Effect of medication and psychotherapy on heart rate variability in panic disorder

Depression and Anxiety (Impact Factor: 4.41). 03/2009; 26(3):251 - 258. DOI: 10.1002/da.20533


Background: Panic disorder (PD) patients have been shown to have reduced heart rate variability (HRV). Low HRV has been associated with elevated risk for cardiovascular disease. Our aim was to investigate the effects of treatment on heart rate (HR) in patients with PD through a hyperventilation challenge. Methods: We studied 54 participants, 43 with Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) PD and 11 controls. Subjects lay supine with their heads in a plastic canopy chamber, resting for 15 min and then breathing at a rate of 30 breaths per minute for 10 min. HRV was sampled for spectral analysis. Clinical and behavioral measures of anxiety were assessed. Treatment was chosen by patients: either 12 weeks of CBT alone or CBT with sertraline. Results: All patients showed significant decrease on clinical measures from baseline and 31 were treatment responders, 8 dropped out of the study before completion of the 12-week treatment phase and 4 were deemed nonresponders after 12 weeks of treatment. Although both treatments led to significant clinical improvement, only CBT alone demonstrated a significant reduction in HR and increase in HRV. Conclusions: Our study replicated the finding that increased HR and decreased HRV occur in PD patients. Given the evidence of cardiac risk related to HRV, CBT appears to have additional benefits beyond symptom reduction. The mechanisms of this difference between CBT and sertraline are unclear and require further study. Depression and Anxiety, 2009. © 2008 Wiley-Liss, Inc.

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    • "In a study of 30 depressed patients with stable CHD (Carney et al., 2000), average heart rate and daytime HRV significantly improved after 16 sessions of CBT, although this finding was only observed in the 12 severely depressed individuals relative to the mildly depressed and control patients. In another study of 54 patients with panic disorder (Garakani et al., 2009), only those administered CBT displayed decreases in heart rate and increases in HRV, while those receiving CBT with sertraline (an SSRI) did not display any change despite significant clinical improvement . These SSRI findings are consistent with those from our own meta-analysis on depression (Kemp et al., 2010), which indicated that antidepressant medication did not increase (or decrease) HRV in MDD patients. "
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    ABSTRACT: Here we review our recent body of work on the impact of the mood and comorbid anxiety disorders, alcohol dependence, and their treatments on heart rate variability (HRV), a psychophysiological marker of mental and physical wellbeing. We have shown that otherwise healthy, unmedicated patients with these disorders display reduced resting-state HRV, and that pharmacological treatments do not ameliorate these reductions. Other studies highlight that tricyclic medications and the serotonin and noradrenaline reuptake inhibitors in particular may have adverse cardiovascular consequences. Reduced HRV has important functional significance for motivation to engage social situations, social approach behaviours, self-regulation and psychological flexibility in the face of stressors. Over the longer-term, reduced HRV leads to immune dysfunction and inflammation, cardiovascular disease and mortality, attributable to the downstream effects of a poorly functioning cholinergic anti-inflammatory reflex. We place our research in the context of the broader literature base and propose a working model for the effects of the mood disorders, comorbid conditions, and their treatments to help guide future research activities. Further research is urgently needed on the long-term effects of autonomic dysregulation in otherwise healthy psychiatric patients, and appropriate interventions to halt the progression of a host of conditions associated with morbidity and mortality.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 06/2013; 89(3). DOI:10.1016/j.ijpsycho.2013.06.018 · 2.88 Impact Factor
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    • "First, drug-naive PD patients had significantly lower HRV than controls. Our findings corroborated the findings of earlier studies (Yeragani et al., 1993; Middleton and Ashby, 1995; Garakani et al., 2009; Wise et al., 2011), suggesting that reduction in HRV is a psychophysiological marker of PD. We believe our findings to be reliable because our study had four important strengths: (i) We excluded subjects with psychiatric and physical comorbidities that could potentially confound the association between PD and cardiac autonomic functions. "
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    ABSTRACT: Cardiac autonomic dysregulation has been proposed in panic disorder (PD), but the results are mixed. Analyses with larger sample sizes and better methodology are needed. Forty-eight drug-naïve individuals with PD and 202 healthy volunteers were recruited for a case-control analysis. We used the Hamilton Anxiety Rating Scale and the Beck Anxiety Inventory to assess anxiety severity. Cardiac autonomic function was evaluated by measuring heart rate variability (HRV) parameters. Frequency-domain indices of HRV were obtained. The obtained results were evaluated in association with personality traits assessed by the Tridimensional Personality Questionnaire. Patients exhibited reduced mean RR interval (816.94 ± 135.92 versus 873.47 ± 143.36 ms, P = 0.014) and HRV levels (Var 6.37 ± 1.32 versus 7.38 ± 0.95, LF 4.90 ± 1.63 versus5.82 ± 1.11 and HF 4.57 ± 1.53 versus 5.62 ± 1.24 [ln(ms2)], all P < 0.001) as compared to controls, which mainly suggested a reduction in cardiac vagal control in PD. The anxiety severity was negatively correlated with HRV levels (r = -0.29 for Var, r = -0.22 for LF and r = -0.28 for HF, all P < 0.001). The harm avoidance score (which has been suggested to be associated with serotonergic activity) was associated with decreased HRV levels (r = -0.22 for Var, P < 0.01, r = -0.14 for LF, P < 0.05 and r = -0.17 for HF, P < 0.01). This study demonstrates that PD is associated with cardiac autonomic dysregulation, highlighting the importance of assessing HRV in PD patients.
    Asia-Pacific Psychiatry 06/2013; 5(2):80-9. DOI:10.1111/appy.12032 · 0.63 Impact Factor
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    • "study, and further reveal that trait PA could be enhanced and the increases in trait PA might be associated with improvement of basal vagal tone independently of changes in trait NA. Although previous studies have found an association between alleviation of negative emotionality (e.g., depression and panic disorder) and increases of vagal tone (Carney et al., 2000; Chambers and Allen, 2002; Garakani et al., 2009), but Oveis et al. (2009) and Wang et al. (2013) have consistently showed that trait NA is unrelated to basal vagal tone. Thus, the findings of null relationship between decreases in trait NA and increases in vagal tone might be due to trait NA, different from other negative emotionality, is unrelated to basal vagal tone. "
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    ABSTRACT: The association between changes of trait affect and changes of vagal tone was investigated in the present study. Basal physiological data were collected from 70 college students of high (n=33) and low trait positive affect (n=37) (HPA vs. LPA) groups selected by Positive and Negative Affect Schedule (PANAS). Then the final LPA participants (n=34) were randomly assigned to either a four months Positive Psychotherapy (PPT) group (n=16) or a control group (n=18), and their basal physiological and PANAS data were collected immediately after the treatment. The study results showed that compared to the LPA group, the HPA group had higher basal respiratory sinus arrhythmia (RSA). Compared to the control group, the PPT group had changes in trait affect and basal RSA, and increases of trait PA were associated with increases of basal RSA independently of decreases of trait NA. These findings suggest that basal vagal tone of individuals with low trait PA might be improved by increasing their trait PA.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 04/2013; 88(2). DOI:10.1016/j.ijpsycho.2013.04.012 · 2.88 Impact Factor
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