This Article Abstract Full Text (PDF) All Versions of this Article: 109/10/1267    most recent 01.CIR.0000118535.15205.8Fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Eaker, E. D. Articles by Benjamin, E. J. Search for Related Content PubMed PubMed Citation Articles by Eaker, E. D. Articles by Benjamin, E. J. Related Collections Acute myocardial infarction Arrhythmias, clinical electrophysiology, drugs Chronic ischemic heart disease Epidemiology Risk Factors

(Circulation. 2004;109:1267-1271.)
© 2004 American Heart Association, Inc.

Clinical Investigation and Reports

Anger and Hostility Predict the Development of Atrial Fibrillation in Men in the Framingham Offspring Study

Elaine D. Eaker, ScD; Lisa M. Sullivan, PhD; Margaret Kelly-Hayes, EdD, RN; Ralph B. D’Agostino, Sr, PhD; Emelia J. Benjamin, MD, ScM

From Eaker Epidemiology Enterprises, LLC, Chili, Wis (E.D.E.); the Department of Mathematics and Statistics, Boston University School of Public Health, Boston, Mass (L.M.S., R.B.D.); the Departments of Neurology and Cardiology, Boston University School of Medicine, Boston, Mass (M.K.-H.); and the National Heart, Lung, and Blood Institutes’ Framingham Heart Study (L.M.S., M.K.-H., R.B.D., E.J.B.), Bethesda, Md.

Correspondence to Elaine D. Eaker, ScD, Eaker Epidemiology Enterprises, LLC, 8975 County Road V, Chili, WI 54420. E-mail eakerepi{at}tznet.com

Received July 1, 2003; de novo received September 11, 2003; revision received November 21, 2003; accepted November 26, 2003.

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
Background— Conflicting findings in the literature with regard to the ability of type A behavior, expressions of anger, or hostility to predict incident coronary heart disease (CHD) have created controversy. In addition, there are no prospective studies relating these characteristics to the development of atrial fibrillation (AF).

Methods and Results— From 1984 to 1987, 3873 men and women, 18 to 77 years of age, participating in the Framingham Offspring Study, were examined and monitored for 10 years for the incidence of CHD, AF, and total mortality. Measures of type A behavior, anger, hostility, and risk factors for CHD and AF were collected at the baseline examination. After controlling for age, diabetes, hypertension, history of myocardial infarction, history of congestive heart failure, and valvular heart disease in Cox proportional hazards models, trait-anger (RR=1.1; 95% CI, 1.0 to 1.4; P=0.04), symptoms of anger (RR=1.2; 95% CI, 1.0 to 1.4; P=0.008), and hostility (RR=1.3; 95% CI, 1.1 to 1.5; P=0.003) were predictive of 10-year incidence of AF in men. After controlling for risk factors for CHD, none of the measures of anger, type A behavior, or hostility were related to incident CHD; however, trait-anger (RR=1.2; 95% CI, 1.1 to 1.4; P<0.01) was related to total mortality in men. None of the psychosocial variables were related to the 3 outcomes in women.

Conclusions— This is the first study to examine and demonstrate a predictive relation between measures of anger and hostility to the development of AF in men. As opposed to type A behavior, measures of anger and hostility may be more productive avenues for research in studying the risk of arrhythmias and total mortality in men.

Key Words: coronary disease • fibrillation • mortality • men • arrhythmia

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
There is conflict in the literature with regard to whether psychosocial factors predict the development of coronary heart disease (CHD) and total mortality. For example, most studies of type A behavior show no association between type A and the development of definite CHD,^1–5 but some demonstrate positive results.^6–8 Evidence for an association between anger and CHD is limited but suggestive,^9,10 but there appear to be no prospective studies of anger and total mortality. Findings from studies of hostility and cardiovascular atherosclerosis demonstrate both negative¹¹ and positive^12,13 findings. Several prospective cohort studies of men examined the associations between hostility, incident CHD, and total mortality.^14–17 Two of these studies found no association between hostility, incident CHD, or total mortality,^14,15 and 2 demonstrated positive findings.^16,17 There is a deficit of prospective studies of hostility and CHD or total mortality in women, but one case-control study of women found that a measure of hostility was significantly associated with the presence of CHD.¹⁸

