Depression and the risk for cardiovascular diseases: Systematic review and meta analysis. International Journal of Geriatric Psychiatry, 22, 613-626

VU University Amsterdam, Amsterdamo, North Holland, Netherlands
International Journal of Geriatric Psychiatry (Impact Factor: 2.87). 07/2007; 22(7):613-26. DOI: 10.1002/gps.1723
Source: PubMed


Depression and cardiovascular diseases are both common among elderly. Depression is suspected to be an independent risk factor for the onset of coronary heart disease, yet it is not clear to what extent and if depression also is associated with the onset of other diseases of the circulatory system.
To estimate the risk of depression as an independent risk factor for various cardiovascular diseases (CVD) and explore the effects of heterogeneity and methodological quality.
Meta-analyses and meta-regression analyses of longitudinal cohort and case-control studies reporting depression at baseline and CVD outcomes at follow-up.
MEDLINE (1966-2005) and PSYCHINFO (1966-2005).
Of the 28 studies that met the inclusion criteria, 11 were assesed as high quality studies. Although depressed mood increased the risk for a wide range of CVDs, heterogeneity was substantial in most cases. Only the overall combined risk of depression for the onset of myocardial infarctions (n=8, OR=1.60, 95%CI 1.34-1.92) was homogenous. Clinically diagnosed major depressive disorder was identified as the most important risk factor for developing CVD.
Depression seems to be an independent risk factor for the onset of a wide range of CVDs, although this evidence is related to a high level of heterogeneity.

