(Circulation. 1996;94:3123-3129.)
© 1996 American Heart Association, Inc.
Articles |
Depression, Psychotropic Medication, and Risk of Myocardial Infarction
Prospective Data From the Baltimore ECA Follow-up
the Department of Epidemiology (L.A.P., D.E.F., R.M.C., H.K.A.) and the Department of Mental Hygiene (R.M.C., J.J.G., W.W.E.), Johns Hopkins School of Hygiene and Public Health; and the Department of Psychiatry (R.M.C.) and the Department of Medicine (D.E.F.), Johns Hopkins School of Medicine, Baltimore, Md.
Correspondence to Laura A. Pratt, Johns Hopkins University, School of Hygiene and Public Health, 615 N Wolfe St, Box 188, Baltimore, MD 21205. E-mail lpratt@welchlink.welch.jhu.edu.
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Abstract |
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Background There is suggestive evidence that depression increases risk of myocardial infarction (MI), but there are no prospective studies in which the measure of depression corresponds to clinical criteria. This study examines prospectively whether a major depressive episode increases the risk of incident MI and evaluates the role of psychotropic medication use in this relationship.
Methods and Results The study is based on a follow-up of the Baltimore cohort of the Epidemiologic Catchment Area Study, a survey of psychiatric disorders in the general population. A history of major depressive episode, dysphoria (2 weeks of sadness), and psychotropic medication use were assessed in 1981, and self-reported MI was assessed in 1994. Sixty-four MIs were reported among 1551 respondents free of heart trouble in 1981. Compared with respondents with no history of dysphoria, the odds ratio for MI associated with a history of dysphoria was 2.07 (95% CI, 1.16 to 3.71), and the odds ratio associated with a history of major depressive episode was 4.54 (95% CI, 1.65 to 12.44), independent of coronary risk factors. In multivariate models, use of barbiturates, meprobamates, phenothiazines, and lithium was associated with an increased risk of MI, whereas use of tricyclic antidepressants and benzodiazepines was not. Among individuals with no history of dysphoria, only lithium use was significantly associated with MI.
Conclusions These data suggest that a history of dysphoria and a major depressive episode increase the risk of MI. The association between psychotropic medication use and MI is probably a reflection of the primary relationship between depression and MI.
Key Words: drugs • myocardial infarction • risk factors • depression
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Introduction |
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Studies of psychiatric patients have shown higher rates of heart disease among depressed patients.1 2 Cross-sectional and case-control studies have shown that rates of depression are higher among patients with coronary artery disease.3 4 Follow-up of patients after MI has shown that post-MI patients with depression have a worse prognosis than nondepressed patients.5 A question with important implications for public health practice is whether antecedent depression increases the risk of incident heart disease in community-dwelling adults. A prospective study based in the NHANES 1 follow-up reported that adults with depressed affect had a relative risk of 1.5 for fatal ischemic heart disease compared with those without depressed affect.6 A second study in a cohort of Johns Hopkins Medical School alumni found a relative risk of 2.2 for fatal and nonfatal coronary heart disease among male physicians with self-reported clinical depression compared with male physicians reporting no depression.7 In both studies, the association remained after adjustment for sociodemographic variables and major coronary risk factors. Other prospective studies, using different measures of depression, found no relationship between baseline depression and subsequent heart disease.8 9 One study among elderly persons reported an increased risk of cardiovascular events related to an increase in Center for Epidemiological Studies–Depression scale (CES-D) scores over follow-up but found no relationship between baseline CES-D–measured depression and subsequent cardiovascular events.10
Tricyclic antidepressants are known to affect the cardiovascular system11 12 ; therefore, some concern exists that psychotropic medication use may contribute to the risk of MI in depressed patients. The results of two recent studies increased the urgency to investigate this hypothesis. A case-control study of fatal MI in young women found an OR of 16.9 for the current use of psychotropic medication and risk of fatal MI.13 A cohort study of risk for both fatal and nonfatal MI found associations with benzodiazepine and antidepressant use.14 Neither study controlled for depression or other mental illness.
Other suggested explanations of the relationship between depression and heart disease include cigarette smoking and comorbid psychiatric disorders. Some studies have found a relationship between phobia or panic disorder and ischemic heart disease15 16 but did not control for depression, which often occurs with the anxiety disorders.
