered an established independent risk factor for CHD outcomes (Glassman & Shapiro, 1998). Unfortunately, there are not yet any randomized controlled trials of sufficient methodological rigor to demonstrate a reduction in CHD morbidity or mortality as a result of treating depression either psychotherapeutically or psychopharmacologically. However, SADHART (Zoloft vs. placebo) and ENRICHD (stress management plus a selective serotonin reuptake inhibitor [SSRI] vs. standard care) are ongoing clinical trials targeting depression in CHD. What can be said with some certainty is that CHD/depression comorbidity does affect patient functionality, compliance, and quality of life such that assessment and aggressive treatment where indicated is an essential part of comprehensive care regardless of the impact on CHD-specific morbidity and mortality.

Anger. The work of Friedman and Rosenman (1974) on the Type A personality identified a number of characteristics that tended to cluster together and appeared to be associated with cardiovascular prognosis. Apart from ambition, “busyness,” and constant effort, these characteristics include cynicism/mistrust, stubbornness/opinionated, perfectionism/demanding, alexithymia, control-ling/overcontrolled, impatient, and worrier/obsessional. Importantly, not one of these characteristics can be argued as patho-gnomonic of the syndrome, nor does any appear to have a direct effect on the genesis or exacerbation of CHD. Rather, these characteristics are of importance because they tend to foster a hostility complex or “AIAI” (aggravation, irritation, anger, and impatience).

Although the literature has been marred by inconsistent operational definitions, psychometric problems with self-report measures, and a more complex relationship between the AIAI construct and CHD than was originally conceived, it nevertheless remains prudent to assess the patient’s ability to modulate anger. AIAI has been proved to be a causal factor for CHD in a randomly assigned, controlled clinical trial of cognitive/behavioral stress management that targeted AIAI and reduced death/MI rates by 37% relative to placebo controls (Dusseldorp, van Elderen, Maes, Meulman, & Kraaij, 1999; Friedman et al., 1986, 1987).

A related issue concerns confrontation avoidance, where conflict with either family members or coworkers often leads to “stewing” (anger) or chronic anxiety. This has been conceptualized as the “anger in/anger out” issue. This can occur for a variety of reasons, including the Type A who despises but will not discuss conflicts with his or her boss and the Type A’s spouse who is afraid of expressing his or her disagreement over even trivial matters due to the consequent verbal assault (e.g., “that’s so stupid”) or cold shoulder. One common example seen is the cardiac patient who has living with him or her a late adolescent who is not working, going to school, or contributing to the workload at home and who may be abusing drugs or even being verbally abusive with the parents.

Anxiety. The data supporting a relationship between anxiety and CHD is perhaps more complex and less compelling than those supporting depression. As stated previously, acute anxiety might play an acute role in plaque ruptures, arrhythmias, and blood pressure. Anxiety has been implicated as a major risk factor for CHD in multiple prospective risk factor studies, particularly for death or sudden death (Kamarck & Jennings, 1991; Ketterer, 1999; Kubzansky, Kawachi, Weiss, & Sparrow, 1998). Unfortunately, no large-scale randomized control trials exist, nor are any under way, to examine treatment in this population and cardiac outcomes. It should be noted that acute digoxin toxicity (e.g., tremor, loss of appetite, confusion) may mimic anxiety.

Alexithymia. Many CHD patients are found to display some degree of alexithymia, which refers to difficulty in identifying and/or labeling emotional states in self and others. Patients with this disorder will display a poverty of vocabulary in reporting their feelings and describing other people’s personalities, and they will typically not explore psychosocial circumstances as possible causes of their problems. They will present as emotionally concrete (as opposed to metaphorical) in talking about what appear to be emotionally charged situations. When exploring their psychosocial circumstances, it is necessary to gently probe for concrete event/behavioral details because these patients rarely volunteer information spontaneously because they frequently view it as irrelevant. Alexithymia can make it difficult for many patients to benefit from traditional psychological intervention, although they are typically good at complying with behavioral assignments.

