Psychosomatics 46:523-528, November-December
doi: 10.1176/appi.psy.46.6.523
© 2005 Academy of Psychosomatic Medicine
Association Between Depressive Episode Before First Myocardial Infarction and Worse Cardiac Failure Following Infarction
Chris Dickens, Ph.D.,
Linda McGowan, Ph.D.,
Carol Percival, Ph.D.,
Jane Douglas, M.Phil.,
Barbara Tomenson, M.Sc.,
Lawrence Cotter, M.D.,
Anthony Heagerty, M.D., F.R.C.P., and
Francis Creed, M.D.
Received June 30, 2004; revision received Dec. 22, 2004; accepted June 30, 2005. From the Psychological Medicine Research Group, Department of Psychiatry, Manchester University, Manchester, U.K.; and the Department of Cardiology, Manchester Royal Infirmary. Address correspondence and reprint requests to Dr. Dickens, Department of Psychiatry, Rawnsley Building, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, U.K.; c.dickens{at}man.ac.uk (e-mail).
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ABSTRACT
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Depression following myocardial infarction is associated with a higher mortality rate. The authors studied 314 patients admitted to the hospital with a first myocardial infarction to assess whether cardiac failure after the infarction, which is also linked to a higher mortality rate, was predicted by psychosocial characteristics present before the myocardial infarction. One-fifth (20.7%) of the subjects met the ICD-10 criteria for depressive episode in the 1 month before the attack. Variables independently associated with worse cardiac failure after the myocardial infarction were greater age, a history of angina preceding the infarction, and a previous depressive episode. The impact of depression on postinfarction outcome may result from the influence of preinfarction depression on the degree of cardiac failure.
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INTRODUCTION
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There are two separate bodies of research concerned with the association between psychosocial risk factors and heart disease. The more recent literature has demonstrated that depression, lack of social support, and environmental stresses are all risk factors for death and other cardiac events in the months or years following myocardial infarction.1–4 Suggested mechanisms for these effects include a potential mediating role of maladaptive behaviors (e.g., smoking, lack of exercise), direct pathophysiological mechanisms (e.g., reduced heart rate variability), and influences on health care received.4,5 Such mechanisms are speculative, however, and the relative importance of each in determining the natural history of coronary heart disease remains to be established.
The other body of research has shown that depression, lack of social support, environmental stress, and hostility are risk factors for the development of coronary heart disease in previously healthy individuals.4,6 In a recent systematic review, Wulsin and Singal confirmed the association between depression and the later development of coronary heart disease, even in studies that controlled for other risks factors (e.g., smoking, hypertension).6 Using meta-analytic techniques, they calculated that depression conferred a relative risk of 1.64, with a 95% confidence interval (CI) of 1.41–1.90, for the development of coronary heart disease, a level of risk greater than that associated with passive smoking.
Very few studies have considered whether there is a continuity of psychosocial risk factors that might contribute to both the development of coronary heart disease and its later outcome, despite evidence that this might be the case. In two studies where depression was detected in patients after myocardial infarction, this depression was shown to have been present before the infarction in 30% to 50% of the subjects.7,8 One of these studies found that previous depression was associated with an increased risk of later cardiac failure (Killip class 2 or above), suggesting that depression contributes to both the development of the myocardial infarction and worse cardiac functioning afterward.8 This latter study included patients who had experienced a previous myocardial infarction, however, which may have confounded the result since a previous myocardial infarction may have been associated with both depression and cardiac failure.
We studied patients admitted to the hospital following the first myocardial infarction in order to investigate whether prior depressive episode and related psychosocial variables were associated with more severe cardiac failure following the first myocardial infarction. We tested the hypothesis that, among these patients, depressive episode, lack of social support, social stresses, and hostility would be independently associated with higher Killip class after control for relevant confounders.
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METHOD
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Study Group
Consecutive patients admitted to four inner-city hospitals with suspected myocardial infarctions between October 1997 and November 1999 were screened for this study. Consenting subjects who had no previous history of myocardial infarction and were less than 80 years of age were considered for inclusion if they met the World Health Organization criteria for myocardial infarction;9 two of the following were required: 1) a history of typical chest pain, 2) characteristic ECG changes, and 3) a serial rise in creatine phosphokinase (CPK) level.