This article reports on a prospective study of depression as a risk factor for nonfatal MI in the Baltimore ECA Follow-up Study. The study examines the hypothesis that an MDE and dysphoria are independent risk factors for MI and assesses the role of psychotropic medication in the relationship between depression and MI. This investigation differs from published prospective studies of the relationship between depression and heart disease in several ways. First, the sample was drawn from the general population and was not restricted to certain age groups, sexes, or clinical populations. Second, unlike other studies that used symptom scales as a measure of depression,6 8 9 10 this study used a structured interview grounded in the standard clinical criteria for MDE as found in the American Psychiatric Association's Diagnostic and Statistical Manual, third edition (DSM-III).17 Third, because baseline measures of other psychiatric illnesses are available, the role of MDE, independent of comorbid psychiatric disorders, can be investigated. This study is the first to include measures of psychiatric disorder in analyses of the role of psychotropic medication in myocardial infarction.
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Methods |
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Research Design
ECA
The ECA program was a national study with the goal of measuring the prevalence and incidence of clinically defined psychiatric disorders in the general population. More than 20 000 persons older than 18 years of age were interviewed in five US cities between 1980 and 1983.18 19 The target population for the Baltimore site of the ECA was the household residents of east Baltimore, an area of 175 000 adult inhabitants. In 1981, an area probability sample was selected, and 3481 individuals were interviewed in their households, a completion rate of 82%. Participants gave informed consent before the interview. The protocol was approved by the Committee on Human Research of the Johns Hopkins School of Hygiene and Public Health. Further details of the ECA study and methods are available elsewhere.20
The instrument used in the ECA program was the National Institute of Mental Health DIS.21 The DIS is a highly structured survey interview designed to produce diagnoses of specific mental disorders according to the criteria of the American Psychiatric Association's DSM-III.17 The DIS consists of close-ended (mostly yes/no) questions and is designed for administration by interviewers with 1 to 2 weeks of training but no clinical experience. The DIS assesses the presence or absence of symptoms needed for a diagnosis and contains probes that eliminate trivial occurrences of symptoms and possible nonpsychiatric causes of the symptoms such as physical illness or ingestion of alcohol or drugs. A computer algorithm combines the responses into diagnostic categories. Studies of the reliability and validity of the DIS show that it has good reliability and acceptable validity.21 The DIS is widely used in psychiatric epidemiology.
Baltimore ECA Follow-up
In 1993 and 1994, the Baltimore cohort of 3481 was the target for tracing and reinterviewing (W.W. Eaton, unpublished data, 1995). Mortality was an important factor in tracing, and 847 respondents were identified who died during the follow-up period. The address of 437 individuals from the 3481 could not be established, and 300 refused to participate. More than 72% of the 2634 survivors, or 1897 individuals, were located and reinterviewed. The 1993/1994 respondents did not differ appreciably from the survivors in terms of age and sex. In other analyses (M.A. Badawi, unpublished data, 1995), it was shown that certain psychiatric disorders (drug abuse/dependence and antisocial personality disorder) were related to attrition among survivors, but depression in 1981 was not related to attrition. The rate of MDEs among those who died over the follow-up period was much lower than among the survivors, presumably because of the younger age composition of the depressed group. Odds of mortality did not differ by depression status after age adjustment.
Study Sample
In the 1981 interview, respondents were asked if they had ever had heart trouble. Of the 1897 individuals interviewed in 1993/1994, 219 had reported a history of heart trouble during the 1981 interview and were excluded from the analyses in order to restrict the outcome to incident MI. Also excluded were those who did not know in 1993/1994 if they had ever had heart trouble or a heart attack (n=20). Finally, those with incomplete information on 1993/1994 heart attack (n=107), a group mainly composed of individuals who required an informant interview, were also excluded. The final number of participants available for analysis and at risk for new MI was 1551.
