Abstract
Objectives: Cardiac repolarization may be affected by psychiatric disorders and/or antidepressant use, but evidence for this is inconclusive. This study examined the relationship between depressive and anxiety disorder and use of antidepressants with T-wave amplitude (TWA) and QT-interval.Methods: Data was obtained from the Netherlands Study of Depression and Anxiety (n = 1,383). Depression/anxiety was diagnosed with the DSM-IV based Composite International Diagnostic Interview. The use of tricyclic antidepressants (TCAs), selective serotonin and noradrenalin reuptake inhibitors (SNRIs), and selective serotonin reuptake inhibitors (SSRIs) was established. T-wave amplitude and QT-interval corrected for heart rate (QTc) were obtained from an ECG measured in a type II axis configuration.Results: Compared to controls, persons with depression or anxiety disorders did not show a significantly different TWA (p = 0.58; Cohen's d = 0.046) or QTc (p = 0.48; Cohen's d = −0.057). In spite of known sympathomimetic effects, TCA use (p = 0.26; Cohen's d = −0.162) and SNRI use (p = 0.70; Cohen's d = −0.055) were not significantly associated with a lower TWA. TCA use (p = 0.12; Cohen's d = 0.225) and SNRI use (p = 0.11; Cohen's d = 0.227) were also not significantly associated with a prolonged QTc.Conclusion: We did not find evidence that either depressive/anxiety disorder or antidepressant use is associated with abnormalities in TWA or QTc. Earlier found sympathomimetic effects of TCAs and SNRIs are not evident in these measures of cardiac repolarization.
Highlights
Depressive and anxiety disorders have been associated with an increased risk of cardiovascular disease (CVD) (Nicholson et al, 2006; Vogelzangs et al, 2010), cardiovascular mortality and sudden death (Frasure-Smith and Lespérance, 2008)
Considering antidepressant use, studies have indicated that the use of tricyclic antidepressants (TCA) are associated with a lower T-wave amplitude (TWA) and a prolonged HR corrected QT-interval (QTc) (Burckhardt et al, 1978; Burgess et al, 1979; Giardina et al, 1979; Wilens et al, 1996; Zemrak and Kenna, 2008), while the effects of selective serotonergic and noradrenergic reuptake inhibitors (SNRIs) and selective serotonin reuptake inhibitors (SSRIs) are less conclusive (Roos, 1983; Glassman et al, 2002; Raskin et al, 2003; Zhang et al, 2007; Baumert et al, 2008; Isbister, 2009; Castro et al, 2013)
26.6% had a current depressive/anxiety disorder, 52.4% had a history of depression/anxiety, and 19.7% used antidepressants (Table 1)
Summary
Depressive and anxiety disorders have been associated with an increased risk of cardiovascular disease (CVD) (Nicholson et al, 2006; Vogelzangs et al, 2010), cardiovascular mortality and sudden death (Frasure-Smith and Lespérance, 2008). Increased sympathetic activity has been found to prolong QTc (Magnano et al, 2002; Baumert et al, 2008) Both abnormalities in TWA (Tan et al, 2008; Okuda et al, 2011) and prolonged QTc (Okin et al, 2000; Mozos and Serban, 2011) have been associated with cardiac morbidity and mortality. If these measures are affected by psychiatric disorders and/or antidepressant use, they could explain part of the comorbidity between poor mental health and cardiovascular disease. Considering antidepressant use, studies have indicated that the use of tricyclic antidepressants (TCA) are associated with a lower TWA and a prolonged QTc (Burckhardt et al, 1978; Burgess et al, 1979; Giardina et al, 1979; Wilens et al, 1996; Zemrak and Kenna, 2008), while the effects of selective serotonergic and noradrenergic reuptake inhibitors (SNRIs) and selective serotonin reuptake inhibitors (SSRIs) are less conclusive (Roos, 1983; Glassman et al, 2002; Raskin et al, 2003; Zhang et al, 2007; Baumert et al, 2008; Isbister, 2009; Castro et al, 2013)
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