Hence, the role of psychological factors in the development of CHD and mortality is controversial. Furthermore, to our knowledge, the relation between psychosocial characteristics and incident atrial fibrillation (AF) has never been examined. The objective of our study, therefore, was to test the hypotheses that type A behavior, measures of anger, and hostility were independently related to the 10-year incidence of CHD, AF, and total mortality in men and women.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
The Framingham Heart Study is a prospective, longitudinal cohort study that began enrollment of the offspring (and spouses) of the original Framingham Heart Study cohort in 1971.¹⁹ From 1984 through 1987, 3873 offspring participants returned for their third follow-up examination. A few weeks before the examination, subjects were mailed psychosocial questionnaires, which were collected at the scheduled clinic visit; 95% were completed. Subjects were excluded from the present study for the following indications: incomplete questionnaire (n=191), prevalent CHD for the analyses of incident CHD (n=107), and prevalent AF (n=25) for the analyses of incident AF.

The Bortner Rating Scale for behavior type (type A/type B) has been found to be related to incident CHD⁸ and was introduced into the Framingham Offspring Study in 1984. The Bortner Rating Scale has 14 items, each comprising 2 statements with a 7-point Likert scale in between the 2 statements. Examples include "never late" on one end of the scale and "casual about appointments" on the other end of the scale. The participant put a check between the two descriptors to indicate what best described him or her.

Anger was assessed through the use of the original Framingham scales for Anger-In, Anger-Out, Anger-Symptoms, and Anger-Discuss.²⁰ These anger scales assessed ways of expressing or coping with anger, such as keeping it to oneself ("anger-in"), taking it out on others ("anger-out"), or talking with a friend or relative ("anger-discuss"). The physical manifestations of anger included such things as getting a headache or feeling weak ("anger-symptoms"). In addition, the 10-item Spielberger Trait-Anger Scale²¹ has been found to significantly predict the development of CHD in a large prospective study⁹ and was included in our study. On the Spielberger scale, participants rated their typical experience with anger on a 4-point Likert scale. A measure of hostility consisted of selected items from the Cook-Medley Hostility Scale.¹³ These selected items were based on the research of Williams et al, demonstrating that patients endorsing these items were more likely to have coronary occlusions.¹³ The Cook-Medley hostility items are characterized by the view that others are inconsiderate, immoral, selfish, and deserving to be punished or hurt. Responses consisted of agreement or disagreement with various statements. The reliability and validity of the particular items selected, relative to the entire hostility subscale, are not known.

For all psychosocial scales, responses were scaled and standardized between 0 and 1, with the higher score indicating more of the trait. A scale score was obtained by calculating an average over the nonmissing values in the scale.

The 3 outcomes of interest included the 10-year incidence of CHD, AF, and total mortality. The definitions of CHD²² and AF²³ have been published previously; the manifestations of interest for CHD in these analyses included myocardial infarction (recognized and unrecognized), coronary insufficiency, and coronary death (both sudden and not sudden). The diagnosis of AF was made if AF or atrial flutter was present on an ECG obtained from the Framingham clinic visit, hospital charts, or physician office record. Atrial fibrillation was diagnosed if p-wave activity was not evident and the ventricular response was irregularly irregular. Atrial flutter was diagnosed if typical flutter (saw-tooth) waves were seen on the ECG. AF electrocardiograms were reviewed and verified by one of two Framingham Study cardiologists. For causes of death, 25% of men and 12% of women died from coronary heart disease. Cerebrovascular accidents accounted for 2.8% and 4.4% of deaths in men and women, respectively. Cancer accounted for 35.4% of deaths in men and 55.4% of deaths in women.

Potential confounders were ascertained at the index examination. Multivariable models predicting the 10-year incidence of CHD and total mortality adjusted for age, systolic blood pressure, body mass index (kg/m²), current cigarette smoking, diabetes (defined as fasting blood glucose of at least 126 mg/dL or on treatment), total cholesterol/high-density cholesterol. Multivariable analyses for AF included characteristics known to be related to its development: age, diabetes, hypertension, history of myocardial infarction or history of congestive heart failure, and valvular heart disease (defined as any diastolic murmur or 3 out of 6 systolic murmur).