Variables Under Study
Main exposure variables
MDE, as described in the DSM-III and measured by the DIS, is a disorder characterized by sadness (dysphoria) or complete loss of interest in things usually enjoyed, occurring concomitantly with symptoms from at least four out of eight symptom groups and lasting 
2 weeks. Any occurrence of MDE before the 1981 interview (lifetime history) placed the respondent in the (hypothesized) highest risk category of exposure. Because the published studies on depression and heart disease have used many definitions of depression and means of measurement and have not shown whether the clinical diagnosis threshold is relevant in explaining increased risk of MI, a history of 2 weeks of unremitting dysphoria was also used in the analyses as the broadest indicator of depression. The exposure variable was a categorical variable of three levels: (1) the reference group consisting of individuals who reported never having had 2 weeks of dysphoria, (2) individuals with a history of dysphoria who had never met clinical criteria for a major depressive episode, and (3) individuals who had met the criteria for MDE at some point in their life. By definition, individuals who did not report dysphoria could not meet the clinical criteria for MDE.
Information on psychotropic medication was gathered in the 1981 household interview through the use of detailed questions that included color photographs of each specific pill. Similar to the MDE variable, analyses considered "ever use" of the particular medication in the respondent's lifetime.
Outcome variables
The 1993-1994 interview contained more detailed questions about heart trouble than the 1981 interview. After the respondent was asked whether he or she had ever had heart trouble, those who responded positively were then asked, "What kind of heart trouble have you had?" The interviewer then read a list of five specific conditions: rheumatic fever, rheumatic heart disease, angina pectoris, a heart attack, and congestive heart failure. Those who reported having a heart attack were considered positive for the outcome; all other 1993-1994 respondents were considered negative.
Covariates
In the 1981 household interview, information was collected about the participant's history of common physical illnesses, including heart disease, hypertension, and diabetes; use of tobacco, alcohol, and other substances; and many sociodemographic variables, including education, household income, and marital status. A history of other psychiatric disorders that might confound the depression–heart disease relationship (ie, DIS/DSM-III alcohol abuse/dependence, panic disorder, and phobia) was obtained in 1981 through the use of the DIS as described above.
Analytical Strategy
The three exposure groups (respondents with a history of major depressive episode, those with a history of dysphoria who did not meet DSM criteria for MDE, and those who did not report a history of dysphoria) were compared in terms of baseline characteristics. Cumulative incidence rates of MI were calculated for each exposure and risk factor group. Crude ORs were obtained with the use of logistic regression for dysphoria and an MDE relative to those without history of dysphoria (Table 3, model 1).
The logistic regression model was then expanded to adjust for known coronary risk factors including age, male sex, cigarette smoking, history of diabetes, history of hypertension, socioeconomic as measured by high school education, and social support as measured by marital status. Data on serum cholesterol were not available. Variables were retained in the model if they were significant at the level of P<.10 or if their removal altered the ORs associated with dysphoria or MDE by >20%. The resulting model (model 2) is referred to as the risk factor model. The other DIS/DSM-III psychiatric disorders, phobia, panic disorder, and alcohol abuse/dependence (model 3), were then added to the risk factor model to assess their confounding potential, as was a broad measure of psychotropic medication use (model 4).
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To study the effect of the specific types of psychotropic medications, crude ORs of MI were calculated for each drug category. Subjects were included in the exposed category for each drug type that they reported ever having taken. Separate logistic regression models were used to calculate ORs for each drug category, holding constant a history of dysphoria, MDE, and the coronary risk factors from model 2. Because psychotropic drug use and depression are highly correlated, the crude and adjusted ORs for each drug category were examined in the group with no history of dysphoria.
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Results |
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The subjects with a history of MDE differed from those without a history of MDE or dysphoria in several ways (Table 1).
Subjects with a history of MDE were younger, more likely to be female, less likely to be married or widowed, more likely to be separated or divorced, and more likely to have graduated from high school or obtained a GED. Subjects with dysphoria also had a younger age distribution than the unexposed group, although they were likely to be older than the participants with a history of MDE. The group with a history of dysphoria was more likely to be female and to be widowed, separated, or divorced than the reference group, but the proportion of high school graduates was similar in both groups. The group without any history of dysphoria tended to have a somewhat higher household income than the other groups. Subjects with a history of MDE and those with dysphoria were more likely to be current cigarette smokers and to have a history of alcohol abuse/dependence than the unexposed group. Both exposure groups were more likely to meet criteria for panic disorder or phobia and to report having taken psychotropic medication than the unexposed. There was no difference between the three groups by race, history of hypertension, or history of diabetes.
