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Depression and Coronary Heart Disease

Large amounts of research has been aimed at substantiating hypothesized psychosocial risk factors for Coronary Heart Disease (CHD), such as Type A Behavior Pattern (TABP), hostility, and anxiety. Comparatively little work, however, has examined whether depression is a significant risk factor for CHD or how it influences other more widely accepted CHD risk factors. The following will contain a review of the literature on depression and cardiovascular disease risk, as well as how depression is assessed and how other known CHD risk factors may be related to depression.

What is depression and how is it assessed?

According to H. Friedman in his book “The Self-Healing Personality”, depression generally involves feelings of sadness, tiredness, indecisiveness, and worthlessness. Depressed people tend to be aware of their problems, and are likely to be prone to excessive stress which manifests itself in a disruption of hormonal systems that are used to maintain internal homeostasis.

The most frequently used measure of depression is probably the Depression scale of the Minnesota Multiphasic Personality Inventory(MMPI). Numerous other measures for depression exist including the Profile of Mood States, the Welsh Depression Scale, the Dempsey Depression Scale, and simple ratings of depression made by an interviewer (Booth-Kewley and Friedman, 1987).

Associations of anxiety with CVDs and known CVD risk factors

The most commonly cited evidence that depression is reliably related to CHD is Booth-Kewley and Friedman’s 1987 meta-analysis of psychological predictors of heart disease. Surprisingly, out of the 18 personality-variable categories that Booth-Kewley and Friedman performed separate meta-analyses on, only SI-assessed TABP was found to be more reliably related to CHD outcomes than depression (r=.205). Depression was found to be a better predictor for CHD outcome than hostility, anger, or anxiety. All 15 studies included in their meta-analysis on depression and CHD used some manifestation of CHD or atherosclerosis as a dependent variable. When their analysis was performed separately for only the six prospective studies, depression was again strongly related to CHD outcome (r=.168), the strongest association seen when only prospective studies were included in the meta- analyses (Goldstein and Niaura, 1992). Although they conclude that more attention should be focused on depression as a component of the coronary-prone personality, the findings remain in question even by Friedman and Booth-Kewley (1988) due to numerous questions over the validity of the studies included. Further doubt over whether depression is a risk factor for CHD comes from Matthews’ 1988 meta-analysis of prospective studies on psychological predictors of heart disease. He did not find depression to be a predictor for coronary artery disease (CAD).Matthews was more conservative in the studies he selected and weighted studies according to the number of participants.

Although patients who develop cardiovascular disease are at a greater risk for subsequent depression (Carney et al., 1988; Littman, 1993), evidence for the converse is not as convincing. In four studies of institutionalized patients diagnosed with depression, two report a positive association between depression and cardiovascular mortality (Baldwin,1980; Dreyfuss et al., 1969), while two fail to report an association (Martin et al., 1985; Tsuang et al., 1980). It should be noted that these studies have been questioned in their validity due to a number of design problems. None of these studies controlled for known cardiovascular disease risk factors. Secondly, these studies were retrospective in design, and therefore any possible cause and effect relationships between depression and cardiovascular disease could not be distinguished. In fact, subjects with symptoms of depression, such as fatigue, palpitations, and decreased energy, may have had undiagnosed cardiovascular problems before the start of the study, because these symptoms are also incipient manifestations of cardiovascular disease (Hayward, 1995). Another problem of these studies comes from using institutionalized patients. This particular bias overestimates the degree of the association, because a patient who has two illnesses, a physical illness and a psychiatric diagnosis, is more likely to be hospitalized than a patient with only one disorder (Berkson, 1946). One study by Murphy et al., 1987 has avoided these particular study design pitfalls. In this prospective study where subject selection was from a community sample, the risk for subsequent cardiovascular disease death was higher among individuals with an affective disorder than among individuals without an affective disorder. The positive association in this study was larger for males(relative risk = 2.5) than for females(relative risk = 1.5).

It has been suggested that if depression increases the risk for later cardiovascular disease, the relationship may be non-linear (Hayward, 1995). In other words, low to intermediate levels of depression, a quite common experience, may have no ascertainable effect of cardiovascular health, but high levels of depression, predominantly only seen in the clinical population, may then pose significant harm to cardiovascular health. Evidencethat low to intermediate levels of depression does not greatly increase cardiovascular disease risk comes from studies that use self-report measures of depression obtained from nonclinical samples. In four prospective studies, there has been no evidence that self-reported symptoms of depression predict cardiovascular disease (Ostfeld et al., 1964; Vogt. et al., 1994; Brozek et al., 1966; Goldberg et al., 1979).