All analyses were sex specific. We examined the relation of the psychosocial measures to education and CHD risk factors classified at baseline with Pearson correlations and ANOVA for continuous and discrete variables, respectively. The 10-year age-adjusted rates and relative risks of CHD, AF, and total mortality were estimated by means of Cox proportional hazards regression. For each psychosocial predictor variable that reached a significance level of P0.10 in the age-adjusted analyses, we examined multivariable-adjusted Cox proportional hazards models. Relative risks for incident disease were presented relative to a 1-SD difference in each measure. In exploratory analysis, we also investigated the impact of adjusting for interim myocardial infarction and interim coronary heart failure in the models for AF.

The Office of Management and Budget approved the use of this survey in the Framingham Offspring Study in 1983.

	Results

Top Abstract Introduction Methods Results Discussion References

 
The study consisted of 1769 men and 1913 women who were a mean age of 48.5 (SD=10.1; range, 18 to 77 years) at baseline. Table 1 and Table 2 present the Pearson correlation coefficients between the measures of type A behavior, anger, hostility, and education and the CHD risk factors for men and women, respectively. In men and women, most of the scales were inversely associated with advancing age except hostility, which was positively associated with age in men. Hostility was inversely related to education and directly associated with smoking in both men and women. Hostility also was directly related to body mass index and total/HDL cholesterol in men. In contrast to men, in women many of the scales were negatively associated with blood pressure. In addition, trait-anger was positively associated with smoking in women.

View this table: [in this window] [in a new window]   TABLE 1. Relation of Type A, Anger, and Hostility Scales to CHD Risk Factors: Men

View this table: [in this window] [in a new window]   TABLE 2. Relation of Type A, Anger, and Hostility Scales to CHD Risk Factor: Women

Table 3 shows the age-adjusted relations between the type A, anger, and hostility variables to the 10-year incidence of CHD, AF, and total mortality in men and women. None of the measures of type A behavior, anger, or hostility reached statistical significance for men or women in relation to incident CHD. Because previous research has shown that anger may have a differential effect by housewife/working woman status,² we reanalyzed the model in women stratifying on this characteristic; the results were not materially altered (data not shown).

View this table: [in this window] [in a new window]   TABLE 3. Age-Adjusted Relative Risks for 10-Year Occurrence of Coronary Heart Disease, Atrial Fibrillation, and Total Mortality

In age-adjusted analyses of AF, increased trait-anger, hostility, and symptoms of anger were significant predictors in men, and anger-out was a significant predictor in women. Trait-anger was positively associated with the age-adjusted total mortality rate in men. None of the variables examined were associated with total mortality in women.

The multivariable analyses for the 10-year incidence of AF and total mortality in men are presented in Table 4. Men with increased trait-anger were at significantly higher risk of developing AF (RR=1.1; 95% CI, 1.0 to 1.4; P=0.04), as were those with increased hostility (RR=1.3; 95% CI, 1.1 to 1.5; P=0.003) or increased symptoms of anger (RR=1.2; 95% CI, 1.0 to 1.4; P=0.008). When interim myocardial infarction or congestive heart failure (during the follow-up) was taken into account, the symptoms of anger and hostility variables remained significant predictors of AF (data not shown). For total mortality, men with increased trait-anger had a relative risk of death of 1.2 (95% CI, 1.1 to 1.4; P<0.01) for each standard deviation increase in scale scores for trait-anger. Anger-out in women was no longer significantly related to AF in the multivariable model.

View this table: [in this window] [in a new window]   TABLE 4. Multivariable Adjusted Relative Risks for 10-Year Occurrence of Atrial Fibrillation and Total Mortality in Men

We examined the clinical features of the AF cases in our study. More than half the cases (66%) occurred before the age of 60 years. Ninety-nine percent of all AF cases had no history of CHF at baseline, and 87% of cases were free of CHF during the follow-up. Ninety-two percent of AF cases were free of myocardial infarction at baseline, and 86% were free of myocardial infarction during the follow-up.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
To our knowledge, our study is the first to systematically examine the predictive relation between psychosocial variables and incident AF in a large prospective cohort. Noteworthy findings from our study are that in men, symptoms of anger and hostility were predictive of incident AF after adjusting for baseline and interim risk factors. It is important to place our AF findings in context. The peak ages for the prevalence of AF are from 70 to 84 years of age.²⁴ The cases we observed in this particular study could be characterized as "early-onset" or "premature" AF, largely occurring without preexisting heart disease. Thus, risk factors for the early development of AF in men appear to be strongly associated with psychosocial risk factors such as anger and hostility.

