ARE THE PHYSICAL AND TABP RISK FACTORS FOR HEART DISEASE UNIQUE TO CHD?

LOGAN WRIGHT

University 01 Oklahoma

Scores of 40 hospitalized CHD patients on 11 Type A-related and 7 physical CHD risk factors were compared to those of 40 hospitalized non-CHD patients. Family history for CHD was the only physical risk factor for which a significant difference was found. CHD patients scored significantly higher on all seven interview-measured Type A and Type A subcomponent variables. Only two of the four Jenkins Activity Survey-measured Type A variables produced significant differences, with one higher for non-CHD subjects. It was concluded that some CHD risk scores also may be associated with other diseases, to the experience of being seriously i l l , and/or to the experience of hospitalization.

Risk for coronary heart disease (CHD) is considered to be associated in part with seven physical risk factors, as well as with the Type A Behavior Pattern (TABP; Rosen- man et al., 1975). The seven traditionally employed physical risk factors include smok- ing, elevated serum cholesterol, high blood pressure, a family history of CHD, diet, exercise, and weight control (Rosenman et al., 1975). The inclusion of Structured Interview-measured TABP as a bona fide CHD risk factor is supported by the (NIH) Review Panel (1981), as well as a more recent meta-analysis by Friedman and Booth- Kewley (1988).

Some earlier studies have examined the relationship of the above-mentioned risk factors to non-CHD disorders. These include, in addition to the numerous investiga- tions of smoking and cancer, the relationship of diet to diabetes (Greenwald, Lanza, & Eddy, 1987); the association between diet and colon cancer (Cranston, McWhinnie, & Collin, 1988); the link between the TABP and duodenal ulcers (Keltikangas-Jarvinen, 1987); and the relationship of the TABP to accidents and illness in general (Niemcryk, Jenkins, Rose, & Hurst, 1987). A prospective study by Suls and Marco (1990) has in- dicated that high TABP subjects are at greater risk for minor illnesses. However, a review by Suls, Wan, and Sanders (1988) concludes that, due to the methodological problems that affect most studies, it is impossible to conclude that the TABP constitutes a general risk factor for a wide variety of physical disorders.

To date, however, the comparative relationship of CHD risk factors to CHD, as compared to non-CHD illnesses, has not been investigated in the same study, with well- controlled conditions. Specifically, no previous studies have compared the effect of CHD risk factors to CHD vs. non-CHD illnesses while controlling for variables such as the experience of hospitalization and seriousness of subjects’ illnesses.

Clinically, it has been this author’s experience that many hospitalized CHD and non-CHD patients tend to exaggerate both their physical and TABP-related life-style abuses. Particularly in retrospective studies, the experience of serious illness and/or hospitalization could greatly influence subjects’ psychological defenses (e.g., the obliterating of denial of life style abuses, increasing one’s need for penitence and/or confession of such abuses). The confessional tendencies of seriously ill subjects could impact their self-reported scores for risk variables such as smoking, diet, exercise, etc.,

Correspondence should be addressed to Logan Wright, Department of Psychology, University of Oklahoma, Norman, OK 73019-0535.

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as well as self-reported TABP-related tendencies such as anger, time urgency, job in- volvement, etc. Thus, lessened denial and/or increased penitence could cause patients to overstate their risk-related behaviors. This, in turn, could produce positive correla- tions between almost any illness and (retrospectively) self-reported perceptions of life style abuses. If so, some of what is assumed to represent CHD risk could actually be an artifact of subjects’ experience of serious illness and/or of hospitalization.

As stated earlier, it is also possible that some of the risk variables that are regarded as unique to CHD may apply to other illnesses as well. Some CHD risk factors could be somewhat generic, with the manifested illness a function of somatic or constitutional weakness. As Garber and Hollon (1991, p. 129) recently have articulated, “A variable may be nonspecific, but still causal, if it is one of several multiple interacting causes.” Thus, it remains uncertain what, if any, portion of risk traditionally associated with CHD is unique to CHD.

The purpose of this study was to begin the process of determining the extent to which some CHD risk scores may be affected by non-CHD variables such as the ex- perience of any serious illness and/or the experience of hospitalization. The CHD risk factor scores of CHD patients, and those of non-CHD medical patients, were compared under conditions that controlled for the effects of hospitalization, age, gender, marital status, socioeconomic status (SES), and severity of illness.

One unique characteristic of this study is that it avoids a weakness of other similar investigations, most of which involve angiography patients (e.g., Barefoot, Beckham, Peterson, Haney, & Williams, 1992). Among angiography patients, those who are free of CHD usually have unexplained chest pains and are highly neurotic (Barefoot et al., 1992). It is felt that by employing a more unusual control group (hospitalized non-CHD patients) our data would provide a useful contrast with earlier studies.