1 Follower
42 Reads
  • Source
    • "Extensive evidence suggests that depression is a robust and independent predictor of cardiovascular disease incidence and progression (Van der Kooy et al., 2007). While a variety of mechanisms – both genetic and behavioral – have been proposed to explain this association, one specific pathophysiological mechanism through which depression is thought to increase cardiac risk is a dysregulation of the autonomic neural control of cardiac function. "
    [Show abstract] [Hide abstract]
    ABSTRACT: In humans, depression is often triggered by prolonged exposure to psychosocial stressors and is often associated with cardiovascular comorbidity. Mounting evidence suggests a role for endocannabinoid signaling in the regulation of both emotional behavior and cardiovascular function. Here, we examined cardiac activity in a rodent model of social stress-induced depression and investigated whether pharmacological inhibition of the enzyme fatty acid amide hydrolase (FAAH), which terminates signaling of the endocannabinoid anandamide, exerts antidepressant-like and cardioprotective effects. Male Wistar Kyoto rats were exposed to five weeks of repeated social stress or control procedure. Starting from the third week, they received daily administration of the selective FAAH inhibitor URB694 (0.1mg/kg, i.p.) or vehicle. Cardiac electrical activity was recorded by radiotelemetry. Repeated social stress triggered biological and behavioral changes that mirror symptoms of human depression, such as (i) reductions in body weight gain and sucrose solution preference, (ii) hyperactivity of the hypothalamic-pituitary-adrenocortical axis, and (iii) increased immobility in the forced swim test. Moreover, stressed rats showed (i) alterations in heart rate daily rhythm and cardiac autonomic neural regulation, (ii) a larger incidence of spontaneous arrhythmias, and (iii) signs of cardiac hypertrophy. Daily treatment with URB694 (i) increased central and peripheral anandamide levels, (ii) corrected stress-induced alterations of biological and behavioral parameters, and (iii) protected the heart against the adverse effects of social stress. Repeated social stress in Wistar Kyoto rats reproduces aspects of human depression/cardiovascular comorbidity. Pharmacological enhancement of anandamide signaling might be a promising strategy for the treatment of these comorbid conditions.
    European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 09/2015; 192(11). DOI:10.1016/j.euroneuro.2015.07.015 · 4.37 Impact Factor
  • Source
    • "Furthermore, it is plausible that different subtypes of depressive disorder may be associated with different inflammatory profiles (Dunjic-Kostic et al., 2013; Kaestner et al., 2005; Karlovic et al., 2012). Similarly, chronic diseases, severity of depressive symptoms and comorbid psychiatric disorders may affect the magnitude of the associations between inflammation and major depression (Hiles et al., 2012b; Howren et al., 2009; Irwin and Miller, 2007; Stuart and Baune, 2012; Van der Kooy et al., 2007). The majority of major depressive patients included in our meta-analysis could be classified as severely or very severely depressed; IL-6, CRP and TNF-a were more strongly associated with severe than non-severe forms of depression. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cumulative meta-analyses are used to evaluate the extent to which further studies are needed to confirm or refute a hypothesis. We used this approach to assess observational evidence on systemic inflammation in individuals with major depressive disorder. We identified 58 studies of four common inflammatory markers in a literature search of PubMed, Embase and PsychInfo databases in May 2014. Pooled data from the earliest eight studies already showed an association between interleukin-6 concentrations and major depression; 23 more recent studies confirmed this finding (d = 0.54, p < 0.0001). A significant association between C-reactive protein levels and major depression was noted after 14 studies and this did not change after addition of six more studies (d = 0.47, p < 0.0001). For these two inflammatory markers, there was moderate heterogeneity in study-specific estimates, subgroup differences were small, and publication bias appeared to be an unlikely explanation for the findings. Sensitivity analyses including only high-quality studies and subjects free of antidepressant medication further verified the associations. While there was a link between tumour necrosis factor-α levels and major depression (d = 0.40, p = 0.002), the cumulative effect remained uncertain due to the extensive heterogeneity in study-specific estimates and inconsistencies between subgroups. No evidence was found for the association between interleukin-1β levels and major depression (d = −0.05, p = 0.86). In conclusion, this cumulative meta-analysis confirmed higher mean levels of interleukin-6 and C-reactive protein in patients with major depression compared to non-depressed controls. No consistent association between tumour necrosis factor-α, interleukin-1β and major depression was observed. Future studies should clarify the specific immune mechanisms involved as well as continue testing anti-inflammatory therapies in patients suffering from major depression.
    Brain Behavior and Immunity 06/2015; 20. DOI:10.1016/j.bbi.2015.06.001 · 5.89 Impact Factor
  • Source
    • "Heart failure, independent of underlying disease, is associated with the activation of several neurotransmitter systems that lead to further ventricular dysfunction and death. Depression, a mood disorder, is a co-morbidity commonly associated with cardiovascular disease [3] [4] [5]. This medical condition also causes an activation of neurohumoral systems, which could facilitate the transition to heart failure. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Depression is a predictor of poor prognosis in patients with heart failure. Selective serotonin (5-HT) reuptake inhibitors (SSRIs) may improve these outcomes. Left ventricular volume overloadinduced hypertrophy that is associated with aortic regurgitation (AR) leads to ventricular dysfunction and heart failure. The aim of this study was to verify the effects of the SSRI paroxetine on cardiac function, as well as on fluid intake and excretion, in subchronic AR. Male Wistar rats (260 to 280 g) received sham (SH) surgery or AR induced by retrograde puncture of the aortic valve leaflets. The presence of AR was confirmed by echocardiography (ECHO) exams. Four weeks after AR surgery, subcutaneous injections of paroxetine (PAR: 10 mg/kg 3 times in a week) or saline were administered. The rats were randomly divided into the following 4 groups and treated for 4 weeks: AR-PAR, ARsaline, SH-PAR and SH-saline. At the end of the treatment period, fractional shortening was preserved in AR-PAR, compared to AR-saline (46.6 ± 2.7% vs 38.3 ± 2.2%, respectively). Daily 0.3 M NaCl intake was reduced in PAR-treated rats. Natriuresis was increased in weeks 2-3 after PAR treatment. Our results suggest that augmentation of central 5-HT levels has a beneficial effect on cardiovascular remodeling following volume overload. The mechanisms underlying this effect are unknown.
    Physiology & Behavior 03/2015; 41. DOI:10.1016/j.physbeh.2015.02.037 · 2.98 Impact Factor
Show more