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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.

Conclusions

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.


References

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Anxiety and Coronary Heart Disease

The idea that a link may exist between anxiety and the heart has been around for as long as the history of medicine has been documented. However despite a wide spread public perception that stress and anxiety are significant risk factors for coronary heart disease(CHD), numerous conceptual and methodological difficulties in studying whether a relationship between anxiety and CHD exists have scared away many researchers from even attempting such studies(Byrne and Rosenman, 1990). It is only very recently, with advances in methodology, that possible associations between certain types of anxiety and CHD have been uncovered.

What is anxiety and how is it assessed?

Anxiety is generally defined as a psychobiological emotional state or reaction that can be distinguished most clearly from other emotions such as anger or sadness by its experiential qualities. An anxiety state consists of unpleasant feelings of tension, apprehension, nervousness, and worry, and activation of the autonomic nervous system. The physiological manifestations in anxiety generally include increased blood pressure; rapid heart rate(palpitations or tachycardia); sweating; dryness of mouth; nausea; vertigo; irregularities in breathing; muscle tension; and muscular-skeletal disturbances such as restlessness, tremors, and feelings of weakness(Spielberger and Rickman, 1990).

Anxiety also refers to relatively stable individual differences in anxiety-proneness as a personality trait. People who have high trait anxiety are most likely to perceive stressful situations as being personally dangerous or threatening and to respond to such situations with elevations in state anxiety. The stronger the anxiety trait, the more often the individual has experienced state anxiety in the past, and the greater the probability that intense elevations in state anxiety will be experienced in threatening situations in the future (Spielberger and Rickman, 1990).

State and trait anxiety are measured using a variety of different approaches. Projective techniques such as the Rorschach inkblots and the Thematic Apperception Test are used extensively in the clinical evaluation of anxiety. However, these tests do not lend themselves to quantification and are therefore limited in the extent they can be used in research. Rating scales and psychometric self-report inventories and questionaires are by far the most popular procedures for assessing anxiety in research. An advantage of such instruments is that they are easily administered and scored and do not require a great deal of expensive professional time. The standard rating scale to measure anxiety, the Hamilton Anxiety Rating Scale(HARS- Hamilton, 1959), is composed of 100 symptoms of anxiety evaluated by the clinical examiner that are aggregated to define 13 scale variables. The most commonly used psychometric self-report inventory is probably Spielberger’s State-Trait Anxiety Inventory (STAI- Spielberger et al., 1970). Major revisions were made to STAI in 1979 to develop a “purer” measure of anxiety in order to provide a firmer basis for differentiating anxiety disorders from depressive reactions. Many other self-report psychometric inventories and questionnaires exist such as the Taylor Manifest Anxiety Scale(MAS-Taylor, 1953), Cattell’s Trait and State Anxiety Measures(Cattell and Scheier, 1963), the Affect Adjective Check List(AACL- Zuckerman and Lubin, 1965), the SCL-90 Symptom Check List(SCL-90 – Derogatis et al., 1973), the Profile of Mood States(POMS- McNair et al., 1971), and the Crown-Crisp experiental index(Crown and Crisp, 1966). (Spielberger and Rickman, 1990).

Associations of anxiety with CHD, cardiovascular disorders, and known cardiovascular disease risk factors

In the mid-1970’s, three studies(Jenkins, 1976; Lebovitis et al., 1975; Zyzanski et al., 1976) reported a positive association between anxiety and coronary heart disease. However, these studies and other studies in the 1960’s and 1970’s showed little evidence that anxiety plays a causal role in the pathogenesis of CHD. These positive assocations can be mostly explained by assuming that patients diagnosed or suffering from cardiovascular problems commonly suffer from anxiety over their cardiovascular health. Five studies during this time period examined the relationship between self-reported anxiety and the risk of subsequent cardiovascular disease. Three of them showed positive associations(Paffenberger et al., 1966; Medalie et al., 1973; Thiel et al., 1973), while the other two found negative associations(Thorne et al., 1968; Wardell and Bahnson, 1973). None of these studies controlled for known cardiovascular disease risk factors.

Many studies in the early 1980’s found that coronary atherosclerosis is nfrequent in subjects with anxiety states(Bass, 1984; Costa, 1981; DeMaria et al., 1980; Schocken et al., 1984; Sprafkin et al., 1984), even suggesting that anxiety may play a protective role against atherosclerosis(Rosenman, 1990). On the basis of finding positive associations between anxiety and angina pectoris(chest pain) and negative relationships between anxiety and coronary artery disease, Costa et al., 1985, suggested that anxiety was a risk factor for being referred for oronary angiography but not for coronary artery disease.