Progress is being made in defining the role of behavioral and emotional stress in the precipitation of cardiac arrhythmias.^25–30 Studies of animals have demonstrated that cardiac arrhythmias were significantly more frequent during social stress than during other challenging situations.²⁵ A recent study in humans found that anger (OR, 1.8; 95% CI, 1.0 to 3.2) can trigger ventricular arrhythmias in patients with implantable cardioverter-defibrillators.²⁸

Our findings with regard to trait-anger and incident CHD differ from prior studies. We found trait-anger to be significantly related to total mortality in men but not incident CHD. Other studies have found that trait-anger¹⁰ or "anger-content"⁹ to be related to incident CHD. The latter study showed significance only after angina pectoris was included in the CHD outcomes.

In the original Framingham Study cohort, it was found that type A behavior was significantly related to angina pectoris but not myocardial infarction or fatal coronary artery disease in both men and women.¹ This finding explains the discrepancies between this report and earlier publications from the original Framingham cohort.³¹ In the present study, angina pectoris was not included as an end point, only definite CHD. As with most prospective studies of type A behavior, the present study of the Bortner scale for type A behavior did not predict definite CHD, AF, or total mortality. In contrast, the VA Normative Aging Study found the MMPI-2 Type A Scale predicted CHD incidence.⁷ This inconsistency probably is due to the conceptualization of type A behavior and how it is measured.

With regard to women, the findings from the present offspring study are similar to those reported previously in the Framingham cohort.² The Framingham scales for anger symptoms, anger-in, anger-out, and anger-discuss were not associated with the incidence of myocardial infarction or coronary death. In the present study, we added trait-anger and hostility, and neither of these variables reached statistical significance for any of the three end points in women. Another research study has shown that "suppressed anger" is not related to nonfatal myocardial infarction in men or women.³²

There is little consensus among previous prospective cohort studies on the effect of hostility on total mortality or incident CHD.^14–17 The present study is in agreement with two other prospective studies^14,15 that failed to support an association between hostility and incident CHD or total mortality. It has been argued that adjusting for potential confounders may be inappropriate and may lead to an erroneous conclusion with regard to hostility.³³ This probably is not the case with the present analyses because even the age-adjusted analyses of hostility did not achieve statistical significance for CHD or total mortality. Some studies have argued that hostility rather than type A behavior is the important risk factor for disease.^34–36 Two of these studies are matched case-control studies,^34,36 and one is a cross-sectional study of peripheral arterial disease.³⁵

The strengths of the Framingham Offspring Study include a prospective design, inclusion of both men and women, a stable cohort, carefully assessed end points, and routinely ascertained information on standard risk factors. One potential limitation is that the psychometrics of the abbreviated measure of hostility used in the present study are not known; its predictive value, however, for AF appears to be adequate in men. Certainly, replication of our findings is necessary before we can generalize the idea that hostility is an etiologic factor for early-onset AF in men; this is particularly important because the effect size that we observed (a maximum relative risk of 1.3) is modest. In addition, the study cohort was predominantly white and middle-aged; the findings may not be generalizable to other ethnicities and the elderly. Because our community sample is middle aged, the event rates were low in women, which limited our power to describe the predictive relations of psychosocial characteristics to these end points (eg, we had power of 29% to detect a relative risk of 1.8 of CHD in women). Our sample in the Framingham Offspring Study, however, constitutes one of the larger data sets with prospective psychosocial data in women.

In summary, we did not observe significant associations between anger, type A behavior, and hostility for the 10-year incidence of CHD, AF, or total mortality in women. For men, however, trait-anger, hostility, and symptoms of anger are independent risk factors for the development of AF. Although hypotheses about emotions and the development of arrhythmias were reasonable, this is the first time an association has been documented specifically between emotions and the development of AF. In addition, trait-anger is also an independent risk factor for total mortality in men. The mechanism of the relation between AF and anger and hostility merits further investigation. Future interventions for the prevention of early onset of AF in men might include anger and hostility recognition and management.

