Significant Reduction In Heart Rate Variability Research Articles

Association between high sensitivity C-reactive protein, heart rate variability and corrected QT interval in patients with chronic inflammatory arthritis

BackgroundThe risk of sudden cardiac death is increased in chronic inflammatory arthritis, particularly rheumatoid arthritis (RA).To evaluate the putative effect of systemic inflammation on heart rate variability (HRV) and ventricular repolarization in chronic inflammatory arthritis, we analyzed in these patients the possible relationship among HRV parameters, QT interval, and high sensitivity C-reactive protein (hsCRP). MethodsOne hundred-one patients with chronic inflammatory arthritis underwent a 15-minute ambulatory twelve-channel electrocardiogram-recording, to evaluate HRV and QT interval, as well as a venous withdrawal for hsCRP as an estimation of ongoing systemic inflammation. ResultsIn patients with chronic inflammatory arthritis, hsCRP is inversely correlated with HRV and directly with QTc duration, but while hsCRP is associated with HRV independently from any other investigated factor, the association between hsCRP and QTc seems to be an indirect consequence of the autonomic dysfunction itself. Within the whole cohort of patients, those subjects having elevated hsCRP levels displayed both a significant reduction in HRV and a prolongation of QTc with respect to patients with a normal hsCRP value. A similar, although less marked, degree of HRV depression and QTc prolongation was found in RA patients when compared to subjects with spondyloarthritis (SpA) and healthy controls. ConclusionsThese data provide evidence of a link between systemic inflammation and the arrhythmic risk in patients with chronic inflammatory arthritis, also putatively explaining, at least in part, how the different inflammatory load characterizing RA and SpA parallels the different risks of cardiovascular death in these two conditions.

The impact of anxiety on heart rate variability at rest and under stress

Event Abstract Back to Event The impact of anxiety on heart rate variability at rest and under stress John Chalmers1*, Daniel S. Quintana1, 2, Maree J. Abbott1 and Andrew Kemp1, 3 1 University of Sydney, Australia 2 Brain and Mind Research Institute, Australia 3 Hospital Universitário, University of São Paulo, Brazil Aims: Anxiety increases the risk of developing cardiovascular disease (CVD), and is associated with poorer prognosis once CVD is diagnosed. Reduced heart rate variability (HRV) – indicative of reduced parasympathetic nervous system (PNS) activity – may be one mechanism underlying this relationship. Low HRV predicts CVD and all-cause mortality, and is associated with a number of anxiety disorders. However, it remains unclear whether anxious apprehension or arousal underpins HRV reductions. This is the goal of the present study, during rest, and stress conditions. Method: Eighty participants (55 controls) were recruited, and administered the Anxiety Disorders Interview Schedule IV and a semi-structured medical interview to assess psychiatric and medical history. Participants also completed measures (i.e. Penn State Worry Questionnaire, GAD-7, Anxiety Sensitivity Index, & Body Sensations Questionnaire) assessing anxiety related symptoms. Five laboratory tasks were administered (baseline rest, anticipation of shock, acute threat of shock, anticipation of serial subtraction, acute serial subtraction) during which electrocardiogram was collected from which indices of HRV were derived. Results: Participants with a primary anxiety disorder displayed significant reductions in HRV at baseline relative to controls (t = 2.58, p = .03) Multiple regression indicated that general apprehension and worry (Penn State Worry Questionnaire) predicted unique variance in HRV at rest. High worriers also exhibited significantly lower resting state HRV than low worriers. Conclusions: Decreased HRV is driven more by symptoms of worry and apprehension, than symptoms of panic and arousal. Keywords: Heart rate variability, Anxiety, Autonomic Nervous System, Parasympathetic Nervous System, Stress, Psychological Conference: ASP2013 - 23rd Annual meeting of the Australasian Society for Psychophysiology, Wollongong, Australia, 20 Nov - 22 Nov, 2013. Presentation Type: Oral Presentation Topic: Other... Citation: Chalmers J, Quintana DS, Abbott MJ and Kemp A (2013). The impact of anxiety on heart rate variability at rest and under stress. Conference Abstract: ASP2013 - 23rd Annual meeting of the Australasian Society for Psychophysiology. doi: 10.3389/conf.fnhum.2013.213.00020 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 Nov 2013; Published Online: 05 Nov 2013. * Correspondence: Mr. John Chalmers, University of Sydney, Sydney, Australia, john.chalmers313@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers John Chalmers Daniel S Quintana Maree J Abbott Andrew Kemp Google John Chalmers Daniel S Quintana Maree J Abbott Andrew Kemp Google Scholar John Chalmers Daniel S Quintana Maree J Abbott Andrew Kemp PubMed John Chalmers Daniel S Quintana Maree J Abbott Andrew Kemp Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