However, also in the 1980’s and continuing into the early 1990’s, six studies examined cardiovascular disease outcomes in patients with anxiety disorders. In two studies, there was a higher than expected death rate from diseases of the circulatory system in patients with panic disorder (Coryell et al., 1982; Coryell et al., 1986). In a third study, anxiety neurosis was associated with higher death from arterioschlerotic disease(Sims and Prior, 1982). Finally, a fourth study, utilizing the Epidemiologic Cachment Area database, also found an association between panic disorder and cardiovascular disease(Weissman et al., 1990). The other two studies failed to observe a relation between anxiety and cardiovascular disease. All of these studies were retrospective, they did not control for known cardiovascular disease risk factors, and, with the exception of one study(Weissman et al., 1990), they used registries for the purpose of case identification.

The more compelling evidence for a relationship between anxiety and CHD comes from studies examining self-reported anxiety and the risk of subsequent cardiovascular disease. As previously mentioned, these types of studies in the 1960’s and 1970’s produced conflicting results. However, in the 1980’s and 1990’s, there have been three such studies, all of which found strong positive associations between anxiety and cardiovascular disease(Haines et al., 1987; Kawachi, Colditz et al., 1994l Kawachi, Sparrow et al., 1994). Additionally, all three of these studies contained large samples, were prospective, and controlled for the effect of known CHD risk factors. Haines et al.(1987) and Kwachi, Colditz et al.(1994) both found that the risk of cardiovascular disease specifically related to the phobic anxiety scale of the Crown-Crisp index(Crown and Crisp, 1966). The study by Kwachi, Colditz et al.(1994) also found that the risk of sudden coronary death to be greater than the risk of nonsudden coronary death. Lastly, the most recent study (Kawachi and Sparrow et al., 1994) used a five-item anxiety symptom scale out of questions from the Cornell Medical Index (Coryell et al., 1982). The five questions selected were similiar to existing, validated psychological assessment scales such as STAI, HARS, and the Crown-Crisp index. Compared with men reporting no symptoms of anxiety, men reporting two or more symptoms had an elevated risk of fatal CHD, and particularly sudden coronary death(after adjusting for potential confounding variables, age-adjusted odds ratio(OR)= 4.46, 95% confidence interval: 0.92-21.6). Unfortunately, all of these studies involved only males. Anxiety disorders are 2-3 times more common in females, and therefore it will be important to replicate these findings in women(Hayward, 1995).

Anxiety has also been linked to known CHD risk factors. High cholesterol levels, a known CHD risk factor, have been reported in patients with anxiety disorders but not in patients with affective disorders(Hayward et al., 1989; Bajwa et al., 1992; Fava et al., 1994). According to a recent review (Hayward, 1995), only only study(Tancer et al., 1990) did not find elevated cholesterol levels in patients with anxiety disorders, suggesting that trait anxiety may be linked to high cholesterol levels. Anxiety has also been hypothesized to be a risk factor for hypertension. According to Hayward, 1995, several studies have found higher rates of hypertension in patients with anxiety disorders(Friedman and Bennet, 1977; Noyes et al., 1980; Katon, 1984; Davidson et al., 1991), while only two studies have failed to find this association (Dunner, 1985; Charney and Heninger, 1986). Most of the studies that have investigated the possible association between anxiety and the development of hypertension have been cross-sectional or have been limited because they had small sample sizes, used persons with borderline hypertension, or had been conducted on other highly selected populations (Jonas et al., 1997).

According to Jonas et al., 1997, a look at prospective studies of anxiety as predictors of hypertension shows that two recent studies did find a positive association for specific age and sex groups (Markovitz et al., 1991; Markovitz et al., 1993), while four earlier studies did not (Jenkins et al., 1983; Russek et al., 1990; Kahn et al., 1972; Sparrow et al., 1982). However, it should be noted that three out of four of these earlier studies did not use a standardized measure of anxiety. Both studies by Markovitz et al., which did find a positive association between anxiety and later development of hypertension, did use a standardized measure of anxiety. Jonas et al., 1997, has provided further evidence favoring a link between anxiety and increased risk for hypertension using longitudinal evidence from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study. Relative risks for hypertension incidence were determined on the basis of age, race, and level of anxiety symptoms. Blacks between the ages of 25-64 and whites between the ages of 45-64, who had a high level of anxiety symptoms, were found to have a higher relative risk of hypertension compared to groups of the same age range and race that possessed intermediate or low levels of anxiety symptoms. Blacks(age 25-64) with high levels of anxiety symptoms showed the highest relative risk of hypertension during the follow-up, with a relative risk of 3.24 of this group later being subscribed antihypertensive medications. In comparison, blacks (age25-64) with low levels of anxiety symptoms had a baseline relative risk of 1.00. Since hypertension is more common in blacks than whites (Fries, 1973; James et al., 1976), it is not surprising that the possible effects of anxiety on hypertension development were most easily seen in blacks. This might be part of the reason why Somova et al.(1995) found that in young blacks(ages 18-23) but not in whites of the same age, anxiety was found as a partial predictor of hypertension. The evidence as a whole is not conclusive, but recent research particularly suggests a link between anxiety and increased risk for hypertension.