Substance Use

Assessment of substance use, particularly tobacco products, is particularly important in any evaluation. Smoking is a powerful predictor for many diseases, including CHD. If the patient is an active or recent smoker, immediate referral for Zyban or an SSRI and possible nicotine replacement should be facilitated (Edwards, Murphy, Downs, Ackerman, & Rosenthal, 1989; Ketterer, Pickering, Stoever, & Wansley, 1987; Murphy, Edwards, Downs, Ackerman, & Rosenthal, 1990). Smoking is such a potent predictor of outcomes that hesitation is not prudent unless the patient insists on thinking it over. The patient should be taught techniques to avoid smoking cues (e.g., bars, sitting around after meals) and to disrupt smoking habits (e.g., smoke with the opposite hand, change brands, smoke menthol), and should be taught relaxation procedures to help control acute urges prior to setting a contracted quit date (preferably during a psychosocially quiescent period). Giving the patient 24-hour-per-day access to the clinician during the first month of cessation is a privilege that will rarely be used or abused, and it seems to assist some patients in managing their impulses.

Although not a common problem in this population, chemical dependency (e.g., cocaine, alcohol) should be ruled out. It is a futile exercise to try to treat emotional distress in someone whose central nervous system is under assault by fluctuating levels of psychoactive substances. Detoxification may be necessary before further treatment can proceed. Note that prolonged alcohol abuse can result in car-diomyopathy. Prevalence rates for cocaine abuse in CHD do not exist, but it is clear that chronic cocaine use, particularly when smoking is the route of administration, can lead to early heart disease. Because cocaine can provoke coronary vasoconstriction, chest pain, and MI as well as depression, it is important to consider this in the history of the patient. Cocaine use is probably the most common single factor precipitating MI in young people (e.g., under age 40 years), so a drug screen may help to account for early CHD.

Sleep Apnea

Sleep apnea is a periodic cessation of breathing during sleep that is an underappreciated comorbidity in CHD. Clinicians should suspect sleep apnea when there are signs of persistent nightly snoring, bed partner complaints or descriptions of choking/gasping/cessation of breathing, and/or chronic fatigue (“excessive daytime sleepiness”). Patients may also manifest subtle signs of cognitive dysfunction or mood symptoms. Suspected apnea should result in referral for evaluation to a sleep center. It is not clear whether treatment of sleep apnea lowers the risk of MI/death, but this seems likely to be the case (Ketterer, Brymer, Rhoads, Kraft, & Kenyon, 1994). Because many apneics develop a reactive depression due to self-attributions regarding their “laziness,” treatment of sleep apnea can improve mood (Dahlof, Ejnell, Hallstrom, & Hdner, 2000).

Cognitive Dysfunction

Of particular importance in this population, particularly given advanced age, are consideration of whether the patient displays any cognitive impairment (often subtle and in the absence of waxing/waning arousal and attention). The use of a cognitive screening tool or procedure (e.g., month, year, three items immediate and delayed, counting backward) at initial evaluation is important. Because of the patient’s vascular disease and/or arrhythmias (particularly those patients who have atrial fibrillation), the likelihood of mild-moderate, early-stage, multi-infarct dementia (often manifesting on magnetic resonance imaging/computerized tomography [MRI/CT] as “periventricular leukomalacia” or “ischemic white matter changes”) is elevated. Although the patient may still be highly functional, irritability/frustration over subtle memory-related problems may be an aggravating factor if he or she externalizes causality. Ruling out alternative, potentially arrestable causes (e.g., a thyroid-stimulating hormone for thyroid problems, a venereal disease research laboratory or a rapid plasma regain test for neurosyphilis) is important, but such causes are only rarely found. Patients often fear a large cerebrovascular accident more than they fear a heart attack. Because prophylaxis of cerebrovascular accidents is the same as the regimen followed for MIs, patients can be reassured that all reasonable steps are being taken, and their concern can be used to further motivate “taking care of themselves.”

The Importance of Collateral Clinical Data

Because of the high rate of denial/mini-mization/alexithymia present in this patient population, the clinician should be somewhat skeptical about the patient’s version of his or her life and circumstances. Although it is important to understand how the patient attributes meaning to events, psychological “holes” in narration (e.g., “Gee, I don’t know why she left me”) should be seen as important and indicative of a chronic coping problem.

