Depression, C-reactive Protein and Two-year Major Adverse Cardiac Events in Men after Acute Coronary Syndromes
Department of Psychiatry and School of Nursing, McGill University, Montreal, Canada. Biological Psychiatry
(Impact Factor: 10.26).
09/2007; 62(4):302-8. DOI: 10.1016/j.biopsych.2006.09.029
We investigated the impact of depression and inflammatory markers, assessed 2 months after acute coronary syndrome (ACS), on major adverse cardiac events over 2 years (MACEs; cardiac death, survived myocardial infarction, survived cardiac arrest, and nonelective revascularization).
Depression symptoms (Beck Depression Inventory-II; BDI-II), major depression, C-reactive protein (CRP), interleukin-6, and soluble intercellular adhesion molecule were assessed in 741 ACS patients (including 602 men).
Some 102 (78 men) experienced at least one MACE. Beck Depression Inventory-II scores of > or =14 predicted MACEs (p = .007). The increase in risk was marked in men (hazard ratio [HR] = 1.96, 95% confidence interval [CI] = 1.24-3.09, p = .004), with little evidence of a relationship in women (p = .85). Subsequent analyses were limited to men. Results were similar after covariate adjustment (HR = 1.72, 95% CI = 1.07-2.77, p = .024). C-reactive protein levels were also associated with increased MACE risk (adjusted HR for CRP > or = 2.0 mg/L = 1.67, 95% CI = 1.07-2.62, p = .025). C-reactive protein levels and BDI-II scores interacted in predicting MACEs. Men with both BDI-II scores of > or =14 and CRP of > or =2.0 mg/L experienced an increase in risk similar to those with only one of these factors.
In men assessed 2 months after ACS, depression and CRP are overlapping prognostic risks. Patients with either risk may benefit from similar therapies.
Available from: Phillip Tully
- "The biological mechanisms of cardio-pathogenesis attributable to depression and anxiety are multifactorial and include the dysregulation of the hypothalamic-pituitary- adrenal axis,– reduced heart-rate-variability,– altered serotonergic pathways, inflammatory response and altered platelet aggregability. An earlier review suggested 20% of variability in CAD and depressive symptoms was attributable to common genetic factors and the authors speculated these could be related to inflammation and serotonin. "
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ABSTRACT: Research to date indicates that the number of coronary artery bypass graft (CABG) surgery patients affected by depression (i.e., major, minor, dysthymia) approximates between 30% and 40% of all cases. A longstanding empirical interest on psychosocial factors in CABG surgery patients highlights an association with increased risk of morbidity in the short and longer term. Recent evidence suggests that both depression and anxiety increase the risk for mortality and morbidity after CABG surgery independent of medical factors, although the behavioral and biological mechanisms are poorly understood. Though neither depression nor anxiety seem to markedly affect neuropsychological dysfunction, depression confers a risk for incident delirium. Following a comprehensive overview of recent literature, practical advice is described for clinicians taking into consideration possible screening aids to improve recognition of anxiety and depression among CABG surgery patients. An overview of contemporary interventions and randomized, controlled trials are described, along with suggestions for future CABG surgery research.
Available from: Renerio Fraguas
- "Depressed patients have higher levels of C-reactive protein and inflammatory cytokines, which play important roles in atherogenesis.24 A recent investigation evaluated direct associations between levels of depression and C-reactive protein concentrations in patients that suffered a myocardial infarction.25 "
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ABSTRACT: Depression and coronary artery disease (CAD) are both extremely prevalent diseases. In addition, compromised quality of life and life expectancy are characteristics of both situations. There are several conditions that aggravate depression and facilitate the development of CAD, as well as provoke a worse prognosis in patients with already established CAD: inferior adherence to medical orientations (medications and life style modifications), greater platelet activation and aggregation, endothelial dysfunction, and impaired autonomic dysfunction (lowered heart rate variability). Recent literature has shown that depression alone is becoming an independent risk factor for cardiac events both in primary and secondary prevention. As the diagnosis of depression in patients with heart disease is difficult, due to similarities of symptoms, the health professional should perform a careful evaluation to differentiate the clinical signs of depression from those related with general heart diseases. After a myocardial infarction, depression is an independent risk factor for mortality. Successful therapy of depression has been shown to improve patients' quality of life and cardiovascular outcome. However, multicentric clinical trials are needed to support this inference. A practical liaison between qualified professionals is necessary for the better management of depressed patients with excess risk in developing CAD. Accordingly, pathophysiological and clinical implications between depression and CAD are discussed in this article.
Available from: Robert Dantzer
- "The association between depression and inflammation has actually turned out to be easier to observe in physically ill patients than in patients with psychiatric disorders who are otherwise considered medically healthy. This is the case in patients with coronary heart disease (Frasure-Smith et al 2007; Joynt et al 2003; Kiecolt- Glaser & Glaser 2002; Lesperance & Frasure-Smith 2007). A similar association between biomarkers of inflammation and depression, especially when measured with psychological instruments (e.g., the Beck Depression Inventory or the Montgomery-Asberg Depression Rating Scale), is commonly found during aging and is exacerbated by obesity and type II diabetes (Bremmer et al 2008; Milaneschi et al 2009; Penninx et al 2003). "
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ABSTRACT: In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms.
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