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: Poor adaptation to stress, alterations in cerebrovascular function and excessive brain inflammation play critical roles in the pathophysiology of many psychiatric and neurological disorders such as major depression, schizophrenia, post traumatic stress disorder, Parkinson's and Alzheimer's diseases and traumatic brain injury. Treatment for these highly prevalent and devastating conditions is at present very limited and many times inefficient, and the search for novel therapeutic options is of major importance. Recently, attention has been focused on the role of a brain regulatory peptide, Angiotensin II, and in the translational value of the blockade of its physiological AT(1) receptors. In addition to its well-known cardiovascular effects, Angiotensin II, through AT(1) receptor stimulation, is a pleiotropic brain modulatory factor involved in the control of the reaction to stress, in the regulation of cerebrovascular flow and the response to inflammation. Excessive brain AT(1) receptor activity is associated with exaggerated sympathetic and hormonal response to stress, vulnerability to cerebrovascular ischemia and brain inflammation, processes leading to neuronal injury. In animal models, inhibition of brain AT(1) receptor activity with systemically administered Angiotensin II receptor blockers is neuroprotective; it reduces exaggerated stress responses and anxiety, prevents stress-induced gastric ulcerations, decreases vulnerability to ischemia and stroke, reverses chronic cerebrovascular inflammation, and reduces acute inflammatory responses produced by bacterial endotoxin. These effects protect neurons from injury and contribute to increase the lifespan. Angiotensin II receptor blockers are compounds with a good margin of safety widely used in the treatment of hypertension and their anti-inflammatory and vascular protective effects contribute to reduce renal and cardiovascular failure. Inhibition of brain AT(1) receptors in humans is also neuroprotective, reducing the incidence of stroke, improving cognition and decreasing the progression of Alzheimer's disease. Blockade of AT(1) receptors offers a novel and safe therapeutic approach for the treatment of illnesses of increasing prevalence and socioeconomic impact, such as mood disorders and neurodegenerative diseases of the brain.Psychoneuroendocrinology 10/2010; 36(1):1-18. DOI:10.1016/j.psyneuen.2010.10.001 · 5.59 Impact Factor
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ABSTRACT: Depression is highly prevalent in cardiac patients, with 20% to 40% of patients meeting criteria for major depressive disorder or experiencing an elevation in depressive symptoms. These depressive symptoms are often chronic and persistent, and they have been associated with the development and progression of coronary artery disease, worse health-related quality of life, poor physical functioning, recurrent cardiac events, and a 2- to 2.5-fold increased risk of mortality. Impaired adherence to health behaviors and adverse physiological effects of depression, including inflammation, endothelial dysfunction, platelet hyperactivity, and autonomic nervous system abnormalities, may link depression with adverse cardiac outcomes. Pharmacologic and psychotherapeutic interventions appear to be safe and effective at reducing depressive symptoms in patients with cardiovascular disease and may impact cardiac outcomes. Unfortunately, depression often is unrecognized and untreated in this population, despite the availability of brief screening tools that can be used for this purpose. We recommend the routine screening of cardiac patients for depression when there are adequate mechanisms for management and referral, such as available consulting psychiatrists or care management programs that facilitate the delivery of pharmacologic and psychotherapeutic treatments in this vulnerable population.Cardiology in review 01/2011; 19(3):130-42. DOI:10.1097/CRD.0b013e31820e8106 · 3.24 Impact Factor
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ABSTRACT: The development of autoimmune myocarditis in rats after a single subcutaneous injection of rat myosin mixed with a complete Freund’s adjuvant (CFA) (400 μg/kg in 200 μl) was studied. The rats from the control group were injected with only CFA. The titer of antibodies to myosin, infiltration of lymphocytes into the myocardium, ultrastructural damage of myofibrils, mitochondria, and nuclei of cardiomyocytes were maximally pronounced on days 14–21 after the immunization with myosin, which indicates a peak of the inflammatory reaction. The content of nitrites and nitrates in the blood serum and myocardium of immunized rats were also studied. A certain contribution to the development of the inflammation is made by CFA: in rats injected with only CFA, morphological signs of myocarditis were found, but to a much lesser degree than in the group immunized with myosin.Biology Bulletin 10/2010; 37(5):511-522. DOI:10.1134/S1062359010050110 · 0.24 Impact Factor