Significant others should always be used as collateral sources of information when evaluating a patient or tracking response to treatment. Sometimes, this can be accomplished by simply asking the patient, “How does your wife [husband] think you are doing?” Other times, it is necessary to obtain independent contact with the significant other because of the patient’s denial/alexithymia or other lack of insight. Often, it is necessary to obtain this data out of the patient’s hearing range given that many spouses report “walking on eggshells” so as not to provoke the patient’s ire. One prudent tactic is to simply tell the patient that “it’s always helpful to have another person’s perspective on how you’re doing.” At a later point in time, the clinician can encourage the patient to use an appropriate significant other as a “monitor” under the mutual contract that the spouse should not be punished for providing accurate but unwelcome feedback.

As an adjunct to interviewing significant others, the Spouse/Friend Ketterer Stress Symptom Frequency Checklist (KSSFC) (Ketterer et al., 1996, 1998, 2002) is recommended for obtaining a significant other’s assessments of the patient’s emotional status. The KSSFC is unique in this feature of allowing both patient self-ratings and ratings by significant others. The spouse/friend KSSFC can be administered by sending it home with minimal written instructions and a stamped addressed envelope to “someone who knows you well.” The patient and significant other should be encouraged to not discuss the questionnaire until after it has been mailed back. If the clinician is seeking direct input from a spouse/significant other on the patient’s routine emotional functioning, it is critical that the conversation occur without the patient being present. It has been demonstrated that spouse/friend-reported depression using the KSSFC is a stronger correlate of coronary artery disease severity (by angiography) than is self-report and that denial of depression (spouse/friend minus self-ratings) is an even stronger correlate (Ketterer et al., 1996). Furthermore, spouse/friend ratings (and not self-ratings) of anxiety were the only predictor of angina at 5-year follow-up, and it was shown that denial of distress (particularly AIAI) is a very strong predictor of mortality (Ketterer et al., 1998). For this reason, the chapter authors routinely send their male patients home with a questionnaire about themselves to be given to “someone who knows you well” to complete and return independently by mail before discussions with the patients. Although not yet documented, it will be interesting to see whether this relationship holds true for female patient/male significant other dyads.

Treatment and Clinical Practice

Stress and Coping Framework

Stress is a concept that most people, including those with CHD, readily accept and for which they have some intuitive understanding. Framing any psychological or behavioral problems within a diathesis stress model rather than using more traditional or formal psychiatric nomenclature (e.g., “crankiness” rather than “anger,” feeling “down” rather than feeling “depressed,” “worried” or “stressed” rather than “anxious”) will typically provoke the least resistance and help to facilitate a therapeutic alliance. Clinicians working within a traditional psychiatric context and looking to develop cardiac referrals will face resistance from patients even before their first visits. Ideally, treatment should be done as part of a multidisciplinary cardiac team or consultation service rather than removed in a separate psychiatric setting to maximize destigmatization. Table 15.5 summarizes some of the treatment studies focusing on stress reduction.

Here the transactional model of Lazarus and Folkman (1984) works nicely. In the most general sense, coping efforts can be presented to patients as taking one of two tacks: problem-focused coping or emotion-focused coping. For heuristic purposes, these two coping efforts can be discussed as if they are separate, independent coping methods, whereas in vivo they most often interact in dynamic fashion and over time the patient will need to integrate them more effectively. Problem-focused coping, or efforts aimed at defining the problem, its solution, and implementation of instrumental actions designed to bring about resolution, is often highly developed in CHD patients. Despite their good problem-solving skills, CHD patients may display poor discrimination skills in situations where problem solving is likely to be ineffective. Consequently, they may manifest an inability to profit from experience (e.g., banging their heads against a brick wall) in apparent defiance of punishing consequences. Repeated failures may lead to AIAI. Consequently, feeling trapped in stressful circumstances is a common experience.

Reliance on problem-focused coping strategies often comes at the expense of good, constructive, emotion-focused coping skills. Issues such as poor self-pacing, inability to relax or tolerate “downtime,” and substance use are indicative of poor emotion-focused coping.

It is usually useful to teach some form of relaxation to new patients. Acute reductions in heart rate and blood pressure, and the subjective benefits (e.g., calming, reduced worry, reduced chest pain, reduced headache, easier sleep onset) that accompany these exercises, provide an immediately perceived sense of control over previously “uncontrollable” events and so reinforce instructions regarding stress and CHD. The chapter authors use such a procedure prior to all group sessions because it also seems to foster psychological mindedness, permitting possible alteration of pathogenic cognitive attributions. Helping patients to master abbreviated relaxation methods, such as a “cleansing breath,” is important in the transfer of relaxation skills to in vivo stressors.