METHOD

Subjects Subjects were 80 married, White males between 40 and 55 years of age who were

hospitalized at a large private medical center in the Southwest. Forty of these subjects were CHD patients, while the other 40 were without documented CHD. The diseases of non-CHD subjects included, among others, diabetes, ulcers, cancer, and general surgical problems. Subjects were matched for age (12 months or less difference), marital status (all married), gender (all male), race (all Caucasian), SES (all within $5,000 annual income and matched for blue collar/white collar employment), and for seriousness of illness. (All matched subjects possessed the same rating on a 1 to 4 Likert-type scale for how life-threatening their illness was and for the same rating on a 1 to 4 Likert-type scale for how badly they were feeling at the time of the interview.) These latter two ratings were performed by the author.

Procedure All subjects completed the Jenkins Activity Survey (JAS; Jenkins, Zyzanski, &

Rosenman, 1979). They also were administered the Augmented Structured Interview (ASI; Wright & Schmidt-Walker, 1990), which includes the Structured Interview (SI; Rosenman, 1978) and 19 additional items designed to improve ratings of TABP sub- components. The AS1 yields ratings for the global TABP and for the TABP subcom- ponents of time urgency, perpetual activation, anger in, anger out, anger control, and anger expression.

Scores also were obtained for the seven traditional physical risk factors for CHD according to a method originally suggested by Rosenman et al. (1975). The smoking score was the average number of cigarettes per day times number of years smoked. The weight control score was a ratio determined by dividing height in inches by weight in

CHD Risk Factors 707

pounds, a method advocated by Stunkard (1986). The other five risk factors were scored as follows:

Self- reported family history 1 = No family history 2 = Secondary family history (aunts, uncles, and grandparents only) 3 =

3 . 5 =

4 =

Family history in only one immediate family member (father, mother, brother, sister) Family history in one or more immediate family member and in one or more secondary family member Family history, multiple; i.e., two or more immediate family members

Serum cholesterol. Average of all available combined HDL/LDL readings. (Avoided utilizing more than one reading in any one year.) The average of multiple readings in one year was employed. Also, no post infarction readings from present hospitalization were employed.

Blook pressure. Systolic and diastolic readings combined - all available readings for blood pressure (combined systolic and diastolic).

1 = below 190 and no medication 2 = 190-210 and no medication 3 = 210-230 and no medication 4 = 230 and above OR on medication 5 = 230 and above AND on medication

1 = Little or no exercise at work or home 2 = Moderate exercise at work. No formal exercise program 3 = Routine vigorous exercise at work or formal exercise program (less vigorous

than level 4) 4 = Vigorous exercise at work and formal exercise program (less vigorous than

level 5) 5 = Formal exercise program (20 minutes or more of vigorous exercise,

excluding walking) done 3 or more days a week Sev-reported diet. Typical diet practiced prior to documentation of CHD. Patients

simply were asked, “Throughout most of your life, and prior to the discovery of your heart disease, what was your typical diet? Subjects were queried until it could be ascer- tained which of the following three ratings applied.

1 = Deliberately restricted high fat foods and chose high fiber foods (i.e., low fat and high fiber)

2 = High fat and high fiber 3 = High fat and low fiber

Self-reported exercise style

Ratings for the six TABP subcomponents listed above were obtained by an SI inter- viewer who was traditionally trained (by a graduate of the Stanford-based R. Rosen- man/M. Chesney program) and was naive as to the purpose of the study. She was told simply that, as a function of her job, she needed to obtain AS1 ratings for 80 subjects. CHD and non-CHD patients were interviewed in a random order. Some CHD patients were hospitalized on a general medical patients unit and vice versa, and the interviewer appeared to remain naive throughout the duration of the data-gathering process.

RESULTS

In order to control Type I error rate for the many dependent 1-tests while concur- rently maintaining adequate power, the multivariate F-statistic (a function of Hotelling’s TZ for correlated measures) was calculated for these data. This statistic is, of course,

108 Journal of Clinical Psychology, November 1992, Vol. 48, No. 6

a test of the multivariate null hypothesis that the population means of the difference scores for all the dependent variables are all simultaneously zero. Rejection of this hypothesis allows one to proceed to test differences between individual variables. For these data, the multivariate analysis yielded F(18,22) = 3.61, p < .0025. Thus, matched pairs t-tests were estimated for the seven traditionally employed physical CHD risk factors, for seven SI-measured Type A and TABP subcomponent measures, and for four JAS-measured Type A and TABP subcomponent measures. These results are shown in Table 1.

