The nature and course of depression following myocardial infarction

Schleifer, Steven J.

doi:10.1001/archinte.149.8.1785

Cited by 203 publications

(176 citation statements)

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“…The prevalence of major depression in patients with CAD is about 3-fold higher than in community samples, ranging from 16% to 23% (Schleifer et al, 1989;Frasure-Smith et al, 1993;Gonzales et al, 1996). Prospective epidemiological studies have demonstrated a significant relationship between depression and the incidence of cardiac events in healthy populations (Aromaa et al, 1994;Ford et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Life-time history of suicide attempts and coronary artery disease in a community-dwelling elderly population

Artéro

Astruc

Courtet

et al. 2006

Int. J. Geriat. Psychiatry

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Section: Introductionmentioning

confidence: 99%

Life-time history of suicide attempts and coronary artery disease in a community-dwelling elderly population

Artéro

Astruc

Courtet

et al. 2006

Int. J. Geriat. Psychiatry

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“…Depression symptoms are independently associated with cardiovascular events in healthy subjects and in patients with heart disease [ [1], [2], [3]]. In the last decade, depression symptoms have also been related to the progression of subclinical atherosclerosis [ [4], [5], [6], [7], [8], [9]].…”

Section: Introductionmentioning

confidence: 99%

Depression symptoms and the progression of carotid intima-media thickness: a 5-year follow-up study

Pizzi

Santarella

Costa

et al. 2013

European Heart Journal

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ObjectiveOnly a few studies have investigated the changes in carotid intima-media thickness (IMT) over time, and uncertainties remain on the underlying mechanisms linking depression and subclinical atherosclerosis. We carried out a prospective cohort study to evaluate whether depression is associated with changes in carotid IMT in subjects with cardiac risk factors but free from coronary heart disease (CHD), and to what extent the atherogenicity of depression can be explained by inflammatory markers and autonomic nervous system dysfunction. MethodsDuring baseline and follow-up visits: all participants were asked to provide blood samples and compile a structured questionnaire; trained physicians assessed depression symptoms using Beck Depression Inventory (BDI); altered cardiac autonomic tone was measured using time-domain components of heart rate variability in 24 h Holter recordings; measurements of carotid IMT were carried out using B-mode ultrasound image acquisition. Logistic and linear regression analyses were used to adjust for potential confounders and explore potential mediators. ResultsA total of 381 subjects completed the 5-year follow-up. The mean carotid IMT significantly increased in all subjects but the amount of increase was significantly larger among subjects with depression symptoms: mean IMT increased by 0.16 ± 0.14 mm; 0.31 ± 0.28 mm and 0.61 ± 0.54 mm among the subjects with no, mild and moderate/severe depression, respectively (all p < 0.01). The association between moderate/severe depression and IMT increase remained highly significant even after controlling for all the variables considered, however when both IL-6 and CRP were included in multivariate models the regression coefficient decreased by 42.3%. Some of the inflammation markers and autonomic nervous system dysfunction were also independently correlated with carotid IMT increase. ConclusionDepression symptoms are independently associated with an accelerated progression of carotid IMT in subjects with CHD risk factors, and inflammation may substantially modulate the association between depression and carotid IMT progression.

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“…In contrast, depression is a recognized risk factor for coronary artery disease. Although the prevalence of major depression in the general population is 2-9% (1), its prevalence among postmyocardial infarct patients may be as high as 45% (34). Major depression doubles the risk that patients with newly diagnosed coronary artery disease will experience an adverse cardiovascular event within 12 mo (6), and the presence of depression is a significant predictor of mortality after myocardial infarction (18).…”

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confidence: 99%

Cytokine mediation of experimental heart failure-induced anhedonia

Grippo

Francis

Weiß

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Immune system dysfunction is hypothesized to influence several disease states, including cardiovascular disease and psychological depression. The comorbidity of depression and coronary artery disease may be influenced by immune system-brain interactions involving proinflammatory cytokines. The present studies evaluated an index of depression in a rodent model of heart failure by measuring responses to rewarding electrical brain stimulation, which provides an experimental procedure to operationally define anhedonia in rats. Heart failure led to a rightward shift in the current-response relationship in the brain stimulation paradigm, indicative of reduced rewarding properties of the brain stimulation (i.e., anhedonia). Acute treatment with a tumor necrosis factor antagonist, etanercept, reduced circulating tumor necrosis factor-α levels in rats with heart failure and restored responding for electrical brain stimulation. The current findings have implications for the study of pathophysiological mechanisms underlying the association of cardiovascular disease and depression.

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The nature and course of depression following myocardial infarction

Cited by 203 publications

References 0 publications

Life-time history of suicide attempts and coronary artery disease in a community-dwelling elderly population

Life-time history of suicide attempts and coronary artery disease in a community-dwelling elderly population

Depression symptoms and the progression of carotid intima-media thickness: a 5-year follow-up study

Cytokine mediation of experimental heart failure-induced anhedonia

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