The core goal of stress management in coronary artery disease patients is to reduce the frequency/intensity/duration (or “density”) of emotional distress (or “stress”). The clinician should consider whether the patient’s psychosocial environment is unusually stressful (i.e., triggers) and should identify one chronic stressor (or a few) and use ongoing life events to alter habitual cognitions/behaviors (“coping”). An alcoholic spouse, a demanding or abusive boss, and kids who are abusing drugs and sponging off the patient all require a different nexus of the intervention. For example, the chapter authors have seen a half dozen cases where getting an angry spouse on an SSRI resolved a patient’s chest pain.

Frequently recurring stressors that lead to problematic emotions/behaviors should be identified and reviewed at each session to see whether the patient is attempting suggested alternatives and whether the alternatives are “working” (i.e., reducing the density of emotional distress). By attacking the largest stressors first, the patient is most likely to succeed at having a big effect quickly. The only exception to this strategy is when the patient is too overwhelmed (fearful) of attempting an alternative response or when response-specific skills deficits are present and require time to remediate. For example, the patient might not know how to behave assertively and/or might not be able to appropriately discriminate between assertive and aggressive behaviors. For such a patient, time must be spent reviewing events and teaching and even role-playing skills until the patient begins to perceive the unavoidability of facing the “dragon” (usually a boss, parent, child, or spouse) and has attained adequate skills. If such attempts are unsuccessful, consideration should be given to involving the dragon in treatment.

The clinician should assess and begin to challenge self/other perceptions (“I’m/He’s the kind of person who …”). Many cardiac patients, while readily labeling others, seem to have lived unexamined lives. This means that the uniqueness (and maladaptiveness) of one’s own personality often is not part of the way in which the patient attributes meaning to events. Once the clinician has a firm grasp on the patient’s habitual ways of thinking/responding, it is critical to find a positive (or humorous) or pragmatic way in which to frame this trait. Thus, an obsessional person can be described as “thorough” or “careful,” or he or she can be described as “picky.” The former will generally be received by the patient as a positive trait (perhaps carried too far at times), whereas the latter will evoke defensiveness. Once rapport is established, teasing/humor can be a powerful tool for getting the patient to cast himself or herself in a new light and for diffusing angry or resentful emotional responses. The locus of the problem then is no longer “out there” but at least partly “in here.” Well-written readings (generally full of stories/cases) on topics such as Type A behavior (Friedman & Ulmer, 1984), assertiveness (Alberti & Emmons, 1975), panic attacks (Sheehan, 1983), and nurturant communication (Gordon, 1970) can be helpful in getting the patient to think about his or her life, beliefs, and behavior. Without such rich biographical examples, the patient tends to restrict his or her perspective (e.g., “I’m right, dammit, and that SOB is going to admit it”) so as to win the battle while losing the war. The clinician who can bring a rich body of personal, historical, or clinical vignettes to bear will teach the patient more quickly than will the clinician who deals only in abstractions (Friedman, 1979).

It is important to review weekly/monthly stressful events with the patient to ascertain frequency of stressors, the cognitive/behavioral response of the patient, whether a suggested alternative response was tried, and the success/failure of the response as well as to encourage alteration of future events. It is common for patients to not recognize that a “new” event is in fact the same as, or at least similar to, a previous pattern. Thus, helping the patient to perceive the similarities is necessary before he or she will experience familiarity and so the opportunity for a new choice. Some patients are deliberately evasive or seem to be truly unable to recall examples of stressful interactions from their own lives. Some such patients will offer relatively trivial or minor events, avoiding discussion of the major stressors. If a patient is reluctant/unable to offer examples from daily life, the clinician should use clinical stories or examples from his or her own life to destigmatize/normalize and provide examples of situations that the clinician thinks are applicable to the patient’s situation. The chapter authors have observed many such patients who, despite no discussion of the significant stressors in their own lives, nonetheless benefited from hearing the counselors’ or others’ stories in group sessions. Indirect feedback (usually from a spouse) indicates that the patient is attempting to alter his or her habitual way of thinking/coping.