However, many recent studies investigating the relationship between depressive symptoms and CHD outcomes in nonclinical samples contradict these null findings, and suggest that self-reported symptoms of depression do actually predict cardiovascular disease. In a study of 2,832 initially healthy U.S. adults, self-reported depressed affect and hopelessness were associated with increased relative risk of fatal and nonfatal ischemic heart disease over a mean follow-up period of 12.4 years (Anda et al., 1993). Depressive symptoms, assessed using the Depression scale of the MMPI, have also been associated with increased risk of myocardial infarction (MI) in a prospective study of 409 initially healthy males and 432 initially healthy females (Barefoot and Schroll, 1996). Lastly, a recent cross-sectional study, where depression was assessed through psychiatric interview of a nonclinical random sample in Finland, has found significant positive associations between depression and increased risk for CVDs (Aromaa et al., 1994). The age-adjusted relative risk of coronary heart disease of those ages 40-64 diagnosed with depression was 4.87 (CI, 2.91-8.16) compared to those ages 40-64 who were free of psychiatric diagnosis. The hypothesis that depression is a risk factor for CVDs definitely deserves further study.

Although the evidence is inclusive in regards to whether depression is a significant risk factor in the development of CHD, there is substantial evidence that depression is associated with known cardiovascular disease risk factors, particularly cigarette smoking. According to Hayward, 1995, 22 out of 25 studies reporting the frequency of cigarette smoking in depressed versus nondepressed people found increased rates of cigarette smoking in the depressed. Additionally, depressed subjects are less successful in attempts to quit smoking (Glassman et al., 1990). In one 9-year follow-up study, depressed smokers were 40 percent less likely than nondepressed smokers to have quit smoking (Anda et al., 1990).

There are far fewer studies investigating whether depression is associated with other known cardiovascular disease risk factors, but positive associations of depression with hypertension have been reported. Cross-sectional studies of depressed persons provide evidence of increased sympathetic activity and increased blood pressure reactivity (Jonas et al., 1997), and suggest that depression may have a pressor effect on the cardiovascular system that could lead to the development of hypertension (Julius, 1988). According to Hayward, 1995, three cross-sectional studies (Heines et al, 1969; Heines, 1970; Reus and Miner, 1985) have found higher rates of hypertension in depression patients, while two cross-sectional studies did not find such an association (Friedman and Bennet, 1977; Yates and Wallace,1987). In the Yates and Wallace study, although higher rates of hypertension were not found in patients with unipolar affective disorder (depression), higher rates of hypertension were found in patients with bipolar affective disorder (mania). According to Jonas et al., 1997, unfortunately only one prospective study (Goldberg et al., 1980) has examined the effects of depression on the subsequent development of hypertension. No association was observed, possibly because of a poor study design that consisted of few subjects (640) and only a 1-3 year follow-up period. Jonas et al., 1997 have further investigated whether symptoms of depression are risk factors for hypertension in their own prospective study that consisted of more subjects (2992) and a much longer follow-up period of 7-16 years. Symptoms of depression were assessed using the General Well-Being Schedule cheerful vs. depressed scale (Fazio, 1977). The risk of experiencing hypertension was increased among whites aged 45 to 64 years who had high depression symptoms scores compared with those who had low symptom scores(Relative risk=1.80, confidence interval, 1.16-2.78) but not among whites aged 25 to 44 years. The risk of experiencing hypertension was even greater among blacks aged 25 to 64 years who had high depression symptom scores (RR=2.99, CI, 1.41-6.33).

Hypertension and smoking are most likely not the only CHD risk factors that will be shown to be more prevelant in the depressed. Physical fitness is a CHD risk factor that has not been adequetely studied among the depressed.

Some studies report physical inactivity as a risk factor for later onset of depression or depressive symptoms (Farmer et al., 1988; Frederick et al., 1988). It is unclear whether physical activity is a risk factor and/or a symptom of depression. There are also strong theoretical ties between depressed mood and various coronary-prone behaviors (Allan and Scheidt, 1996). Type A Behavior Pattern (TABP) is thought to be a reaction against an underlying, unconscious depression. As long as the Type A individual is engaged in driven, ambition-related activities, he or she is protected from awareness of the depression. When such, activities cease, however, such as after acute MI, depression often becomes unmasked. Clearly, depression is embodied within the cynical and pessimistic orientation to life assessed by the Cook-Medley Ho scale, a standard self-report measure of hostility. In classic psychoanalytic theory, depression is sometimes considered “anger turned inward,” suggesting a strong theoretical link between hostility and depression. Lastly, depression has been found to contribute to self-destructive behavior and motivates people in the direction of “quick fix” forms of satisfaction, such as cigarettes, alcohol, and fast foods high in saturated fat (Allan and Scheidt, 1996).

