Coronary Heart Disease

Coronary Heart Disease Risk Factors and Biobehavioral Mechanisms

Coronary heart disease is the leading cause of death in industrialized countries. Several biological, behavioral, and psychological factors are associated with elevated risk for coronary artery disease (CAD) and its clinical manifestations. In the following sections, a brief review is provided of (1) the epidemiology and pathophysiology of CAD, (2) traditional risk factors for first and recurrent cardiac events (e.g., hypertension, elevated cholesterol), (3) common diagnostic procedures and treatments for patients with CAD, (4) biopsychosocial perspective, including the description of the three main categories of psychological risk factors for coronary syndromes (chronic, episodic, and acute psychological risk factors) based on the pathophysiology of coronary artery disease; and (5) potential implications for psychological interventions.

Epidemiology and Pathophysiology of Coronary Heart Disease

Coronary heart disease (CHD) refers to a broad range of disorders of the heart muscle. A total of 13 million individuals in the United States have CHD. Coronary heart disease is the most common cause of mortality in industrialized countries, accounting for one of five deaths—in the United States, 515,204 deaths in 2000. In this section, common cardiologic terminology is discussed because such information is pertinent to interdisciplinary communication with other professionals in cardiovascular medicine.

The pathophysiology of CHD is determined by multifactorial processes. The heart muscle (myocardium) pumps oxygenated blood through the body and, as is the case for all muscles, this requires adequate myocardial blood supply through the coronary arteries. Myocardial ischemia occurs when cardiac demand for oxygenated blood is not met by the supply of oxygenated blood through the coronary arteries, resulting in insufficient blood perfusion of the heart. Disease of the heart valves and weakening of the heart muscle (cardiomyopathy) are sometimes also categorized under CHD, but is not discussed here. Coronary artery disease is caused by gradual plaque formation (atherosclerosis) of the coronary blood vessels. Serious complications (heart attacks and sudden cardiac death) can occur when the coronary blood supply is abruptly blocked as a result of plaque rupture and/or blood clot (thrombus) formation. These “acute coronary syndromes” are commonly caused by myocardial ischemia and include severe chest pain or pressure (unstable angina pectoris), permanent damage to the heart (myocardial infarction), and malignant heart rhythm disturbances (cardiac arrhythmias).

Coronary atherosclerosis is not a linear process and progresses in phases. Early stages of coronary atherosclerosis are characterized by gradual deposition of lipids (e.g., cholesterol) and other blood particles in the vessel wall. At later stages of CAD, immune system-related molecules (cytokines) play a role in formation of lipid-laden cells in the vessel wall, resulting in impairment of coronary function. When severe CAD has developed, several factors may promote instability of the atherosclerotic plaque and thinning of the cap covering the plaque, both increasing the chance of plaque rupture. Plaque rupture causes partial or complete closure of the coronary artery. The sudden transient coronary obstruction that thus results can cause severe cardiac ischemia and chest pain, whereas complete sustained occlusion leads to myocardial infarction. Although plaque ruptures occur at progressed CAD stages, the actual atherosclerotic narrowing of coronary arteries is generally mild to moderate (20-70 percent) rather than severe. Biological and psychological risk factors differentially affect these increasing stages of coronary pathophysiology. The stage of underlying coronary disease is therefore a major determinant of pathophysiologic mechanisms by which psychological risk factors promote the onset of acute coronary syndromes.

In summary, early stages of atherosclerosis are generally asymptomatic because blood supply to the heart is still well preserved. Narrowing of the coronary arteries (i.e., astenosis >50 percent of the vessel diameter) may lead to decreased coronary blood supply and cause ischemia when cardiac demand exceeds coronary supply (e.g., in response to exercise or acute mental stress). Myocardial infarction may occur as a result of sudden plaque rupture and blood clot formation, causing prolonged and severe myocardial ischemia. Psychological and biological risk factors for clinical manifestations of CAD thus differ with the stage of underlying disease.