Optimizing Self-Management: Using a Family Practice Model

The goal of the therapist is generally to make himself or herself obsolete as soon as possible, although the idea of a “cure” in any psychotherapeutic relationship is untenable (Hoyt, 1995). The chapter authors find the family practice model (Hoyt, 1995; Morrill, 1978) attractive for the CHD patient. In this light, they find it helpful to think of themselves as “coaches” rather than as “doctors” or “therapists” who serve as periodic resources for reality testing and problem solving. Although the initial stages of therapy may follow a more traditional pathway, the course of treatment is best conceived of as intermittent but longitudinal, with the ultimate treatment goal of assisting the patient in fitting disease self-management into the unique circumstances of his or her own life.

Treatment episodes evolve into “tune-up” or “booster” sessions that reinforce skills already acquired or focus narrowly, in a problem-solving manner, on current stressors with which the patient is stuck. The therapy should also secondarily serve to support and reinforce adherence to secondary prevention efforts given that long-term adherence rates in cardiac rehabilitation are generally poor (Burke, Dunbar-Jacobs, & Hill, 1997). This is an often neglected aspect of the coaching role. It is critical to recognize, accept, and work within the patient’s cognitive, emotional, behavioral, intellectual, fiscal, and life structure limitations so as to help him or her reengineer a healthier lifestyle. One issue in particular pertains to helping the patient to distinguish between a lapse (i.e., momentary slip in behavior) and a relapse (return to baseline level of the problem behavior). It is not uncommon for patients to have lapses, and these should be normalized for the patient. The intent here is to circumvent the patient from allowing lapses to evolve into relapses (e.g., “Well, I already smoked two cigarettes, so I might as well smoke the whole pack”).


Behavioral clinicians are often less familiar with the types of medications used in treating cardiac diseases. Thus, Table 15.6 provides a list of the classifications of the most common medications along with a summary of the functions associated with each medication type. Importantly, patients can develop tolerance to these drugs, rendering them less effective over time with frequent use.

The advent of the newer antianxiety/antidepressive agents (mostly serotonin and noradrenalin reuptake inhibitors but also atypi-cals such as Buspar and Wellbutrin) has revolutionized psychopharmacotherapy in CHD patients. Although these new agents are no more effective at treating anxiety/depression than are the older agents, the older agents (tricyclic or heterocyclic antidepressants) have anticholinergic properties (e.g., dry mouth, blurry vision, orthostatic hypotension) that make adherence problematic. In CHD patients, these agents prolong the “QRS” interval that is thought to place some patients at risk for possibly fatal arrhythmias. However, in the only (nonrandomized) comparison of patients on tricyclic antidepressants (TCAs), death rates were actually lower (Pratt et al., 1996).

Table 15.6 Common Cardiac Medications Listed by Function

  • Nitrates (e.g., Sublingual nitroglycerin, Nitropatch, Isordil, Sorbitrate, Ismo, Imdur): Drugs that produce vasodilation, used particularly for the relief of angina
  • ACE inhibitors (e.g., Capoten/Vasotec, Monopril, Destril, Prinivil, Altace, Accupril): Vasodilators that are used as antihypertensives
  • Beta blockers (e.g., Inderal, Lopressor, Toprol, Corgard, Sectral): Drugs that serve as beta-division adrenergic blockers, thereby reducing heart rate, blood pressure, and strength of heart contraction used for hypertension and relief of angina
  • Calcium channel blockers (e.g., Cardizem, Dilacor, Procardia, Norvasc, Isoptin): Central and peripheral vasodilators that serve as antihypertensives and anti-ischemics used to treat chest pain, hypertension, and irregular heartbeats
  • Digoxin (e.g., Lanoxin, Digitoxin): Decreases the strength of heart contractions and allows the heart to keep beating regularly; used for arrhythmias
  • Diuretics (e.g., Lasix, Dyazide, Esidrix): Medications to increase urinary output and decrease fluids in the body and cardiovascular system; particularly used in heart failure
  • Anticoagulants (e.g., asprin, Coumadin, Ticlid, Persantine, Plavix, Lovenox, Ecotrin, Heparin): Change the blood’s viscosity by acting as blood “thinners”
  • Antilipidemics (e.g., Lipitor, Zocor, Mevacor, Lopid, Lescol, Niacin): Medications that affect blood lipids by reducing low-density lipoprotein (LDL, bad cholesterol) and total cholesterol and by increasing high-density lipoprotein (HDL, good cholesterol)
  • Antiarrhythmics (e.g., Quinidine, Betapace, Amniodarone, Norpace, Rythmol): Help to prevent both atrial and ventricular arrhythmias