Subjects were excluded if they 1) died before the assessment or were too ill or too cognitively impaired to complete the assessment (N=62), 2) had insufficient English or suffered substantial sensory impairment that precluded completion of the assessments even with assistance (N=18), 3) lived outside the area (N=14), 4) suffered from a significant psychiatric illness other than depression (N=4), 5) were diagnosed late (N=2), or 6) initiated their own discharge (N=1). Of the 357 eligible patients, 314 (88.0%) gave informed consent and completed baseline assessments. On average, the assessments took place 3.6 days (SD=3.3) after the index infarction.
We recorded age, gender, marital status, years of education (12 or more versus fewer than 12), separation from parents of 1 year or more before 17 years of age, current or past smoking, use of alcohol and illegal drugs, past medical history (including previous cardiovascular disease in the patient and his or her family), and past psychiatric history. Details of any current noncardiac illnesses were also recorded, including diabetes and hypertension.
Ethical permission was granted by the local research ethics committees, and this study complied with the Declaration of Helsinki. All participants provided written informed consent.
Assessments
Severity of cardiac failure was assessed by using the Killip class.10 This brief scale (scored 1 to 4) rates clinical signs of cardiac failure as follows: 1) Killip class 1 indicates no clinical signs of cardiac failure, 2) Killip class 2 indicates mild to moderate signs of cardiac failure (pulmonary rales, S3 gallop rhythm, and venous hypertension, 3) Killip class 3 indicates that severe cardiac failure was detected (frank pulmonary edema), and 4) Killip class 4 indicates cardiogenic shock (hypotension, peripheral vasoconstriction). The ratings were based on the findings of the clinical examination by the admitting physician/cardiologist. This measure has been shown to be an important risk factor for death after a myocardial infarction.1,11 Furthermore, in a previous study we found that Killip class was a significant independent predictor of cardiac events in the year following a myocardial infarction; the present study group includes patients who were also in that study.12
Socioeconomic status was assessed by using the job class criteria of Goldthorpe and Hope, which are based on current employment of the subject, the partner’s job if the subject is on sick leave, and the last job if the subject is retired.13 Subjects were classified in this study into two groups, referred to as middle and lower socioeconomic status.
Social support was assessed first as the degree of intimacy of the closest relationship(s). To do this we classified individuals as having, or not having, a close confidant—i.e., someone with whom the subject lived or contacted regularly and with whom she or he could share sensitive personal information and gain support.14 This is almost identical to an item from the ENRICHD Social Support Instrument,15 which predicts further cardiac events in subjects with ischemic heart disease.16–18 The second assessment concerned frequency of social contacts: people were classified as socially isolated if these were very few.19
Social stress was measured by using the Life Events and Difficulties Schedule.14 This measures the severity of social stress independent of the tendency of depressed persons to perceive their environments as more stressful than do nondepressed persons. The proportion of subjects who had experienced a severe event (e.g., bereavement, divorce) over the previous year is reported. Ongoing social difficulties (e.g., seriously ill relative, marked marital discord) are presented as a score representing the number and severity of such difficulties at the time of the myocardial infarction. We excluded any difficulties relating to the patient’s physical health (e.g., limitations of home or work life secondary to other illness).
The diagnosis of depressive episode preceding the myocardial infarction was made by using the Schedule for Clinical Assessment in Neuropsychiatry (SCAN) interview.20 This semistandardized research interview assessed each possible psychiatric symptom over the 30 days before the infarction. The interviewer asked detailed questions to establish the timing and nature of the symptoms, and only the symptoms that were clearly persistent during the month preceding the myocardial infarction contributed to the diagnosis of depressive episode. The interview data were entered directly into a computer, allowing an ICD-10 or DSM-IV diagnosis to be derived by computerized algorithm. This report concerns only subjects who met the ICD-10 criteria for depressive episode (mild, moderate, or severe) in the month preceding the infarction. The small number of subjects with other psychiatric disorders (mostly generalized anxiety disorder and dysthymia) were grouped together in the "not depressed" group. Excluding these subjects altogether did not change our findings.
Hostility was measured by using the Cook-Medley Hostility Scale.21 This self-rated assessment provides scores on two dimensions of hostility, hostility and aggressive responding, with high scores indicating greater hostility.
Statistics
Descriptive data are presented by using means (with standard deviations) or numbers (with percentages) of patients, as appropriate. For group comparisons we used the t test, chi-square test, and Fisher’s exact test.