Risk Factors for Coronary Artery Disease

The major risk factors for CAD are age, male gender, diabetes mellitus, high blood pressure, adverse lipid profile, positive family history/genetic factors, overweight, physical inactivity, and tobacco smoking. The exact risk for each of these factors ranges from 50 percent to fivefold, depending on the nature of the risk factor, the population under study, the time between risk factor assessment and cardiac endpoint, and the cutoff used for presence versus absence of these risk factors. The odds ratio (OR) reflects the ratio of disease incidence among individuals exposed to a risk factor, divided by disease incidence of individuals without the risk factor. If the OR is significantly greater than one, then the risk factor is more likely to promote a particular disease. If, for example, the OR is equal to 3, than a person with the risk factor is three times more likely to have the disease than a person who does not have the risk factor. The 95 percent confidence interval is a measure of the accuracy of the estimate and ORs are statistically significant at p < 0.05 if the interval does not include the value 1.0. Ranges of estimated risks are as follows: positive family history, 1.5-2.0; diabetes mellitus, 2.4—2.8; hypertension, 1.8-2.0; elevated total cholesterol, 1.7-3.4; obesity, 1.2-1.7; and physical inactivity, 1.5-2.4. Risk factors often cluster and are frequently overrepresented in ethnic and racial minority groups. Socioeconomic status plays an important role in these associations, but cannot account for all the observed differences. A detailed review of the interaction of the multiple cardiovascular risk factors for CAD is beyond the scope of this article. It is important to differentiate between modifiable (e.g., overweight, physical inactivity, and tobacco smoking) and nonmodifiable risk factors (e.g., age, sex, family history).

Coronary Heart Disease Diagnostic Procedures and Interventions

Several diagnostic procedures exist for determining presence or absence of CAD. The most common sequence of events is that patients experience typical or atypical anginal symptoms (chest pain or pressure, shortness of breath, palpitation, or extreme fatigue). These symptoms may lead to referral for cardiac diagnostic testing. Electrocardiographic assessments are made during exercise to determine inducibility of myocardial ischemia by increasing exercise-induced cardiac demand. These assessments are often combined with noninvasive outpatient procedures involving (1) imaging of cardiac blood perfusion by radioisotope labeling of myocardial tissue using thallium or technetium or (2) determination of cardiac function by echocardiography or radionuclide ventriculography. New developments in cardiac electron beam computed tomography scanning allow for detection of subclinical coronary calcification with high sensitivity for detecting CAD. If inducible ischemia is detected, when patients have typical anginal symptoms, in case of severe coronary calcification, or when patients have a very unfavorable risk profile, coronary angiography is performed to visualize the coronary arteries by intracoronary injection of a radioactive dye. This diagnostic procedure takes approximately 1 hr and patients are generally discharged the same day.

Interventions for CAD have three generally overlapping targets: risk reduction of myocardial infarction and other cardiovascular complications, improvement of cardiac function, and alleviation of symptoms plus optimizing quality of life. Risk reduction of CAD and its clinical manifestations involves pharmacological and behavioral modification of risk factors and intervention targeted at improving coronary supply in patients with documented CAD.

When angiography indicates that CAD has progressed to coronary narrowing of >50 percent, various procedures exist that restore coronary blood supply. Percutaneous transluminal coronary angioplasty (PTCA) involves placement of a balloon-tipped catheter at the site of the stenosis, where it is inflated to reopen the blood vessel. Small metal tubes (stents) are commonly placed at the site of angioplasty to prevent recoil of the artery. Recent developments use coated stents with biological agents that can help prevent renarrowing of the opened arteries. Patients generally stay overnight postangioplasty for monitoring purposes. When angioplasty is not possible, coronary artery bypass graft (CABG) surgery is a common treatment option. During CABG, healthy vessels from the leg or near the chest are taken and placed on the coronary arteries to bypass the blockage. CABG is major surgery and requires long-term (1 week) hospitalization and recovery. In addition to these two methods of improving coronary supply (PTCA and bypass surgery), patients with high vulnerability for life-threatening rhythm disturbances can be provided with an implantable cardioverter defibrillator, which delivers a shock when a malignant arrhythmia is detected. Medications are generally used to improve cardiac function, reduce biological risk factors such as high blood pressure (hypertension) and adverse lipid profile, and decrease symptoms. Most medications have side effects that interfere with patients’ quality of life, including fatigue, headache, and reduced sexual function or interest. Behavioral and psychological interventions are used to reduce the risks associated with adverse health behaviors (e.g., overweight and smoking) and psychological factors (e.g., depression). In addition, these interventions may also improve quality of life (as discussed later).

Biopsychosocial Perspective of Coronary Heart Disease

Psychological risk factors for CAD can be classified into three categories, based on their duration and temporal proximity to coronary syndromes: (1) chronic factors, among which are negative personality traits (e.g., hostility) and low socioeconomic status; (2) episodic factors, which are transient, with a duration of several weeks up to 2 years and recurring throughout the life span (e.g., depression and exhaustion); and (3) acute triggers, including mental stress and outbursts of anger. These three types of psychological risk factors are associated with pathophysiologic mechanisms relevant to CAD progression and their effects as risk factors change with progressive stages of coronary disease.