Over the 13 years of follow-up, there were 6 MIs among the 73 people with a history of MDE (a rate of 8.2 per 100), 21 heart attacks among the 371 people with dysphoria who did not meet criteria for MDE (a rate of 5.7 per 100), and 37 heart attacks among the 1107 unexposed people (a rate of 3.3 per 100; Table 2). A 
2 test for trend was significant at the level of P=.008. Frequencies of MI by other risk factors are also shown in Table 2.
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Respondents with a history of MDE had 2.6-times-higher odds of MI than respondents with no history of dysphoria, with 95% CIs that did not include 1.0 (Table 3, model 1). The crude OR for respondents with history of dysphoria compared with the unexposed was 1.7 and was borderline statistically significant. Because age is negatively related to depression and positively related to MI, it is likely to be a major confounder. As expected, after adjustment for age (not shown), the OR for MI among those with a history of dysphoria compared with the reference group increased to 2.0 (95% CI, 1.1 to 3.5) and the OR for those with a history of major depressive episode compared with the reference group increased to 4.8 (1.8 to 12.7). In a logistic regression model adjusting for coronary risk factors, the covariates sex, age, marital status, and history of hypertension were all significant at the level of P<.10 and were retained in the final risk factor model (model 2, Table 3). As shown in model 2 (Table 3), the odds of MI in persons with a history of dysphoria are 2.1 times higher than the odds of MI in persons with no history of 2 weeks of dysphoria, independent of other coronary risk factors. Respondents with a history of MDE had odds of MI 4.5 times higher than that of respondents with no history of dysphoria, independent of other coronary risk factors.
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To test whether the association was independent of comorbid psychiatric disorders, history of DIS/DSM III alcohol abuse/dependence, panic disorder, and phobia was added to the coronary risk factor model. The odds of MI associated with depression decreased only slightly and remained significant. None of the relationships between the other psychiatric disorders and MI was large or approached significance (alcohol abuse dependence OR, 1.4; panic disorder OR, 1.2; phobia OR, 1.2; model 3). When psychotropic medication use was added to the coronary risk factor model, similar results were obtained (model 4).
There was a significantly increased risk of MI associated with a wide variety of medication groups: barbiturates, phenothiazines, lithium, and meprobamates (Table 4). There was no increased risk associated with tricyclic antidepressants or benzodiazepines. Dysphoria and MDE remained significant predictors of MI in each model.
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To separate the effects of the psychotropic medications from those of depression, we looked at the odds for MI associated with each medication grouping among the respondents who reported never having had 2 weeks of dysphoria (n=1107). Among respondents who reported no history of dysphoria, only the use of lithium was significantly associated with increased odds of MI (crude OR, 10.1 [95% CI, 1.0 to 99.3]; adjusted OR, 23.5 [1.8 to 300.9]; data not shown). This result is based on only 4 individuals who reported taking lithium but not having a history of dysphoria, one of whom reported an MI.
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Discussion |
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A history of DIS/DSM-III–defined MDE was associated with odds of MI more than four times higher than that among individuals with no history of MDE or dysphoria in this cohort of people who did not report having any heart trouble 13 years earlier. This increased risk was independent of major coronary risk factors. Comorbid psychiatric disorders and psychotropic medication use did not explain the relationship between depression and MI. Although rates of cigarette smoking were higher among individuals with a history of MDE or dysphoria than among those without dysphoria, cigarette use did not explain the excess risk of MI among depressed individuals. This result is consistent with that reported by Ford et al7 among male Johns Hopkins Medical School Alumni in the Precursors Study.
A single question that captures the most important feature of depressive disorder, dysphoria ("In your lifetime, have you ever had 2 weeks or more during which you felt sad, blue, depressed, or when you lost all interest and pleasure in things that you usually cared about or enjoyed?"), was associated with 107% increased odds of MI that was independent of major coronary risk factors. This result is consistent with that reported by Anda et al6 in the NHANES follow-up study, in which a single question on hopelessness was predictive of increased risk of fatal ischemic heart disease after adjustment for coronary risk factors.
