The relationships among heart rate variability, inflammatory markers and depression in coronary heart disease patients.
ABSTRACT Studies show negative correlations between heart rate variability (HRV) and inflammatory markers. In cardiac patients, depression is related to both. We investigated links between short-term HRV and inflammatory markers in relation to depression in acute coronary syndrome (ACS) patients. We measured C-reactive protein (CRP), interleukin-6 (IL-6), depression symptoms (Beck Depression Inventory, BDI-II), and SDNN, high frequency (HF) and low frequency (LF) power at rest in 682 (553 men) patients approximately two months post-ACS. There were no differences in HRV measures between those with and without elevated depressions symptoms (BDI-II >or= 14). However, all HRV measures were negatively and significantly associated with both inflammatory markers. Relationships were stronger in patients with BDI-II >or= 14. Differences were significant for CRP and not explained by covariates (including age, sex, previous MI, left ventricular ejection fraction, coronary bypass surgery at index admission, diabetes, smoking, body mass index (BMI), fasting cholesterol, fasting glucose, angiotensin-converting-enzyme inhibitors, beta-blockers, statins, and antidepressants). HRV independently accounted for at least 4% of the variance in CRP in the depressed, more than any factor except BMI. Relationships between measures of inflammation and autonomic function are stronger among depressed than non-depressed cardiac patients. Interventions targeting regulation of both autonomic control and inflammation may be of particular importance.
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ABSTRACT: We aimed to explore links between heart rate variability (HRV) and clinical depression in patients with acute coronary syndrome (ACS), through a review of recent clinical research literature.Neuropsychiatric Disease and Treatment 01/2014; 10:1335-47. · 2.00 Impact Factor
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ABSTRACT: Sepsis, a clinical syndrome occurring in patients following infection or injury, is a leading cause of morbidity and mortality worldwide. Current immunological mechanisms do not explain the basis of cellular dysfunction and organ failure, the ultimate cause of death. Here we review current dogma and argue that it is time to delineate novel immunometabolic and neurophysiological mechanisms underlying the altered cellular bioenergetics and failure of epithelial and endothelial barriers that produce organ dysfunction and death. These mechanisms might hold the key to future therapeutic strategies.Immunity 04/2014; 40(4):463-475. · 19.75 Impact Factor
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ABSTRACT: Depression is accompanied by an array of neurobiological variations, including altered HPA axis activity, monoamine, growth factor and inflammatory immune functioning. In addition, a recent perspective has entertained the possible role for oxytocin in depressive disorders. Given the involvement of oxytocin in prosocial behaviors such as attachment, affiliation, trust, and social support seeking, it is not surprising this neuropeptide might be involved in the development or maintenance of depressive disorders. This view is supported by evidence that oxytocin interacts with various neuroendocrine, neurotransmitter, and inflammatory processes that have previously been implicated in depression. Thus, it might be profitable to consider the contribution of oxytocin in the context of several neurobiological changes provoked by stressors. The current review examines the relation between oxytocin and depression with a specific focus on the interactions between the oxytocinergic system and stressor-provoked biological and psychosocial responses. The possibility is also considered that oxytocin might increase the salience of social cues, such that positive or negative experiences result in exaggerated responses that may influence affective states.Neuroscience & Biobehavioral Reviews 09/2014; · 10.28 Impact Factor