Article

Depression Is Associated With Decreased Blood Pressure, but Antidepressant Use Increases the Risk for Hypertension

Vrije Universiteit Medical Center, Department of Psychiatry, AJ Ernststraat 887, 1081 HL, Amsterdam, The Netherlands.
Hypertension (Impact Factor: 7.63). 03/2009; 53(4):631-8. DOI: 10.1161/HYPERTENSIONAHA.108.126698
Source: PubMed

ABSTRACT The present study compared blood pressure levels between subjects with clinical anxiety and depressive disorders with healthy controls. Cross-sectional data were obtained in a large cohort study, the Netherlands Study of Depression and Anxiety (N=2981). Participants were classified as controls (N=590) or currently or remittedly depressed or anxious subjects (N=2028), of which 1384 were not and 644 were using antidepressants. Regression analyses calculated the contributions of anxiety and depressive disorders and antidepressant use to diastolic and systolic blood pressures, after controlling for multiple covariates. Heart rate and heart rate variability measures were subsequently added to test whether effects of anxiety/depression or medication were mediated by vagal control over the heart. Higher mean diastolic blood pressure was found among the current anxious subjects (beta=0.932; P=0.03), although anxiety was not significantly related to hypertension risk. Remitted and current depressed subjects had a lower mean systolic blood pressure (beta=-1.74, P=0.04 and beta=-2.35, P=0.004, respectively) and were significantly less likely to have isolated systolic hypertension than controls. Users of tricyclic antidepressants had higher mean systolic and diastolic blood pressures and were more likely to have hypertension stage 1 (odds ratio: 1.90; 95% CI: 0.94 to 3.84; P=0.07) and stage 2 (odds ratio: 3.19; 95% CI: 1.35 to 7.59; P=0.008). Users of noradrenergic and serotonergic working antidepressants were more likely to have hypertension stage 1. This study shows that depressive disorder is associated with low systolic blood pressure and less hypertension, whereas the use of certain antidepressants is associated with both high diastolic and systolic blood pressures and hypertension.

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    • "The question of whether the presence of depression is associated with increased blood pressure, HbA1c, and body mass index (BMI) among people with diabetes is largely unexamined, but studies that have analyzed these relationships are described later. Of the nondiabetes specific studies that examined the relationship between blood pressure and depression, some found a decrease in blood pressure among those who are depressed [8] [9]. However, Nabi and colleagues showed that age-related risks of hypertension increase more within the depressed group than the nondepressed group, arguing that "
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    ABSTRACT: Diabetic patients are nearly three times as likely to have depression as their nondiabetic counterparts. Patients with diabetes are already at risk for poor cardiovascular health. Using cross-sectional data from the translating research into action for diabetes (TRIAD) study, the authors tested the association of depression with cardiovascular risk factors in diabetic patients. Depression was measured using the patient health questionnaire (PHQ8). Patients who scored greater than 9 on the PHQ8 were classified as depressed and were compared with those who were not depressed (n = 2,341). Depressed patients did not have significantly different blood pressure levels than those who were not depressed. However, those who were depressed had higher HbA1c levels than those who were not depressed (P < 0.01) and higher BMIs than those who were not depressed (P < 0.01). These results indicate that depressed diabetic patients are at greater risk of having poor control of cardiovascular risk factors and suggest that depression screening should be a standard practice among this patient group.
    International Journal of Endocrinology 11/2012; 2012:747460. DOI:10.1155/2012/747460 · 1.52 Impact Factor
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    • "The potential for confounding of autonomic effects by antidepressants was clearly demonstrated in our own recent research on the association between major depressive disorder (MDD) and anxiety disorders and cardiac vagal activity and blood pressure (Licht et al, 2008, 2009b, c), where we found that especially the use of tricyclic antidepressants (TCAs) and serotonergic and noradrenergic reuptake inhibitors (SNRIs) were associated with decreased vagal activity and increased blood pressure. We confirmed these findings with longitudinal evidence indicating that starting the intake of TCAs and SNRIs caused a decrease in vagal activity paired to an increase in heart rate (HR) (Licht et al, 2010). "
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    ABSTRACT: Increased sympathetic activity has been hypothesized to have a role in the elevated somatic disease risk in persons with depressive or anxiety disorders. However, it remains unclear whether increased sympathetic activity reflects a direct effect of anxiety or depression or an indirect effect of antidepressant medication. The aim of this study was to test longitudinally whether cardiac sympathetic control, measured by pre-ejection period (PEP), was increased by depression/anxiety status and by antidepressant use. Cross-sectional and longitudinal data were from a depression and anxiety cohort: the Netherlands Study of Depression and Anxiety (NESDA). Baseline data of 2838 NESDA subjects (mean age 41.7 years, 66.7% female) and 2-year follow-up data of 2226 subjects were available for analyses. Included were subjects with and without depressive/anxiety disorders, using or not using different antidepressants at baseline or follow-up. The PEP was measured non-invasively by 1.5 h of ambulatory impedance cardiography. Cross-sectional analyses compared PEP across psychopathology and antidepressant groups. Longitudinal analyses compared 2-year changes in PEP in relation to changes in psychopathology and antidepressant use. Cross-sectional analyses showed that antidepressant-naïve depressive/anxious subjects had comparable PEP as controls, whereas subjects using tricyclic (TCA) or combined serotonergic/noradrenergic antidepressants (SNRI) had significantly shorter PEP compared with controls. In contrast, subjects using selective serotonin re-uptake inhibitors (SSRIs) had longer PEP than controls. Longitudinal results confirmed these findings: compared with 2-year change in PEP in continuous non-users (+2 ms), subjects who started TCA or SNRI treatment showed significantly shortened PEP (-11 ms, p=0.005 and p<0.001), whereas subjects who started SSRI treatment showed significant prolongation of PEP (+9 ms, p=0.002). Reversed findings were observed among those who stopped antidepressant use. These findings suggest that depressive and anxiety disorders are not associated with increased cardiac sympathetic control. However, results pose that TCA and SNRI use increases sympathetic control, whereas SSRI use decreases sympathetic control.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 07/2012; 37(11):2487-95. DOI:10.1038/npp.2012.107 · 7.83 Impact Factor
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    • "At first sight the direction of this association appears contrary to studies in which adults with more depressive symptoms were at increased risk of hypertension (Davidson et al., 2000; Delaney et al., 2010). However a study by Licht et al. (2009) showed that adults who were depressed, excluding those taking anti depressant, had lower blood pressure while depression defined by antidepressant use increased the risk of hypertension. Alternatively this relationship may depend on adult behaviors and responses to environmental stress (Lett et al., 2004). "
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