Logistic regression with forward conditional selection of variables was used to examine which of the baseline characteristics were independently associated with Killip class (Killip class 2 or 3 versus Killip class 1). All variables that were significant (p<0.05) or nearly significant (p<0.2) predictors of Killip class in univariate analyses were entered into the logistic regression. In addition, any recognized risk factor for coronary heart disease, irrespective of whether it was associated with outcome in the univariate analyses, was also entered into the regression equation. Independent variables were entered in blocks: demographic variables were entered in block 1 (age, sex, social class, educational level), recognized risk factors for coronary heart disease were entered in block 2 (history of angina, hypertension, diabetes, hypercholesterolemia, smoking, and serum cholesterol level on admission), and psychosocial variables were entered in block 3 (depressive episode and marked life difficulties in year before the myocardial infarction). The analyses were performed by using Statistics Package for Social Sciences (SPSS), version 11.5 (SPSS, Chicago).
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RESULTS
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The mean age of subjects was 57.6 years (SD=11.2). Of the 314 participants, 199 (63.4%) were male. All were admitted following their first myocardial infarction, although 44 (14.0%) had experienced angina previously. They were predominantly white Caucasians (N=296, 94.3%). Sixty-two subjects (19.7%) reported some degree of social isolation; 23 (7.3%) did not have a close confidant.
Sixty-five subjects (20.7%) met the ICD-10 criteria for a depressive episode in the 4 weeks before the myocardial infarction. Coexisting noncardiac medical problems were present in 199 subjects (63.4%). The distribution among the Killip classes was as follows: class 1: N=230 (73.2%), class 2: N=78 (24.8%), and class 3: N=6 (1.9%).
In the univariate analysis (Table 1), it was found that the subjects with cardiac failure in Killip class 2 or 3 were older (p=0.003) than the remainder of the subjects; they were more likely to have experienced angina prior to the myocardial infarction (p=0.002), to suffer from diabetes (p=0.05), and to have rheumatological disorders (p=0.03). The group with Killip class 2 or 3 cardiac failure had a nonsignificantly smaller proportion of subjects with 12 or more years of education (p=0.08) and higher proportions with a depressive episode in the month preceding the myocardial infarction (p=0.09) and with marked ongoing social difficulties (p=0.08). Hostility, lack of a close confidant, and social isolation were not associated with higher Killip class. In a logistic regression with Killip class 1 versus Killip class 2 or 3 as the dependent variable, higher age (OR=1.04, p=0.006, 95% CI=1.01–1.05), a history of angina (OR=2.67, p=0.007, 95% CI=1.31–5.46), and having a depressive episode in the month before myocardial infarction (OR=2.14, p=0.03, 95% CI= 1.07–4.26) made significant independent contributions to the final model.
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TABLE 1. Univariate Associations Between Killip Class of Cardiac Failure and Demographic, Medical, and Psychosocial Measures in 314 Patients With a First Myocardial Infarction
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When the history of taking antidepressant medication was entered into the logistic regression model in addition to all the other variables, depressive episode remained significantly associated with higher Killip class (OR=2.26, p=0.03, 95% CI=1.12–4.57).
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DISCUSSION
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In this study of consecutive patients with a first myocardial infarction, those with a depressive episode in the month preceding the infarction had a risk of cardiac failure afterward that was twice as high as that for nondepressed subjects. Lack of a confidant, social isolation, hostility, and ongoing life difficulties showed no such independent association with Killip class. This association between depressive episode and Killip class was independent of the effects of conventional risk factors for coronary heart disease, such as smoking, hypercholesterolemia, and noncardiac illnesses, such as diabetes and hypertension.
Our study has a number of methodological strengths. First, we recruited patients who had not experienced a previous myocardial infarction, which might confound the association between depression and Killip class. We screened consecutive patients admitted following the first myocardial infarction and were able to recruit a high proportion to this study (88.0%), and as the result, our subjects were typical of patients admitted to the hospital following a first myocardial infarction in the United Kingdom. We measured a wide range of psychosocial variables and used very thorough research interviews to measure depressive episode, social support, and social stress.