If anxiety is indeed a risk factor for hypertension and high serum cholesterol, it still does not necessrily mean that it is the emotional state of anxiety that directly leads to these physiological effects. Anxiety may influence behaviors and habits that are relevant to cardiovascular disorders, which then lead to development of physiological cardiovascular disease risk factors such as hypertension and high serum cholesterol levels (Rosenmen, 1990). An example of a behavioral CHD risk factor is physical inactivity or lack of fitness. There is evidence that psychiatric patients with anxiety disorders, specifically panic disorder, are more likely to be physically unfit(Taylor et al., 1987; Gaffner et al., 1988). Although this area has not been adequately studied to make any conclusions about how the relationship between anxiety and physical fitness effects cardiovascular health, it serves as an example as to how anxiety could influence behavior that is relevant to the development of CHD.

Finally, it must be noted that commonly used measures of trait anxiety have been found to have a distinct lack of validity and instead seem to measure a single general trait labeled dysphoria, neuroticism, or negative affectivity (Smith, 1985). Individuals high on this trait are hypothesized to report(italicized) more dissatisfaction and have low psychological well-being. Past studies on the effects of anxiety on CHD have usually not controlled for the possible confounding effects of “negative affectivity” or “neuroticism.”

Is trait anxiety linked to cardiovascular reactivity to stress only during anxiety provoking situations?

Investigators have proposed that excessive physiological cardiovascular reactivity (CVR) to psychological stress may constitute an important physiological link which mediates the relationships between psychological traits and CHD (Glass, 1977; Goldband et al., 1979; Kranz and Manuck, 1984). If this is so for anxiety, it is expected that anxiety levels should predict CVR to stressful situations. While studies addressing the issue of whether trait anxiety is linked to CVR to stress have not produced convincing evidence (Houston, 1986), partial relationships have been found for anxiety-specific trait measures and cardiovascular reactivity. Test anxiety, social anxiety, performance anxiety, and specific phobias have all been found in separate studies to be related to cardiovascular reactivity, but many null findings have also been found. One hypothesis accounting for null findings include the failure to match specific dimensions of anxiety with situations that are appropriately anxiety-provoking (Burns, 1995). Relationships observed in most studies between stimulus-specific anxiety(eg., test anxiety, social anxiety) and cardiovascular reactivity most likely depend on whether the laboratory task mimics natural anxiety-producing stimuli (Ward, 1990). Turner et al.(1986) found evidence supporting the importance of specific situations emphasizing social evaluative cues in distinguishing an association between social anxiety and CVR. Additionally, studies by Burns (1995) support the hypothesis that specific dimensions of anxiety may be related to CVR only under appropriately anxiety-provoking situations.

Anxiety, job strain, psychological distress 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. Furthermore, Stansfeld et al.(1995) have found positive associations between anxiety and conflicting psychological work demands, work pace, and low control. Few studies have examined whether work environments that are high in job strain are particularly anxiety-provoking, although Bourbonnais et al.(1996) provide evidence for a positive association between job strain and psychological distress. Psychological distress was assessed in this study using the Psychiatric Symptom Index, which measures the presence and intensity of anxiety, aggressivity, depressive symptoms, and cognitive trouble. In contrast, in the New York City blood pressure study, trait anxiety was not correlated with job strain (Landsbergis et al., 1992; Schnall et al., 1992). However, the measures of trait anxiety used in this study lacked validity in that they are more a measure of negative affectivity. The relationship between high job strain and high employee anxiety remains for the most part unknown. Furthermore, how job strain and anxiety interact in regards to cardiovascular health also remains largely unknown.

Anxiety and its determinants

There has also been remarkably little research on the determinants anxiety, 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.

Conclusions

Although there is a large amount of conflicting results in the literature regarding the hypothesized link between high levels of anxiety and CHD, recent research for the most part supports that the relationship exists to some extent. Recent positive findings tying anxiety to higher serum cholesterol levels and later development of hypertension showed anxiety may be related to a number of important cardiovascular disease risk factors. There is an obvious need for finding better ways to assess anxiety, and past lack of validity in anxiety assessment adds uncertainty to the positive findings, as well as to the null findings. Possibly, associations will be easier to distinguish if more consideration is taken into what situations are best used to elicit the dimensions of anxiety being studied. There is also a lack of studies that have examined the relationship between job strain and anxiety, and whether they are independent or mutually reinforcing risk factors for the development of coronary heart disease. Finally, more research is needed on the determinants of anxiety, such as social class and job stress.


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