Change in Depression as a Precursor of Cardiovascular Events

Wassertheil‐Smoller, Sylvia; Applegate, William B.; Berge, Kenneth G.; Chang, Chee Jen; Davis, Barry R.; Grimm, Richard H.; Kostis, John B.; Pressel, Sara L.; Schron, Eleanor B.

doi:10.1001/archinte.1996.00440050111012

Cited by 263 publications

(86 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Also, depressive symptoms that are not sufficient in magnitude to meet the criteria for major depression occur at least as commonly among cardiac patients. 2,3 Recent epidemiological studies evaluating the relationship between depression and CAD among healthy [3][4][5][6][7][8][9][10][11] and CAD [12][13][14][15][16][17][18][19] populations consistently demonstrate a significant prospective relationship between the occurrence of major depression episodes and the incidence of cardiac events (Table 1). Two additional findings are notable.…”

Section: Depression and Related Syndromesmentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

View full text Add to dashboard Cite

Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

show abstract

Section: Depression and Related Syndromesmentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

View full text Add to dashboard Cite

show abstract

“…In the present study, a subsyndromal depressive mood was assessed by the DEEX scale, which is among the less rigorous options to assess depressive mood although a recent reexamination of its validity and reliability is promising. 15 Clinically, the DEEX scale identified symptoms of reduced vitality, weakness and 'vital exhaustion' 44 but without a negative self-concept and feelings of guilt feelings, 45 which provides sufficient coverage for all important facets of subsyndromal depressive mood of negative affectivity in the context of cardiovascular medicine. 46,47 Additionally, depression was measured at one time point, so that transient states of depression could not be distinguished from persistent states.…”

Section: Strength and Limitations Of The Studymentioning

confidence: 99%

Synergistic effects of depressed mood and obesity on long-term cardiovascular risks in 1510 obese men and women: results from the MONICA–KORA Augsburg Cohort Study 1984–1998

et al. 2006

View full text Add to dashboard Cite

Objective: To examine the contribution of depressed mood in obese subjects on the prediction of a future coronary heart disease event (CHD). Design: A prospective population-based cohort study of three independent cross-sectional surveys with 6239 subjects, 45-74 years of age and free of diagnosed CHD, stroke and cancer. During a mean follow-up of 7 years, 179 CHD events occurred among men and 50 events among women. Subjects: A total of 737 (23%) male and 773 (26%) female subjects suffering from obesity (BMI X30 kg/m 2 ). Measurements: Body weight determined by trained medical staff following a standardized protocol; standardized questionnaires to assess subsyndromal depressive mood and other psychosocial features. Results: The main effect of obesity to predict a future CHD (hazard ratio, HR ¼ 1.38, 95% CI 1.03-1.84; P ¼ 0.031) and the interaction term of obesity by depression (HR ¼ 1.73, 95% CI 0.98-3.05; P ¼ 0.060) were borderline significant, both covariate adjusted for multiple risk factors. Relative to the male subgroup with normal body weight and no depression, the male obese group with no depression was not at significantly increased risk for CHD events (HR ¼ 1.17, 95% CI 0.76-1.80; P ¼ 0.473) whereas CHD risk in males with both obesity and depressed mood was substantially increased (HR ¼ 2.32, 95% CI 1.45-3.72, P40.0001). The findings for women were similar, however, not significant probably owing to lack of power associated with low event rates. Combining obesity and depressed mood resulted in a relative risk to suffer from a future CHD event of HR 1.84 (95% CI 0.79-4.26; P ¼ 0.158). Conclusions: Depressed mood substantially amplifies the CHD risk of middle-aged obese, but otherwise apparently healthy men. The impact of depression on the obesity risk in women is less pronounced.

show abstract

“…In the last fifteen years this link has become the focus of a growing literature of prospective, epidemiological studies (Carney et al, 1988;Thomas et al, 1992;Andaetai, 1993;Aromaa et al, 1994;Vogt et al, 1994;Frasure-Smith et al, 1995;Lapaneefa/., 1995;Wassertheil-Smollerefa/., 1996;Barefoot & Schroll, 1996;Pratt et al, 1996;Bingefors et al, 1996;Ford et al, 1998;Sesso et al, 1998;Cohen et al, 2000;Penninx et al, 2001). Almost all have reported some positive, statistically significant association of depression with cardiovascular disease (CVD), although one found the association with change in depression status rather than baseline depression (Wassertheil-Smoller et al, 1996), and another found the association with all-cause mortality but not CVD mortality (Vogt et al, 1994). One did not report any association at all (Thomas et al, 1992).…”

Section: Hillel W Cohen and James Davidmentioning

confidence: 99%