It is important to keep in mind that depressed patients are a very heterogeneous group. Just as only those depressed patients with increased rates for known CVD risk factors may be at a greater risk for CVDs, it is possible that only certain types of depression lead to substantially increased risk for CVDs. Fava et al., 1996 hypothesized that patients with anxious or hostile depression may have a greater risk of mortality from coronary artery disease(CAD) than other depressed patients. They tested their hypothesis by assessing the relationship between CAD risk factors and anxiety and hostility in a sample of 138 depressed outpatients. They found that patients with anxious or hostile depression had a profile of greater CAD risk compared with patients with depression who had low anxiety and hostility scores. The most significant association seen in the anxious or hostile depression groups was with increased serum cholesterol levels. Fava et al., 1997 further suggest that the heterogeneity of major depression might account for null findings among unipolar depressed patients of increased risk for CVDs and known CVD risk factors. Limitations of the study include that their findings are derived from outpatients with mild-to-moderate major depression and may not be generalizable to more sever forms of depression. Also, this study did not control for other known CVD risk factors. Although more studies are surely needed before any reliable conclusions can be made, depression may only lead to significantly increased CVD risk when psychosocial CVD risk factors other than depression, such as hostility and anxiety, are present as well.

Depression, Job strain, and CHD

“Job strain” has been defined by Karasek (1979) as work in jobs with high psychological demands (work pace + conflicting demands) and low decision latitude (control + variety and skill use). In a half-dozen epidemiological studies over the last decade, occupational stress researchers have found job strain to be a significant risk factor for CHD. To our knowledge, there have been no published studies examining possible relationships between depression and job strain. Although it has been suggested, the potential influence of job characteristics in the development of psychological states, such as depression, has rarely been studied (Schnall et al., 1994). According to Schnall et al., 1994, it is unlikely though that personality variables such as depression account for the association between job strain and hypertension or CVD. Research is needed to develop a theory that specifies possible interactions between environmental stressors(e.g., job strain) and personality characteristics(e.g., depression), and to improve the methodology of such studies.

Depression and its determinants

There has been remarkably little research on the determinants of depression, particularly social class and job stress. Such factors might shape personality development in childhood. For example, certain parental behavior patterns (i.e., overly strict, critical and demanding of conformity) are more common in low SES households, and may be viewed as a reflection of the parents’ occupational and other life experiences, which are characterized by low control and insecurity. Similarly, an adult’s experience, which might include stressful, low control jobs, may shape their personality development (Kohn and Schooler, 1982). Thus, research on the social determinants of personality measures believed to be associated with illness outcomes needs to be a major priority in future research.


Although it is widely accepted that depression is commonly observed in CHD patients, the question of whether depression can significantly contribute to the etiology of CHD remains in debate. Recent prospective studies that have found depressive symptoms to predict common CHD endpoints, such as myocardial infarction and ischemic heart disease, provide strong evidence for considering depression a CHD risk factor, but more studies of this sort are needed to settle this issue. There is overwhelming evidence, however, that depressed people are more likely to lead a self-destructive lifestyle that leads to increased risk for other known CHD risk factors, primarily smoking. Furthermore, depression has been theoretically tied to more proven coronary-prone behaviors, such as TABP and hostility. One possibility for the null findings regarding associations between depression and CVDs is that only certain types of depression may pose harm to cardiovascular health. As one study (Fava et al, 1996) suggests, only anxious or hostile depressed patients may be at significantly increased risk for future development of CVDs. More studies are needed which investigate how depression interacts with other heavily studied coronary-prone behaviors in relation to their combined effects on cardiovascular health. Similarly, further research is needed to develop theories as to how hypothesized CHD risk factor personality characteristics, such as depression, interact with environmental stressor models of CHD risk, such as job strain, and improve the methodology of such studies. Lastly, additional research is needed to elucidate the social determinants of depression, particularly social class and job stress.


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