Table 1 Matched Pairs 1-test Results for Eighteen Study Variables

Variable t

AS1

Time urgency

Perpetual activation

Anger in Anger out

Anger control

Anger expression

JAS

Type A Speed and Impatience

Job Involvement Hard Driving/Competitiveness

Phyical risk

Smoking

Cholesterol Blood pressure

Family history

Exercise

Diet

Weight control

2.23

2.53

2.34 3.18

- 3.42

3.60

1.56 2.25

.26

-2.51

.85

.I3 - .I2

3.16

1.12

.21

.24

< .05

< .05

< .05

< .005

< .oos < .oo5

< .05

< .05

< ,001

With respect to differences between CHD and non-CHD hospitalized patients, sig- nificant differences were found on all seven ASI-measured TABP subcomponent variables; CHD patients scored higher in each case. (The negative T score for anger control indicates less anger control and, therefore, more TABP-like behavior).

Only two of the four JAS-measured variables attained significance. The Type A and Job Involvement subscales did not. The Speed and Impatience subscale was signifi- cant at the .05 level; CHD subjects scored higher. However, the Hard Driving/Com- petitiveness subscale was significant at the .05 level; the non-CHD subjects scored higher. A family history of CHD was the only physical risk factor that differentiated the CHD sample from non-CHD subjects in this study.

Based on T-score values, the variable of anger expression represents the most sig- nificant difference between the two study groups, which, in turn, suggests that anger expression may be the primary TABP-related risk factor for CHD. This finding is highly consistent with the earlier findings of Williams and his colleagues (Dembrowski &

CHD Risk Factors 709

Williams, 1989; Williams, 1984), who believed anger expression to be the primary coronary-prone culprit. Anger expression is calculated by adding subjects’ scores for anger-in and anger-out, then subtracting the anger control score. (Anger control represents adaptive means of preventing or overcoming anger, rather than suppression or repression of anger.) In this study, the high anger expression scores of the CHD sample appear to be more a function of anger out and lack of anger control than of anger in.

The time urgency scores and, to a lesser extent, perpetual activation scores based on ASI-obtained data also produced significant differences between the CHD and non- CHD groups. These findings support the earlier conclusions of Wright (1 988), which have suggested an association of both time urgency and perpetual activation to CHD.

The JAS-related findings obtained here suggest that global TABP and job involve- ment may be no more highly associated with CHD than with other serious diseases that require hospitalization. The finding of no difference between CHD and non-CHD sub- jects on the job involvement subscale is consistent with the results of an earlier meta- analysis by Friedman and Booth-Kewley (1988), who report a lack of relationship between job involvement and CHD.

JAS-measured Speed and Impatience as assessed in this study appears more related to CHD than to other serious illnesses. This finding also appears to support the earlier conclusions of Wright (1988) with respect to the possible relationship of time urgency to CHD. However, JAS-measured Hard Driving Competitiveness (as found in this investigation) was more related to non-CHD illness than to CHD. That finding is somewhat surprising, but not necessarily inconsistent with the earlier meta- analysis-based conclusion, which states that Hard Driving/Competitiveness, as measured by the JAS, is related to CHD. Our results, however, raise the additional question of whether Hard Driving/Competitiveness also could be associated with other, non-CHD illnesses.

The finding of significant differences between groups for family history of CHD provides some minimal support for the notion that familial risk tends to be illness specific. The other six physical risk factors employed here have been consistently associated with an increased incidence of CHD in numerous other studies (e.g., Rosenman et al., 1975). Thus, these findings suggest that some of these other six risk factors also may be associated with non-CHD illness and/or to subjects’ emotional reactions to being seriously ill or possibly to their experience of being hospitalized.

DISCUSSION

Obviously, no attempt has been made to assess differences between either of our hospitalized patient samples and normal subjects. Thus, no data exist as to how each of the two study groups might differ from normal controls. However, the findings of this investigation do lend some support to the belief that a family history for CHD, and the TABP subcomponents of anger and time urgency/perpetual activation, con- stitute greater risk for CHD than for other serious, non-CHD illnesses that require hospitalization.

Future research should focus on separating the effects of: (a) serious illness; (b) hospitalization; and (c) the possible association between CHD risk factors and non-CHD illness. Future studies also could investigate the relationship of the risk variables employed here to single non-CHD illnesses. Such efforts should help to determine the relative im- portance of the traditional CHD risk factors for CHD, in comparison to their associa- tion with other disease endpoints. It is hoped that this study may serve the heuristic purpose of stimulating further research on the relationshp of CHD risk factors both to other diseases and to non-CHD factors, such as being seriously ill and/or being hospitalized.

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