	Acknowledgments

 
The National Heart, Lung, and Blood Institute supported this study: 1-R03-HL-67426-01 and N01-HC-25195.

	References

Top Abstract Introduction Methods Results Discussion References

 

1. Eaker ED, Abbott RD, Kannel WB. Frequency of uncomplicated angina pectoris in type A compared with type B persons (the Framingham Study). Am J Cardiol. 1989; 63: 1042–1045.[CrossRef][Medline] [Order article via Infotrieve]
   
2. Eaker ED, Pinsky J, Castelli WP. Myocardial infarction and coronary death among women: psychosocial predictors from a 20-year follow-up of women in the Framingham Study. Am J Epidemiol. 1992; 135: 854–864.[Abstract/Free Full Text]
   
3. Hemingway H, Marmot M. Evidence based cardiology: psychosocial factors in the aetiology and prognosis of coronary heart disease: systematic review of prospective cohort studies. BMJ. 1999; 318: 1460–1467.[Free Full Text]
   
4. Ragland DR, Brand RJ. Type A behavior and mortality from coronary heart disease. N Engl J Med. 1988; 318: 65–69.[Abstract]
   
5. Bass C, Wade C. Type A behaviour: not specifically pathogenic? Lancet. 1982; 2: 1147–1150.[Medline] [Order article via Infotrieve]
   
6. Houston BK, Chesney MA, Black GW, et al. Behavioral clusters and coronary heart disease risk. Psychosom Med. 1992; 54: 447–461.[Abstract/Free Full Text]
   
7. Kawachi I, Sparrow D, Kubzansky LD, et al. Prospective study of a self-report type A scale and risk of coronary heart disease: test of the MMPI-2 type A scale. Circulation. 1998; 98: 405–412.[Abstract/Free Full Text]
   
8. French-Belgian Collaborative Group. Ischemic heart disease and psychological patterns: prevalence and incidence studies in Belgium and France. Adv Cardiol. 1982; 29: 25–31.[Medline] [Order article via Infotrieve]
   
9. Kawachi I, Sparrow D, Spiro A III, et al. A prospective study of anger and coronary heart disease: the Normative Aging Study. Circulation. 1996; 94: 2090–2095.[Abstract/Free Full Text]
   
10. Williams JE, Paton CC, Siegler IC, et al. Anger proneness predicts coronary heart disease risk: prospective analysis from the atherosclerosis risk in communities (ARIC) study. Circulation. 2000; 101: 2034–2039.[Abstract/Free Full Text]
    
11. Helmer DC, Ragland DR, Syme SL. Hostility and coronary artery disease. Am J Epidemiol. 1991; 133: 112–122.[Abstract/Free Full Text]
    
12. Knox SS, Adelman A, Ellison RC, et al. Hostility, social support, and carotid artery atherosclerosis in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Cardiol. 2000; 86: 1086–1089.[CrossRef][Medline] [Order article via Infotrieve]
    
13. Williams RB Jr, Haney TL, Lee KL, et al. Type A behavior, hostility, and coronary atherosclerosis. Psychosom Med. 1980; 42: 539–549.[Abstract/Free Full Text]
    
14. Hearn MD, Murray DM, Luepker RV. Hostility, coronary heart disease, and total mortality: a 33-year follow-up study of university students. J Behav Med. 1989; 12: 105–121.[CrossRef][Medline] [Order article via Infotrieve]
    
15. Barefoot JC, Dahlstrom WG, Williams RB Jr. Hostility, CHD incidence, and total mortality: a 25-year follow-up study of 255 physicians. Psychosom Med. 1983; 45: 59–63.[Abstract/Free Full Text]
    
16. McCranie EW, Watkins LO, Brandsma JM, et al. Hostility, coronary heart disease (CHD) incidence, and total mortality: lack of association in a 25-year follow-up study of 478 physicians. J Behav Med. 1986; 9: 119–125.[CrossRef][Medline] [Order article via Infotrieve]
    
17. Shekelle RB, Gale M, Ostfeld AM, et al. Hostility, risk of coronary heart disease, and mortality. Psychosom Med. 1983; 45: 109–114.[Abstract/Free Full Text]
    