We found crude associations between many psychotropic drug categories and odds of MI. Unlike Thorogood et al,13 however, we found no increased risk associated with tricyclic antidepressants or benzodiazepines, the most commonly used psychotropic medications among people with depression at the time of the 1981 interview. After adjustment for dysphoria, major depressive episode, and coronary risk factors, four drug groupings remained associated with increased odds of MI. Three of these, lithium, phenothiazines, and meprobamates, have known cardiac effects, whereas the other group, the barbiturates, is not generally thought to have cardiopathic effects. As discussed in the Lancet editorial after the Thorogood article, because the association with MI was not specific to a particular drug type, it is likely that the OR reflects an association with the underlying condition that led a health provider to prescribe the drug rather than to the drug itself.22 Lithium was the only psychotropic medication significantly associated with increased odds of MI among respondents who reported no history of dysphoria. This result, although based on extremely small numbers, could reflect a true cardiopathic effect of lithium23 or it could be a reflection of an increased risk of MI associated with mania,24 an affective disorder for which lithium is commonly indicated.
Research into the mechanisms by which MDE increases the risk for MI could contribute to the prevention of MI as well as the prevention of major depression. The biological abnormalities found in some subjects with major depression could cause either atherosclerosis or clinical coronary events. A dysregulated neurotransmitter system in depression characterized by surges in blood catecholamine levels as described by Siever and Davis25 could lead to endothelial injury,26 increased platelet aggregation, or electrical instability.27 Insulin resistance, which has been seen in major depression,28 has been hypothesized to contribute to atherosclerosis.29 Dalack and Roose30 suggest that decreased heart rate variability seen in depressed patients may increase the risk of cardiovascular mortality.
Study Limitations
There are several limitations to our study that should be discussed. First, the outcome measure was based on self-report and therefore is subject to misclassification. The results of studies assessing the agreement between self-reported data and medical records vary, depending on criteria used to define MI. A study in Finland that accepted a physician diagnosis as confirmation found that 81% of self-reported MIs were confirmed by medical records.31 The Nurse's Health Study, which used WHO criteria to define MI and excluded "silent" infarctions diagnosed by ECG alone, confirmed only 68% of self-reported MIs, although most of the nonconfirmed MI cases did have cardiac disease.32 If the misclassification of outcome is nondifferential with respect to the exposure, it will not affect the conclusions drawn from the data.
Second, although the DIS has been shown to have good reliability and acceptable validity,21 there is a possibility of misclassification of exposure. A study that compared DIS diagnoses with clinical diagnoses found that the DIS tended to err in underascertainment of an MDE and not in overascertainment.33 It is likely, therefore, that those in our MDE group were true-positives. Also, it is likely that any individuals with a history of MDE not captured by our MDE group would be included in the group with a history of dysphoria, thereby not contaminating the reference group. Third, we were unable to look at mortality from MI. Our results for nonfatal MI were similar to those reported by Anda et al6 and Ford et al7 for both fatal and nonfatal MI. Current knowledge suggests that depression is related to a worse prognosis after MI.5 34 Therefore, restricting the study to survivors only should be a conservative approach, resulting in a bias toward the null, if any. The relationship between phobic anxiety and MI reported in the Health Professionals Follow-up Study was restricted to a relationship with sudden death,16 which may explain the lack of association between phobia and MI in our study. We were unable to adjust for length of time of medication use or dosage, and our ascertainment of usage was by self-report. It was impossible to assess the effect of each medication group independent of the others because most respondents who had used psychotropic medication reported using drugs from more than one category. This was true of every drug category except benzodiazepines.
As in most community-based cohort studies, losses to follow-up did occur in our study, but those missing did not differ significantly by exposure from those successfully reinterviewed. Information on other coronary risk factors such as cholesterol level or exercise would strengthen our study. Studies of the relationship between cholesterol levels and depression have reported conflicting results,35 so it is difficult to predict how the inclusion of information on cholesterol would have affected our conclusions. The NHANES-based study adjusted for both cholesterol levels and exercise, and such adjustment did not change the results.6
Conclusions
Our study has several strengths. It is a population-based investigation with good representation of blacks and whites and both sexes. It is prospective in design, which allows more confidence in our assessment of the temporal relationship that the MDE preceded the MI. The measurement of exposure was based on clinical criteria rather than symptom count, which can be more heavily influenced by the presence of physical illness.36 Unlike previous studies, the effect of comorbid mental disorders could be examined.