A Single 4 mg Dose of Nicotine Decreases Heart Rate Variability in Healthy Nonsmokers: Implications for Smoking Cessation Programs

The vast majority of work on the physiological effects of nicotine in humans has been done in smokers or smokers trying to quit. Such studies can be confounded by tolerance, desensitization of receptors, or withdrawal. Because of these difficulties, there is still some dispute as to whether nicotine is proparasympathetic or prosympathetic in humans. To circumvent these difficulties, we assessed the effect of nicotine on autonomic function by measuring changes in heart rate variability (HRV) in nicotine-naive healthy subjects. Twenty males and 20 females aged between 18 and 25 years received 4 mg oral nicotine lozenge or placebo. HRV was assessed in 15-min periods before, during, and after ingestion. There were no significant changes in any measure after placebo administration. During and after nicotine ingestion, heart rate increased to 78 ± 2 beats per minute (bpm) from a baseline level of 75 ± 2 bpm (p < .01). Nicotine significantly increased low frequency (LF; normalized units) from 66 ± 2 at baseline to 70 ± 2 at 15-30 min postingestion (p < .01) and decreased high frequency (HF; normalized units) from 28 ± 2 to 24 ± 1 (p < .01). LF/HF ratio was therefore substantially increased from 2.9 ± 0.3 to 3.7 ± 0.3 (p < .01). A single dose of 4 mg oral nicotine produces a significant reduction in HRV (i.e., a proportional decrease in high-frequency variability) in healthy young nonsmokers consistent with a reduced vagal activity. This has implications for nicotine replacement treatments aimed at cessation of smoking.

Effect of methamphetamine dependence on heart rate variability

Methamphetamine (METH) is an increasing popular and highly addictive stimulant associated with autonomic nervous system (ANS) dysfunction, cardiovascular pathology and neurotoxicity. Heart rate variability (HRV) has been used to assess autonomic function and predict mortality in cardiac disorders and drug intoxication, but has not been characterized in METH use. We recorded HRV in a sample of currently abstinent individuals with a history of METH dependence compared to age- and gender-matched drug-free comparison subjects. HRV was assessed using time domain, frequency domain, and non-linear entropic analyses in 17 previously METH-dependent and 21 drug-free comparison individuals during a 5 minute rest period. The METH-dependent group demonstrated significant reduction in HRV, reduced parasympathetic activity, and diminished heartbeat complexity relative to comparison participants. More recent METH use was associated with increased sympathetic tone. Chronic METH exposure may be associated with decreased HRV, impaired vagal function, and reduction in heart rate complexity as assessed by multiple methods of analysis. We discuss and review evidence that impaired HRV may be related to the cardiotoxic or neurotoxic effects of prolonged METH use.