18. Lahad A, Heckbert SR, Koepsell TD, et al. Hostility, aggression and the risk of nonfatal myocardial infarction in postmenopausal women. J Psychosom Res. 1997; 43: 183–195.[CrossRef][Medline] [Order article via Infotrieve]
    
19. Kannel WB, Feinleib M, McNamara PM, et al. An investigation of coronary heart disease in families: the Framingham offspring study. Am J Epidemiol. 1979; 110: 281–290.[Abstract/Free Full Text]
    
20. Haynes SG, Levine S, Scotch N, et al. The relationship of psychosocial factors to coronary heart disease in the Framingham study, I: methods and risk factors. Am J Epidemiol. 1978; 107: 362–383.[Abstract/Free Full Text]
    
21. Spielberger C, Jacobs G, Russell S, et al. Assessment of anger: the State-Trait Anger Scale. In: Butcher JNSC, ed. Advances in Personality Assessment. Vol 2. Hillsdale, NJ: Lawrence Erlbaum Associates; 1983: 161–189.
    
22. Abbott RD, McGee DL. The probability of developing certain cardiovascular diseases in eight years at specified values of some characteristics. The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease, Section 37. Bethesda, Md: National Heart, Lung, and Blood Institute; 1987.
    
23. Benjamin EJ, Wolf PA, D’Agostino RB, et al. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998; 98: 946–952.[Abstract/Free Full Text]
    
24. Feinberg WM, Blackshear JL, Laupacis A, et al. Prevalence, age distribution, and gender of patients with atrial fibrillation: analysis and implications. Arch Intern Med. 1995; 155: 469–473.[Abstract]
    
25. Sgoifo A, Koolhaas JM, Musso E, et al. Different sympathovagal modulation of heart rate during social and nonsocial stress episodes in wild-type rats. Physiol Behav. 1999; 67: 733–738.[CrossRef][Medline] [Order article via Infotrieve]
    
26. Verrier RL. Mechanisms of behaviorally induced arrhythmias. Circulation. 1987; 76: I-48–I-56.[Medline] [Order article via Infotrieve]
    
27. Hofmann B, Ladwig KH, Schapperer J, et al. Psycho-neurogenic factors as a cause of life-threatening arrhythmias. Nervenarzt. 1999; 70: 830–835.[CrossRef][Medline] [Order article via Infotrieve]
    
28. Lampert R, Joska T, Burg MM, et al. Emotional and physical precipitants of ventricular arrhythmia. Circulation. 2002; 106: 1800–1805.[Abstract/Free Full Text]
    
29. Mittleman MA, Maclure M, Sherwood JB, et al. Triggering of acute myocardial infarction onset by episodes of anger: Determinants of Myocardial Infarction Onset Study Investigators. Circulation. 1995; 92: 1720–1725.[Abstract/Free Full Text]
    
30. Friedman EH. Anger and myocardial infarction. Circulation. 1996; 94: 1788.
    
31. Haynes SG, Feinleib M, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study, III: eight-year incidence of coronary heart disease. Am J Epidemiol. 1980; 111: 37–58.[Abstract/Free Full Text]
    
32. O’Connor NJ, Manson JE, O’Connor GT, et al. Psychosocial risk factors and nonfatal myocardial infarction. Circulation. 1995; 92: 1458–1464.[Abstract/Free Full Text]
    
33. Hemingway H, Marmot M. Authors’ reply to Relation between hostility and coronary heart disease. BMJ. 1999; 319: 917–918.Letter.[Free Full Text]
    
34. Dembroski TM, MacDougall JM, Costa PT Jr, et al. Components of hostility as predictors of sudden death and myocardial infarction in the Multiple Risk Factor Intervention Trial. Psychosom Med. 1989; 51: 514–522.[Abstract/Free Full Text]
    
35. Deary IJ, Fowkes FG, Donnan PT, et al. Hostile personality and risks of peripheral arterial disease in the general population. Psychosom Med. 1994; 56: 197–202.[Abstract/Free Full Text]
    
36. Hecker MH, Chesney MA, Black GW, et al. Coronary-prone behaviors in the Western Collaborative Group Study. Psychosom Med. 1988; 50: 153–164.[Abstract/Free Full Text]
    