  1. Chronic psychological risk factors involve stable characteristics, which are associated with elevated long-term risk of first myocardial infarction. The predictive value for recurrent events is less consistent for chronic psychological risk factors. The most common chronic factors are hostile personality (Type A behavior pattern), social isolation, and low socioeconomic status. Recent reports also document the role of Type D personality (a combination of high negative affectivity and high social inhibition) and mixed results have been reported regarding trait anxiety (RR =1.9; confidence interval [CI] = 0.5-8.6). There has been substantial controversy about the predictive validity of the Type A behavior pattern. Evidence over the past 15 years suggests that hostility is the toxic component of Type A behavior. Meta-analysis indicates that the elevated risk of hostility is often significant, but results are variable (RR = 1.6; CI = 0.73.3).

Low socioeconomic status predicts first cardiac events (estimated risk = 2.7), and the increased risk is not limited to the lowest strata only. Among the factors determining socioeconomic status are education level, income, occupation, economic resources, and social standing. Social isolation and elevated psychological distress are more prevalent among individuals of low socioeconomic status. Aspects of low social support can be construed as a chronic psychological risk factor as well. Social support is defined by the availability of social contacts to promote personal goals or needs. Low social support is associated with increased risk of cardiac events (RR = 1.9; CI = 0.3-13.9). Structural social support refers to the number of available individuals (e.g., marital status, number of friends). Functional social support refers to the utility of social support, including instrumental (i.e., actual help in accomplishing tasks), informational, and emotional support. Both domains of social support have been associated with increased risk of CAD. More research is needed to further disentangle the cardiovascular consequences related to socioeconomic status, chronic social stresses related to racism or adverse stigmata among disadvantaged individuals, social isolation, and sustained low perceived social support.

  1. Episodic risk factors for CAD include major depressive disorder and (vital) exhaustion.* These factors are transient (with a duration ranging from several weeks to 2 years) and are recurring over the life span. Episodic risk factors predict first as well as recurrent cardiac events. The risk of depression for first myocardial infarction is greater than 50 percent above normal (OR = 1.6, CI = 1.3—2.1), and recurrent events are significantly predicted by depression with risk ratios ranging from 3.0 to 7.8. Depression in patients with coronary disease (and other medical conditions) is often atypical, and not primarily characterized by depressed mood and/or loss of interest. Exhaustion (extreme fatigue, increased irritability, and feelings of demoralization) is a significant risk factor for incident and recurrent cardiac events. Risk associated with episodic risk factors is of similar magnitude to traditional CAD risk factors (see earlier discussion).

Major life events (e.g., loss of a spouse, unemployment and financial crisis) often precede the onset of episodic risk factors. The risk of CAD associated with episodic risk factors is primarily observed within the first 2 years following assessment. The long-term (>2 years) predictive value of depression and other episodic risk factors for adverse cardiac health outcomes is probably explained by the recurring nature of these types of risk factors.

Job-related stress can be episodic or chronic, depending on the nature of the profession. An imbalance between effort and reward, a combination of low control or autonomy and high job demand, and low job satisfaction have been associated with increased CAD risk factors and myocardial infarction. Job strain should be considered in the context of family demands as well. For example, working women with children may be at elevated risk of myocardial infarction, whereas working outside the home by itself is not associated with elevated risk of cardiac events.

  1. Acute psychological risk factors (states) can act as triggers of myocardial infarction. Disasters such as earthquakes and missile attacks increase the risk of cardiac events. Acute outbursts of anger are associated with a greater than twofold risk of myocardial infarction. However, these incidents of anger-induced myocardial infarction are very rare, and researchers and clinicians have therefore also focused on acute psychological states of milder intensity (e.g., frustration, tension, annoyance). These acute psychological factors can trigger more common but less severe cardiac events, such as transient myocardial ischemia. Acute mental stress in standardized laboratory conditions causes myocardial ischemia in 30-60 percent of patients with CAD. Mental stress-induced ischemia is generally asymptomatic (silent), in contrast to exercise-induced ischemia, during which chest pain is common.