It is difficult to make conclusions about long-term effects of medications from observational studies because so many characteristics of a patient contribute to a physician's decision to prescribe a medication. This study controlled for the presence of mental disorders more successfully than previous reports. We conclude that dysphoria and an MDE increase the risk of MI and that the associations found with psychotropic medication probably are only reflections of this primary relationship.
The public health implications of our study findings include the need to identify patients with depression and to evaluate both their mental health profile and their cardiovascular profile. The finding that 28% of the Baltimore ECA cohort endorsed the dysphoria question and that this one question was associated with a twofold increase in the odds of MI suggest the possibility of simple screening for this risk factor in the primary care context.
Our study does not show whether treatment of depression would help to lessen the risk of MI associated with depression, but other authors have suggested that this might be the case.4 37 38 A recent study conducted in Austria, Canada, Denmark, and Germany reported that lithium treatment for more than 2 years reduced mortality from cardiovascular disease in patients with major affective disorder, including patients with major depression, mania, and schizo-affective psychosis.37 Another study, from the 1970s, reported that depressed patients adequately treated with either tricyclic antidepressants or electroconvulsive therapy had a lower heart disease mortality than inadequately treated depressed patients.38 Further longitudinal research is needed to determine whether treatment of depression by medication and/or cognitive therapy is an effective means of reducing the excess risk of MI associated with depression.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This research was supported by National Institute of Mental Health grant MH47447. Laura Pratt was supported by National Heart, Lung, and Blood Institute Cardiovascular Epidemiology Institutional Training Grant 5-T32-HL-07024-21. Dr Crum was supported by a Scientist Development Award for Clinicians from the National Institute on Alcohol Abuse and Alcoholism, K20-AA000168.
Received May 6, 1996; revision received August 16, 1996; accepted August 31, 1996.
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S. Herbst, R. H. Pietrzak, J. Wagner, W. B. White, and N. M. Petry Lifetime Major Depression is Associated With Coronary Heart Disease in Older Adults: Results From the National Epidemiologic Survey on Alcohol and Related Conditions Psychosom Med, October 1, 2007; 69(8): 729 - 734. [Abstract] [Full Text] [PDF]
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J. M. McCaffery, N. Frasure-Smith, M.-P. Dube, P. Theroux, G. A. Rouleau, Q. Duan, and F. Lesperance Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin. Psychosom Med, March 1, 2006; 68(2): 187 - 200. [Abstract] [Full Text] [PDF]
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P. P. Rieker and C. E. Bird Rethinking Gender Differences in Health: Why We Need to Integrate Social and Biological Perspectives J. Gerontol. B. Psychol. Sci. Soc. Sci., October 1, 2005; 60(suppl_Special_Issue_2): S40 - S47. [Abstract] [Full Text] [PDF]
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J.P. Empana, D.H. Sykes, G. Luc, I. Juhan-Vague, D. Arveiler, J. Ferrieres, P. Amouyel, A. Bingham, M. Montaye, J.B. Ruidavets, et al. Contributions of Depressive Mood and Circulating Inflammatory Markers to Coronary Heart Disease in Healthy European Men: The Prospective Epidemiological Study of Myocardial Infarction (PRIME) Circulation, May 10, 2005; 111(18): 2299 - 2305. [Abstract] [Full Text] [PDF]
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L J Tata, J West, C Smith, P Farrington, T Card, L Smeeth, and R Hubbard General population based study of the impact of tricyclic and selective serotonin reuptake inhibitor antidepressants on the risk of acute myocardial infarction Heart, April 1, 2005; 91(4): 465 - 471. [Abstract] [Full Text] [PDF]