The use of SSRIs in the treatment of stress among CHD patients requires thorough initial instructions, careful monitoring of side effects, comparatively low dosing, and consideration of possible drug-drug complications. Doses typically used in this population are at or below the generally recognized therapeutic range in psychiatric patients. Thus, 10 to 20 milligrams of Celexa or 25 to 50 milligrams of Zoloft is adequate for perhaps 90% of this population. Because the delay in onset is slow and variable, the adage “start low, go slow” is advisable. Many patients will stop the medication if no change is observed during the first few days unless the importance of at least a 1-month trial is emphasized repeatedly. With some SSRIs (e.g., Paxil, Remeron), there often is an immediate soporific effect, and these should initially be tried at night. Otherwise, the medications are taken in the morning to avoid interfering with sleep and with food to minimize gastrointestinal distress (i.e., abdominal cramping or diarrhea). Most of the improvements will “sneak up” on patients over 10 days to 6 weeks. Indeed, it is common for patients to say “I don’t feel any different” but for family members and/or coworkers to notice a change in the patients. Prepping patients about the subtle effects of these medications can go a long way toward circumventing unrealistic expectations and potential nonadherence. Tracking a symptom (e.g., chest pain, fatigue, sleep onset delay, nocturnal awakening) in an empirical fashion can help to document improvements. Patients may be inclined to attribute improvements to other factors. It is critical that clinicians indicate their belief that the medication is probably the cause.

Common side effects within 24 to 48 hours of starting therapy include diarrhea/abdominal cramping (about 10% of patients). Half of those experiencing diarrhea/abdominal cramping are only mildly affected, and it should resolve within 10 days. The remainder must be tried on other agents. Headache occurs in about 3% of patients and generally resolves within 10 days. In addition, intense anxiety occurs in about 1% of patients. Over several weeks, about one quarter of patients develop loss of libido or erectile problems. Alternative agents, or referral to a psychiatrist for additional agents, should be considered. Some weight gain (7 to 10 pounds) may occur.

The chapter authors have observed several adverse effects of SSRIs that are unique to this population. Some patients, usually with a history of prior atrial fibrillation, may develop worsened atrial fibrillation on SSRIs. The authors believe that consultation with a psychiatrist is necessary to select a safe and effective agent (e.g., Buspar, Wellbutrin). Likewise, because of the effect of some SSRIs on cytochrome P450 metabolic pathways in the liver, some drugs will be removed from the bloodstream more slowly, thereby raising bioavailability. Management can include reduced dosing of the affected agent or use of another SSRI that is less likely to have this effect. Celexa and Zoloft are minimally likely to interfere with other medications and so are generally first-choice agents. Among the medications potentially affected in cardiac patients are digoxin and beta blockers. Digoxin toxicity can result in confusion/cognitive impairment, loss of appetite, and a resting tremor. Potentiation of beta blockers by use of an SSRI can result in lowered heart rate and blood pressure. Clinically, patients will complain of worsened fatigue or tiredness, dizziness, or light-headedness. Because of the effects on the liver, hepatic strain will sometimes result from use of an SSRI. This is most common in patients with prior liver injury (e.g., history of alcohol abuse or hepatitis) or in patients receiving other hepatically difficult medications (e.g., lipid-lowering agents). In severe enough cases, weakness, nausea, and loss of appetite will indicate low-level hepatic failure and should result in immediate cessation of the drug until liver function tests can be obtained. Some SSRIs may be less likely to have this effect.

Many patients will resist referral to a psychiatrist but will accept these agents from a cardiologist or a primary care physician. If one is attempting a first trial, working with the cardiologist/primary care physician may be adequate. But if special circumstances occur (e.g., nonresponse, intolerance of two agents, multiple or problematic side effects such as sexual dysfunction, need for larger doses, recent history of substance abuse, propensity for somatization), referral to a psychiatrist should become a goal of psychological treatment.

