Article

Low Heart Rate Variability and the Effect of Depression on Post–Myocardial Infarction Mortality

Duke University, Durham, North Carolina, United States
Archives of Internal Medicine (Impact Factor: 17.33). 08/2005; 165(13):1486-91. DOI: 10.1001/archinte.165.13.1486
Source: PubMed

ABSTRACT

Depression is associated with an increased risk for mortality after acute myocardial infarction (MI). The purpose of this study was to determine whether low heart rate variability (HRV) mediates the effect of depression on mortality.
Twenty-four-hour ambulatory electrocardiograms were obtained from 311 depressed patients with a recent acute MI who were enrolled in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial and from 367 nondepressed patients who met the ENRICHD medical inclusion criteria. Standard HRV indexes were extracted from the recordings.
The log of very low-frequency (LnVLF) power, an index of HRV derived from power spectral analysis of the electrocardiogram signal (0.0033-0.04 Hz [in milliseconds squared]), was lower in the depressed than in the nondepressed patients (P<.001). There were 47 deaths (6.1%) during a 30-month follow-up. After adjusting for potential confounders, the depressed patients remained at higher risk for all-cause mortality compared with the nondepressed patients (hazard ratio, 2.8; 95% confidence interval [CI], 1.4-5.4; P<.003). When LnVLF power was entered into the model, the hazard ratio for depression dropped to 2.1 (95% CI, 1.1-4.2; P = .03). The proportion of the risk for depression attributable to LnVLF power was 0.27 (95% CI, 0.23-0.31; P<.001).
Low HRV partially mediates the effect of depression on survival after acute MI. This finding helps to clarify the physiological mechanisms underlying depression's role as a risk factor for mortality in patients with coronary heart disease. It also raises the possibility that treatments that improve both depression and HRV might also improve survival in these patients.

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Available from: Robert M Carney, Aug 14, 2014
    • "Consistent with the link between vagal tone and emotion regulation (Berntson et al., 1997, 1993; Porges, 1995a, 1994, 1996), low vagal tone at baseline is associated with negative emotional traits (Beauchaine, 2001; Thayer and Lane, 2000). Further, a number of studies in adult samples find an association between low HRV and depressive disorders (Carney et al., 2005; Gorman and Sloan, 2000; Licht et al., 2008; Rechlin et al., 1995, 1994; Roose et al., 1989). Fewer studies have examined the relation between HRV and depression in adolescents and children. "
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    ABSTRACT: Background: Work examining the link between lower heart rate variability (HRV) and depression in children and adolescents is lacking, especially in light of the physiological changes that occur during pubertal development. Method: We investigated the association between spectral measures of resting HRV and depressive symptoms among 127 children and adolescents, ages 10-17. Using spectral analysis, we evaluated (1) the association between relative high frequency (HF) HRV and depressive symptoms; (2) the predictive power of relative HF HRV for depressive symptoms in the context of relative low frequency (LF) and relative very low frequency (VLF) HRV; and (3) the relationship between relative HF, LF, and VLF band activity, age and pubertal maturation. Results: Consistent with previous work, results revealed that relative HF HRV was negatively associated with self-reported depressive symptoms. As well, relative VLF HRV was positively associated with depressive symptoms. Regression analyses revealed that relative HF HRV and relative VLF HRV significantly predicted self-report depressive symptoms while controlling for age, sex and pubertal maturation, with relative VLF HRV emerging as the strongest indicator of depressive symptoms. Developmental findings also emerged. Age and pubertal maturation were negatively associated with relative HF HRV and positively correlated with relative VLF HRV. Conclusions: Results provide support for the relationship between HRV and depression and suggest that both HF and VLF HRV are relevant to depression symptom severity. Findings also reinforce the importance of considering pubertal development when investigating HRV-depression associations in children and adolescents. Limitations: Influences on cardiac control including physical activity levels and exercise patterns could be controlled in future work. Our data speak to a depressive symptom dimension and relative spectral power HRV. Thus, we cannot make strong claims about relative spectral power HRV and clinical depression.
    No preview · Article · Jul 2015 · Journal of Affective Disorders
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    • " ) , such as genetic polymorphism in the glutathione S - transferase gene ( Nunes et al . , 2014 ) ; dysregulation in the hypothalamic – pituitary – adrenal axis ; alterations in norepinephr - ine and serotonin ( Musselman et al . , 1998 ) ; increased serotonin and platelet activation ( Schins et al . , 2004 ) ; diminished heart rate variability ( Carney et al . , 2005 ) ; autonomic dysfunction ( Wang et al . , 2013 ) ; antidepressant toxicity ( Otte et al . , 2004 ) ; noncom - pliance with medical treatment ( Gehi et al . , 2005 ; Ziegelstein et al . , 2000 ; Di Matteo et al . , 2000 ) and dietary factors , including lowered omega - 3 fatty acid levels ( Frasure - Smith et al . , 2004 ; Berk et al . "
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    ABSTRACT: Background There is a robust comorbidity between mood disorders and cardiovascular disorder (CVD). The atherogenic index of plasma (AIP) and the atherogenic coefficient (AC) are important atherogenic indexes. The aims of this study were to delineate whether AIP and AC are increased in mood disorders especially when comorbid with tobacco use disorder (TUD). Methods In this case-control study we included 134 patients with mood disorders, bipolar disorder and unipolar depression (cases), and 197 individuals without mood disorder (controls) divided into those with and without TUD (defined as never-smokers). Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were measured. AIP and AC were computed as log (TG/HDLc) and non-HDLc/HDLc, respectively. Results The AIP and AC indexes were significantly increased in patients with mood disorders versus controls, both in depression and bipolar disorder. Patients with mood disorder without TUD and patients with TUD without mood disorder showed higher AIP and AC values than never-smokers while those with comorbid mood disorders and TUD showed significantly higher AIP and AC levels than all other individuals. A large part of the variance in the AIC (26.4%) and AC (20.4%) was explained by mood disorders, TUD, male gender and body mass index. Conclusions The findings suggest that lipid abnormalities leading to an increased atherogenic potential are involved in the pathophysiology of mood disorders (depression and bipolar disorder) and especially comorbid mood disorder and TUD. The comorbidity between mood disorders and CVD may be partly explained increased through AIP and AC indexes, impacting increments in atherogenic potential.
    Full-text · Article · Feb 2015 · Journal of Affective Disorders
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    • " ) , such as genetic polymorphism in the glutathione S - transferase gene ( Nunes et al . , 2014 ) ; dysregulation in the hypothalamic – pituitary – adrenal axis ; alterations in norepinephr - ine and serotonin ( Musselman et al . , 1998 ) ; increased serotonin and platelet activation ( Schins et al . , 2004 ) ; diminished heart rate variability ( Carney et al . , 2005 ) ; autonomic dysfunction ( Wang et al . , 2013 ) ; antidepressant toxicity ( Otte et al . , 2004 ) ; noncom - pliance with medical treatment ( Gehi et al . , 2005 ; Ziegelstein et al . , 2000 ; Di Matteo et al . , 2000 ) and dietary factors , including lowered omega - 3 fatty acid levels ( Frasure - Smith et al . , 2004 ; Berk et al . "

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