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R. M. Carney, K. E. Freedland, and D. S. Sheps Depression is a Risk Factor for Mortality in Coronary Heart Disease Psychosom Med, November 1, 2004; 66(6): 799 - 801. [Full Text] [PDF]
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M. W. Ketterer, G. Mahr, J. J. Cao, M. Hudson, S. Smith, and W. Knysz What's "Unstable" in Unstable Angina? Psychosomatics, June 1, 2004; 45(3): 185 - 196. [Abstract] [Full Text] [PDF]
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D. E. Ford and T. P. Erlinger Depression and C-Reactive Protein in US Adults: Data From the Third National Health and Nutrition Examination Survey Arch Intern Med, May 10, 2004; 164(9): 1010 - 1014. [Abstract] [Full Text] [PDF]
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P. Ciechanowski, E. Wagner, K. Schmaling, S. Schwartz, B. Williams, P. Diehr, J. Kulzer, S. Gray, C. Collier, and J. LoGerfo Community-Integrated Home-Based Depression Treatment in Older Adults: A Randomized Controlled Trial JAMA, April 7, 2004; 291(13): 1569 - 1577. [Abstract] [Full Text] [PDF]
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H. Tiemeier, W. van Dijck, A. Hofman, J. C. M. Witteman, T. Stijnen, and M. M. B. Breteler Relationship Between Atherosclerosis and Late-Life Depression: The Rotterdam Study Arch Gen Psychiatry, April 1, 2004; 61(4): 369 - 376. [Abstract] [Full Text] [PDF]
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H. Luukinen, P. Laippala, and H.V. Huikuri Depressive symptoms and the risk of sudden cardiac death among the elderly Eur. Heart J., November 2, 2003; 24(22): 2021 - 2026. [Abstract] [Full Text] [PDF]
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R. A.H. Stewart, F. M. North, T. M. West, K. J. Sharples, R.J. Simes, D. M. Colquhoun, H. D. White, A. M. Tonkin, and for the Long-Term Intervention With Pravastatin in Depression and cardiovascular morbidity and mortality: cause or consequence? Eur. Heart J., November 2, 2003; 24(22): 2027 - 2037. [Abstract] [Full Text] [PDF]
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W. H. Sauer, J. A. Berlin, and S. E. Kimmel Effect of Antidepressants and Their Relative Affinity for the Serotonin Transporter on the Risk of Myocardial Infarction Circulation, July 8, 2003; 108(1): 32 - 36. [Abstract] [Full Text] [PDF]
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M. Danner, S. V. Kasl, J. L. Abramson, and V. Vaccarino Association Between Depression and Elevated C-Reactive Protein Psychosom Med, May 1, 2003; 65(3): 347 - 356. [Abstract] [Full Text] [PDF]
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R. E. Clouse, P. J. Lustman, K. E. Freedland, L. S. Griffith, J. B. McGill, and R. M. Carney Depression and Coronary Heart Disease in Women With Diabetes Psychosom Med, May 1, 2003; 65(3): 376 - 383. [Abstract] [Full Text] [PDF]
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J. M. McCaffery, R. Niaura, J. F. Todaro, G. E. Swan, and D. Carmelli Depressive Symptoms and Metabolic Risk in Adult Male Twins Enrolled in the National Heart, Lung, and Blood Institute Twin Study Psychosom Med, May 1, 2003; 65(3): 490 - 497. [Abstract] [Full Text] [PDF]
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L. R. Wulsin and B. M. Singal Do Depressive Symptoms Increase the Risk for the Onset of Coronary Disease? A Systematic Quantitative Review Psychosom Med, March 1, 2003; 65(2): 201 - 210. [Abstract] [Full Text] [PDF]
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D. J. Jones, J. T. Bromberger, K. Sutton-Tyrrell, and K. A. Matthews Lifetime History of Depression and Carotid Atherosclerosis in Middle-aged Women Arch Gen Psychiatry, February 1, 2003; 60(2): 153 - 160. [Abstract] [Full Text] [PDF]
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L. Borowicz Jr., R. Royall, M. Grega, O. Selnes, C. Lyketsos, and G. McKhann Depression and Cardiac Morbidity 5 Years After Coronary Artery Bypass Surgery Psychosomatics, December 1, 2002; 43(6): 464 - 471. [Abstract] [Full Text] [PDF]