We acknowledge the limitations of our current study. First, our assessment of depression was retrospective. The prevalence of a depressive episode in our subjects immediately before the myocardial infarction, 20.7%, is over four times that seen in the general population.22 This figure is much higher than the 5.4% seen in the study by Lesperance and colleagues,8 probably reflecting the inner-city area in which our study was performed.11,23 It is conceivable that retrospective assessment of depression in the days following the myocardial infarction may have resulted in the overreporting of depressive symptoms in those who were most ill following the infarction. However, the SCAN interview is extremely detailed, and assessors are allowed to ask any number of clarifying questions to ascertain when the symptoms of depression began. Only symptoms that the interviewer felt certain started before the myocardial infarction contributed to the diagnosis of depression. For these reasons, we do not believe that our retrospective assessment of depression was in any way invalidated. We accept that any inferences regarding the causal associations between depression and cardiac failure must be cautious.
A second limitation to our study relates to the fact that our assessment of cardiac failure (Killip class) relied on the clinical findings from the physical examination on admission to the hospital. Because this measure was clinically based, its reliability might be imperfect (reliability was not assessed in the current study), although we believe its main advantage, that it was brief and available to all subjects on admission, outweighed this. Furthermore, using the Killip class as a dichotomous measure (class 1 versus Killip class 2 or 3, i.e., signs of cardiac failure versus no signs of cardiac failure) is likely to have maximized its reliability. We can be sure that Killip class had good validity since it was shown to be predictive of increased morbidity and mortality in a number of previous studies.1,11,12 For these reasons, clinical assessment of cardiac failure was considered suitable.
We interpret our finding as indicating that a depressive episode contributes to the development of coronary heart disease but may also affect the severity of the myocardial infarction, leading to cardiac failure after the infarction. If this conclusion is correct, studies investigating the impact of depression on outcome after a myocardial infarction that control for the effects of the severity of the infarction may underestimate the magnitude of the effect of depression on outcome.24 The reasons for the observed association between depression before myocardial infarction and Killip class are not clear. Our further analysis suggests that this finding cannot be attributed to cardiotoxic effects of antidepressant drugs in the depressed subjects. Other reasons for the association between depression and Killip class may be the result of depressed subjects’ delay in seeking medical attention once the symptoms of the myocardial infarction start.25 We regret that we did not record the duration of symptoms prior to admission in our study group.
It is clear from this study that there is a continuum of risk for coronary heart disease in patients with depression consistent with the model in Figure 1. The magnitude of the effect was particularly large, and this may, in part, reflect the high degree of social deprivation in the group under investigation. Further studies are required to investigate the relative importance of the full range of psychosocial risks, particularly depression and lack of social support, to the development and natural history of coronary heart disease. Consideration should be given to the timing and duration of exposure to the psychosocial risks and their impact on outcome after a myocardial infarction. Possible mechanisms of effect should be explored by assessing the associations of depression and lack of social support with other risk factors (smoking, poor diet, lack of exercise, and poor compliance with treatments) and potential physiological mechanisms, such as changes to platelet and autonomic nervous system functioning. By these means, it may be possible to identify potential targets for intervention that could be incorporated into primary and secondary prevention programs for coronary heart disease.
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ACKNOWLEDGMENTS
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This study was funded by the Medical Research Council (U.K.) and the British Heart Foundation.
The authors thank Dick Heller, Professor of Public Health, Manchester University, for his helpful comments during the preparation of this manuscript.