Another option may be to use the herbal St. John’s wort, which is widely used in Europe for the treatment of depression. Several dozen randomized clinical trials on St. John’s wort have demonstrated an effectiveness equivalent to that of TCAs (and therefore presumably SSRIs) but with fewer side effects than TCAs (Linde & Mulrow, 1999), although other reports have called these data into question. Preparations by reputable manufacturers (e.g., Centrum, Quanterra) should be used because smaller sources have not carefully standardized source or dose given that these supplements are not regulated by the U.S. Food and Drug Administration. Because St. John’s wort is not viewed as “artificial” or a “psychiatric medication,” patients will sometimes try it (or even insist on it) rather than the better understood and tested SSRIs. Importantly, St. John’s wort is known to decrease digoxin levels by about 25% to 33%.

Case Study

The case of “Harriet R.” is a useful one that illustrates many of the psychological aspects of CHD. Harriet was a 46-year-old, white, married mother of three children who was referred for stress management by her cardiologist after she had experienced an MI 6 months earlier. No risk factors were detected other than her constant stress.

Harriet lived with constant tension over avoiding confronting her sometimes outspoken and opinionated husband. One of the early examples of tension was that her husband frequently “forgot” to do things he was supposed to do, and Harriet was resentful that she had to remind her husband to do things and was often criticized by him for her constant reminding (which he described as “nagging”). For example, she reported that she always had to remind him to take his hymnal to choir practice. Not only did she feel angry over always having to remind him, but she frequently experienced chest pain when thinking about these interactions. Harriet’s husband seemed quite concerned but was not able to empathize with her. Rather, he too would get angry when she reminded him to do things.

Following suggestions from the therapist, Harriet agreed to “deliberately not remind” her husband for a week. He “spontaneously” began remembering things himself, and it became apparent to Harriet that her worry/resentment was totally wasted energy. Not only did it seem that she did not need to remind her husband so often, but the number of negative interactions that the couple experienced went down and the frequency with which Harriet experienced angina was greatly reduced.

At this point, discussions with Harriet’s therapist shifted her concerns to the belief that her daughter might be gay and that her husband would ban the daughter from the family if he found out. Like her experiences with “reminding her husband,” whenever she began to worry about her daughter’s sexual orientation, Harriet experienced frequent angina. After reviewing why Harriet thought her daughter was gay, the therapist agreed that it was likely and encouraged her to discuss this with her daughter. Pointing out that Harriet had previously sold her husband short, the therapist coached the patient on how to approach the topic with her husband. He responded with surprise and disappointment, but after pondering the possibility for a few days, he stated that he would still love her and want her in the family.

These experiences helped Harriet learn that much of her concern and worry were generated by her own expectations and that her perceived negative outcomes were not always as predictable as she had once believed. Over the course of treatment, Harriet became better at recognizing the role of her beliefs and expectations in her stress levels, and she was able to greatly reduce the frequency with which she became angry at others. This resulted in remarkable reductions in the frequency and severity of her angina. Harriet reported to her therapist that when she would begin to feel any anger, she could quickly assess the potential “validity” of what was making her angry, and most of the time the anger went away immediately when she realized that the situation was not as negative as she had initially thought.

The chapter authors have not yet found it necessary to refer a patient for electroconvulsive therapy (ECT). But if a patient presents an otherwise intractable depression, special considerations are necessary. Heart failure, aneurysm, and arrythmias are considered contraindications to ECT.

Summary and Conclusions

There is mounting evidence that psychological and behavioral factors play an independent and critical role in the development, maintenance, and exacerbation of CHD. The clinical behavioral sciences, including health psychologists of all stripes, have played a significant role in moving this scientific literature forward. More recent trends have allowed for practitioners to play more central roles in clinical settings such as Phase II cardiac rehabilitation and consultation services targeting cardiology patients. These trends are likely to continue, thereby allowing greater and more varied practice opportunities with this patient population. This chapter has attempted to provide an experienced and practical set of recommendations for working clinically with the CHD patient. There is a continued need for more practice-based writing in this arena that combines evidence-based literature with clinical experience. In addition, novel methods of integration into service delivery behavioral interventions must be explored for all manner of secondary prevention targets (Trask et al., 2002).