Mechanisms accounting for chronic psychological risk factors include sympathetic nervous system-mediated proatherogenic processes, including increased lipid deposition and inflammatory processes. These factors play a crucial role in early stages of CAD. In addition to the direct pathophysiologic pathways, chronic psychological factors also promote development of episodic psychological risk factors (e.g., elevated distress levels and depression in low-socioeconomic status groups), and are associated with increased reactivity to acute stressors. Consequently, the predictive value of chronic psychological risk factors for CAD progression is mediated in part by their association with other (episodic and acute) psychological risk factors for CAD. Mechanisms related to episodic risk factors differ from chronic factors because of their transient (i.e., nonchronic) nature. Most studies have not found significant correlations between episodic factors and CAD severity. Therefore, processes involved in the transition from stable to unstable atherosclerotic plaques are probable candidates accounting for the marked predictive value of depression and other episodic factors for acute coronary syndromes. These include autonomic nervous system- and neurohormonally mediated changes in the likelihood of thrombus formation, immune system alterations, and cardiac arrhythmias. Mechanisms related to acute psychological risk factors include sympathetic nervous system-mediated increases in catecholamines, cardiac demand (heart rate and blood pressure), and stress-induced decreases in plasma volume and transient narrowing of the coronary arteries [for a detailed discussion see Krantz et al. (1996) and Kop (1999)]. These stress-induced responses can result in myocardial ischemia and plaque rupture in advanced stages of CAD

In summary, there are three types of psychological risk factors for coronary artery disease: chronic, episodic, and acute. Chronic psychosocial risk factors are involved in the early stages of CAD and play a role at advanced disease stages primarily because of their association with increased presence of co-occurring episodic and acute psychological risk factors. Episodic risk factors play a role in the transition from stable coronary disease to clinical manifestations such as myocardial infarction. Acute risk factors are primarily important at progressed CAD stages because these factors may cause myocardial ischemia and in rare cases plaque rupture or life-threatening arrhythmias.

Coronary Heart Disease and Psychological Interventions

The majority of cardiovascular behavioral medicine intervention studies have targeted patients with established coronary disease or those with elevated cardiovascular risk factors. Psychological intervention studies reported in the 1970s and 1980s generally demonstrated beneficial effects on reducing psychological risk factors as well as preventing recurrent cardiac events. In contrast, more recent studies have failed to support the earlier positive results regarding improved cardiovascular health outcomes. A few excellent reviews and meta-analyses have been published on the efficacy of psychological interventions in reducing (recurrent) cardiac events (see Bibliography). On average, psychological and educational interventions reduce cardiac mortality by 34 percent and recurrent myocardial infarction by 29 percent. These effects are similar to traditional medical interventions. In addition, improving the psychological aspects of quality of life is a valid goal irrespective of its impact on CAD. There is also a strong relationship between psychological measures and perceived symptoms such as shortness of breath and chest pain.

Psychological interventions are most effective in reducing recurrent cardiac events if they have initial beneficial effects on proximal medical (e.g., blood pressure, exercise tolerance) and psychological (e.g., depression) measures that are risk factors for these cardiac events. Interventions targeting chronic psychological risk factors often include various forms of stress management. Episodic risk factor interventions typically use common cognitive-behavioral techniques in combination with stress management and group support sessions. In patients with medical disorders, these interventions do generally not fully eradicate episodic risk factors, which in turn interferes with the ability of such interventions to prevent recurrent cardiac events. Psychological interventions can play a key role in reduction of adverse health behaviors such as smoking, physical inactivity, and poor diet. It is likely that a combination of patient-tailored psychological and pharmacological intervention is needed to sufficiently reduce and maintain psychological risk factors in patients at high risk of recurrent cardiac events.


  1. Kop, W. J. (1999). Chronic and acute psychological risk factors for clinical manifestations of coronary artery disease. Psychosomatic Medicine, 61′(4), 476-487.
  2. Krantz, D. S., Kop, W. J., Santiago, H. T., and Gottdiener, J. S. (1996). Mental stress as a trigger of myocardial ischemia and infarction. Cardiology Clinics, 14(2), 271-287.
  3. Linden, W. (2000). Psychological treatments in cardiac rehabilitation: Review of rationales and outcomes. Journal of Psychosomatic Research, 48(4-5), 443-454.
  4. Rozanski, A., Blumenthal, J. A., and Kaplan, J. (1999). Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation, 99(16), 2192-2217.
  5. Sebregts, E. H., Falger, P. R., and Bar, E W. (2000). Risk factor modification through nonpharmacological interventions in patients with coronary heart disease. Journal of Psychosomatic Research, 48(4-5), 425-441.

Back to Health Psychology.