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REFERENCES
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- Frasure-Smith N, Lesperance F, Talajic M: Depression following myocardial infarction: impact on 6-month survival. JAMA 1993; 270:1819–1825[Abstract/Free Full Text]
- Irvine J, Basinski A, Baker B, et al: Depression and risk of sudden cardiac death after acute myocardial infarction: testing for the confounding effects of fatigue. Psychosom Med 1999; 61:729–737[Abstract/Free Full Text]
- Welin C, Lappas G, Wilhelmsen L: Independent importance of psychosocial factors for prognosis after myocardial infarction. J Intern Med 2000; 247:629–639[CrossRef][Medline]
- 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]
- Rozanski A, Blumenthal JA, Kaplan J: Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 1999; 99:2192–2217[Abstract/Free Full Text]
- Wulsin LR, Singal BM: Do depressive symptoms increase the risk for the onset of coronary disease? A systematic quantitative review. Psychosom Med 2003; 65:201–210[Abstract/Free Full Text]
- Lloyd GG, Cawley RH: Psychiatric morbidity after myocardial infarction. QJM 1982; 201:33–42
- Lesperance F, Frasure-Smith N, Talajic M: Major depression before and after myocardial infarction: its nature and consequences. Psychosom Med 1996; 58:99–110[Abstract/Free Full Text]
- World Health Organization: Monitoring of cardiovascular disease and risk factor trends: experiences from the World Health Organization/MONICA project. Ann Med 1994; 26:61–65[Medline]
- Killip T, Kimball JT: Treatment of myocardial infarction in a coronary care unit: a two year experience with 250 patients. Am J Cardiol 1967; 20:457–464[CrossRef][Medline]
- Lane D, Carroll D, Ring C, et al: Mortality and quality of life 12 months after myocardial infarction: effects of depression and anxiety. Psychosom Med 2001; 63:221–230[Abstract/Free Full Text]
- Dickens CM, McGowan L, Percival C, et al: Lack of a close confidant, but not depression, predicts further cardiac events after myocardial infarction. Heart 2004; 90:518–522[Abstract/Free Full Text]
- Goldthorpe JH, Hope K: The Social Grading of Occupations: A New Approach and Scale. London, Oxford University Press, 1974
- Brown G, Harris T: Social Origins of Depression: A Study of Psychiatric Disorder in Women. London, Tavistock, 1978
- ENRICHD Investigators: Enhancing Recovery in Coronary Heart Disease (ENRICHD) study intervention: rationale and design. Psychosom Med 2001; 63:747–755[Abstract/Free Full Text]
- Williams RB, Barefoot JC, Califf RM, et al: Prognostic importance of social and economic resources among medically treated patients and angiographically documented coronary artery disease. JAMA 1992; 267:520–524[Abstract/Free Full Text]
- Berkman LF, Leo-Summers L, Horwitz RI: Emotional support and survival after myocardial infarction: a prospective, population-based study of the elderly. Arch Intern Med 1992; 117:1003–1009
- Gorkin L, Schron EB, Brooks MM, Wiklund I, Kellen J, Verter J, Schoenberger JA, Pawitan Y, Morris M, Shumaker S: Psychosocial predictors of mortality in the Cardiac Arrhythmia Suppression Trial-1 (CAST-1). Am J Cardiol 1993; 71:263–267[CrossRef][Medline]
- Brown G, Bilfulco A, Veiel HO, et al: Self-esteem and depression II: social correlates of self-esteem. Soc Psychiatry Psychiatr Epidemiol 1990; 25:225–234[CrossRef][Medline]
- World Health Organization Division of Mental Health: Schedule for Clinical Assessment in Neuropsychiatry, Version 2. Geneva, WHO, 1996
- Barefoot JC, Dodge KA, Peterson BL: The Cook-Medley Hostility Scale: item content and ability to predict survival. Psychosom Med 1989; 51:46–57[Abstract/Free Full Text]
- Meltzer H, Gill B, Petticrew M, Hinds K: The prevalence of psychiatric morbidity among adults living in private households, in OPCS Surveys of Psychiatric Morbidity in Great Britain. London, HMSO (Her Majesty’s Stationery Office), 1995, pp 1, 76
- Creed FH, Morgan R, Fiddler, et al. Depression and anxiety impair health-related quality of life and are associated with increased costs in general medical inpatients. Psychosomatics 2002; 43:302–309[Abstract/Free Full Text]
- Mendes de Leon CF: Depression and social support in recovery from myocardial infarction: confounding and confusion. Psychosom Med 1999; 61:738–739[Free Full Text]
- Schwarz B, Schoberberger R, Rieder A, et al: Factors delaying treatment of acute myocardial infarction. Eur Heart J 1994; 15:1595–1598[Abstract/Free Full Text]
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J. C. Huffman, F. A. Smith, M. A. Blais, A. M. Taylor, J. L. Januzzi, and G. L. Fricchione
Pre-Existing Major Depression Predicts In-Hospital Cardiac Complications After Acute Myocardial Infarction
Psychosomatics,
July 1, 2008;
49(4):
309 - 316.
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C. Dickens and F. Creed
Authors' reply
The British Journal of Psychiatry,
March 1, 2007;
190(3):
273 - 273.
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ABSTRACT
INTRODUCTION