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C. A. Shively, J. K. Williams, K. Laber-Laird, and R. F. Anton Depression and Coronary Artery Atherosclerosis and Reactivity in Female Cynomolgus Monkeys Psychosom Med, September 1, 2002; 64(5): 699 - 706. [Abstract] [Full Text] [PDF]
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J. E. Morley and J. H. Flaherty Editorial It's Never Too Late: Health Promotion and Illness Prevention in Older Persons J. Gerontol. A Biol. Sci. Med. Sci., June 1, 2002; 57(6): M338 - 342. [Full Text]
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S. A. Williams, S. V. Kasl, A. Heiat, J. L. Abramson, H. M. Krumholz, and V. Vaccarino Depression and Risk of Heart Failure Among the Elderly: A Prospective Community-Based Study Psychosom Med, January 1, 2002; 64(1): 6 - 12. [Abstract] [Full Text] [PDF]
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M. JOUKAMAA, M. HELIOVAARA, P. KNEKT, A. AROMAA, R. RAITASALO, and V. LEHTINEN Mental disorders and cause-specific mortality The British Journal of Psychiatry, December 1, 2001; 179(6): 498 - 502. [Abstract] [Full Text] [PDF]
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W. H. Sauer, J. A. Berlin, and S. E. Kimmel Selective Serotonin Reuptake Inhibitors and Myocardial Infarction Circulation, October 16, 2001; 104(16): 1894 - 1898. [Abstract] [Full Text] [PDF]
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B. W. J. H. Penninx, A. T. F. Beekman, A. Honig, D. J. H. Deeg, R. A. Schoevers, J. T. M. van Eijk, and W. van Tilburg Depression and Cardiac Mortality: Results From a Community-Based Longitudinal Study Arch Gen Psychiatry, March 1, 2001; 58(3): 221 - 227. [Abstract] [Full Text] [PDF]
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H. W. Cohen, S. Madhavan, and M. H. Alderman History of Treatment for Depression: Risk Factor for Myocardial Infarction in Hypertensive Patients Psychosom Med, March 1, 2001; 63(2): 203 - 209. [Abstract] [Full Text] [PDF]
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A. House, P. Knapp, J. Bamford, and A. Vail Mortality at 12 and 24 Months After Stroke May Be Associated With Depressive Symptoms at 1 Month Stroke, March 1, 2001; 32(3): 696 - 701. [Abstract] [Full Text] [PDF]
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A. A. Ariyo, M. Haan, C. M. Tangen, J. C. Rutledge, M. Cushman, A. Dobs, and C. D. Furberg Depressive Symptoms and Risks of Coronary Heart Disease and Mortality in Elderly Americans Circulation, October 10, 2000; 102(15): 1773 - 1779. [Abstract] [Full Text] [PDF]
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D. L. Musselman, U. M. Marzec, A. Manatunga, S. Penna, A. Reemsnyder, B. T. Knight, A. Baron, S. R. Hanson, and C. B. Nemeroff Platelet Reactivity in Depressed Patients Treated With Paroxetine: Preliminary Findings Arch Gen Psychiatry, September 1, 2000; 57(9): 875 - 882. [Abstract] [Full Text] [PDF]
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R. M. Carney, K. E. Freedland, P. K. Stein, J. A. Skala, P. Hoffman, and A. S. Jaffe Change in Heart Rate and Heart Rate Variability During Treatment for Depression in Patients With Coronary Heart Disease Psychosom Med, September 1, 2000; 62(5): 639 - 647. [Abstract] [Full Text] [PDF]
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J. L. Januzzi Jr, T. A. Stern, R. C. Pasternak, and R. W. DeSanctis The Influence of Anxiety and Depression on Outcomes of Patients With Coronary Artery Disease Arch Intern Med, July 10, 2000; 160(13): 1913 - 1921. [Full Text] [PDF]
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A. K. Ferketich, J. A. Schwartzbaum, D. J. Frid, and M. L. Moeschberger Depression as an Antecedent to Heart Disease Among Women and Men in the NHANES I Study Arch Intern Med, May 8, 2000; 160(9): 1261 - 1268. [Abstract] [Full Text] [PDF]
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W. Coryell, C. Turvey, A. Leon, J. D. Maser, D. Solomon, J. Endicott, T. Mueller, and M. Keller Persistence of Depressive Symptoms and Cardiovascular Death Among Patients With Affective Disorder Psychosom Med, November 1, 1999; 61(6): 755 - 761. [Abstract] [Full Text] [PDF]
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