This article has been cited by other articles:

				H. Nabi, A. Singh-Manoux, M. Shipley, D. Gimeno, M. G. Marmot, and M. Kivimaki Do Psychological Factors Affect Inflammation and Incident Coronary Heart Disease: The Whitehall II Study Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1398 - 1406. [Abstract] [Full Text] [PDF]

				H. Nabi, M. Kivimaki, M. G Marmot, J. Ferrie, M. Zins, P. Ducimetiere, S. M Consoli, and A. Singh-Manoux Does personality explain social inequalities in mortality? The French GAZEL cohort study Int. J. Epidemiol., June 1, 2008; 37(3): 591 - 602. [Abstract] [Full Text] [PDF]

				M. S. Player, D. E. King, A. G. Mainous III, and M. E. Geesey Psychosocial Factors and Progression From Prehypertension to Hypertension or Coronary Heart Disease Ann. Fam. Med, September 1, 2007; 5(5): 403 - 411. [Abstract] [Full Text] [PDF]

				E. D. Eaker, L. M. Sullivan, M. Kelly-Hayes, R. B. D'Agostino Sr, and E. J. Benjamin Marital Status, Marital Strain, and Risk of Coronary Heart Disease or Total Mortality: The Framingham Offspring Study Psychosom Med, July 1, 2007; 69(6): 509 - 513. [Abstract] [Full Text] [PDF]

				J. E. Williams, D. J. Couper, R. Din-Dzietham, F. J. Nieto, and A. R. Folsom Race-Gender Differences in the Association of Trait Anger with Subclinical Carotid Artery Atherosclerosis: The Atherosclerosis Risk in Communities Study Am. J. Epidemiol., June 1, 2007; 165(11): 1296 - 1304. [Abstract] [Full Text] [PDF]

				G. A. Fava, S. Fabbri, L. Sirri, and T. N. Wise Psychological Factors Affecting Medical Condition: A New Proposal for DSM-V Psychosomatics, April 1, 2007; 48(2): 103 - 111. [Abstract] [Full Text] [PDF]

				W. Rosamond, K. Flegal, G. Friday, K. Furie, A. Go, K. Greenlund, N. Haase, M. Ho, V. Howard, B. Kissela, et al. Heart Disease and Stroke Statistics--2007 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Circulation, February 6, 2007; 115(5): e69 - e171. [Full Text] [PDF]

				I. Rebollo and D. I. Boomsma Genetic and Environmental Influences on Type A Behavior Pattern: Evidence From Twins and Their Parents in The Netherlands Twin Register Psychosom Med, May 1, 2006; 68(3): 437 - 442. [Abstract] [Full Text] [PDF]

				E. D. Eaker, L. M. Sullivan, M. Kelly-Hayes, R. B. D'Agostino Sr, and E. J. Benjamin Tension and Anxiety and the Prediction of the 10-Year Incidence of Coronary Heart Disease, Atrial Fibrillation, and Total Mortality: The Framingham Offspring Study Psychosom Med, September 1, 2005; 67(5): 692 - 696. [Abstract] [Full Text] [PDF]

				S Vale Psychosocial stress and cardiovascular diseases Postgrad. Med. J., July 1, 2005; 81(957): 429 - 435. [Abstract] [Full Text] [PDF]

				23 Apr 2004 to 23 Jul 2004 Evid. Based Nurs., October 1, 2004; 7(4): e4 - e4. [Full Text] [PDF]

				R. Soufer Neurocardiac Interaction During Stress-Induced Myocardial Ischemia: How Does the Brain Cope? Circulation, September 28, 2004; 110(13): 1710 - 1713. [Full Text] [PDF]

				Other articles noted Evid. Based Med., September 1, 2004; 9(5): e5 - e5. [Full Text] [PDF]

This Article Abstract Full Text (PDF) All Versions of this Article: 109/10/1267    most recent 01.CIR.0000118535.15205.8Fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Eaker, E. D. Articles by Benjamin, E. J. Search for Related Content PubMed PubMed Citation Articles by Eaker, E. D. Articles by Benjamin, E. J. Related Collections Acute myocardial infarction Arrhythmias, clinical electrophysiology, drugs Chronic ischemic heart disease Epidemiology Risk Factors