Depression, C-reactive protein and two-year major adverse cardiac events in men after acute coronary syndromes.
ABSTRACT 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.
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ABSTRACT: Major depression is a highly prevalent disorder and is predicted to be the second leading cause of disease burden by 2020. Although many antidepressant drugs are currently available, they are far from optimal. Approximately 50% of patients do not respond to initial first line antidepressant treatment, while approximately one third fail to achieve remission following several pharmacological interventions. Furthermore, several weeks or months of treatment are often required before clinical improvement, if any, is reported. Moreover, most of the commonly used antidepressants have been primarily designed to increase synaptic availability of serotonin and/or noradrenaline and although they are of therapeutic benefit to many patients, it is clear that other therapeutic targets are required if we are going to improve the response and remission rates. It is clear that more effective, rapid-acting antidepressants with novel mechanisms of action are required. The purpose of this review is to outline the current strategies that are being taken in both preclinical and clinical settings for identifying superior antidepressant drugs. The realisation that ketamine has rapid antidepressant-like effects in treatment resistant patients has reenergised the field. Further, developing an understanding of the mechanisms underlying the rapid antidepressant effects in treatment-resistant patients by drugs such as ketamine may uncover novel therapeutic targets that can be exploited to meet the Olympian challenge of developing faster, better and stronger antidepressant drugs.European Journal of Pharmacology 08/2014; · 2.68 Impact Factor
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ABSTRACT: We aimed to explore links between heart rate variability (HRV) and clinical depression in patients with acute coronary syndrome (ACS), through a review of recent clinical research literature.Neuropsychiatric Disease and Treatment 01/2014; 10:1335-47. · 2.00 Impact Factor
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