Cardiac autonomic function does not improve after liver transplantation for familial amyloidotic polyneuropathy

Objective Liver transplantation is the only potentially curative treatment for familial amyloidotic polyneuropathy (FAP). We investigated cardiac autonomic function in 63 transplanted Swedish FAP patients. Methods Heart rate variability (HRV) was recorded between 1–17 (mean 8) months before, and 10–40 (mean 20) months after transplantation. HRV was analysed by power spectrum analysis, but only in patients without arrhythmia ( n = 38). Results Patients with moderate cardiac autonomic dysfunction showed a statistically significant reduction in HRV after transplantation, as compared to the pre-transplant recording. Patients with severe cardiac autonomic dysfunction presented unchanged HRV after liver transplantation. Twenty patients were excluded because they presented cardiac arrhythmia, five of these presented increased HRV after transplantation but had developed subtle arrhythmias, thus, they had not improved cardiac autonomic control. Five patients were excluded because they were pacemaker-treated. Conclusions The reason why HRV decreased after transplantation remains unclear, but there are several possibilities: 1) liver transplantation did not stop the deterioration in cardiac autonomic function; 2) the deterioration continued until transplantation and was then halted; or 3) a sudden reduction in HRV occurred in connection with the transplantation procedure. Nonetheless, this study failed to disclose any improvement in cardiac autonomic function after liver transplantation for FAP.

Heart rate variability in bipolar mania and schizophrenia

Background Autonomic nervous system (ANS) dysfunction and reduced heart rate variability (HRV) have been reported in a wide variety of psychiatric disorders, but have not been well characterized in bipolar mania. We recorded cardiac activity and assessed HRV in acutely hospitalized manic bipolar (BD) and schizophrenia (SCZ) patients compared to age- and gender-matched healthy comparison (HC) subjects. Method HRV was assessed using time domain, frequency domain, and nonlinear analyses in 23 manic BD, 14 SCZ, and 23 HC subjects during a 5 min rest period. Psychiatric symptoms were assessed by administration of the Brief Psychiatric Rating Scale (BPRS) and the Young Mania Rating Scale (YMRS). Results Manic BD patients demonstrated a significant reduction in HRV, parasympathetic activity, and cardiac entropy compared to HC subjects, while SCZ patients demonstrated a similar, but non-significant, trend towards lower HRV and entropy. Reduction in parasympathetic tone was significantly correlated with higher YMRS scores and the unusual thought content subscale on the BPRS. Decreased entropy was associated with increased aggression and diminished personal hygiene on the YMRS scale. Conclusion Cardiac function in manic BD individuals is characterized by decreased HRV, reduced vagal tone, and a decline in heart rate complexity as assessed by linear and nonlinear methods of analysis. Autonomic dysregulation is associated with more severe psychiatric symptoms, suggesting HRV dysfunction in this disorder may be dependent on the phase of the illness.

Impaired cardiac autonomic nervous control after cardiac bypass surgery for congenital heart disease

We undertook a study to describe changes in heart rate variability (HRV) postoperatively in children undergoing cardiac bypass surgery for congenital heart disease (CHD). HRV was recorded for a 1-h period preoperatively and a 24-h period postoperatively in 20 children with CHD. We found a highly significant reduction in HRV in both time and frequency domain indices compared to preoperative values, which was sustained throughout the 24-h study period. There was a negative correlation between both time and frequency domain HRV measurements and length of cardiac bypass. HRV is reduced postoperatively and correlates with cardiac bypass time. Length of cardiac bypass time may be one mechanism whereby HRV is reduced following surgery.

Autonomic neurocardiac function in patients with major depression and effects of antidepressive treatment with nefazodone

Background: Major depression (MD) is associated with an augmented risk of cardiovascular mortality. One possible explanation for this association is that MD influences autonomic neurocardiac regulation (ANR). However, previous studies on this subject revealed conflicting results. Methods: Using an autonomic test battery, which consisted of standardised measurements of heart rate variability (HRV) and blood pressure, we (1) compared ANR between 25 patients with DSM-III-R diagnosed MD and 60 healthy controls, and (2) investigated the autonomic effects of antidepressive treatment with nefazodone. Results: Following multivariate analysis of all tests a significant reduction in HRV could only be shown for the Valsalva ratio amongst the depressives compared to controls. There was a significant inverse correlation between the HRV during deep respiration and both the severity of depression and the duration of the depressive episode. Serial HRV recordings revealed that both the mean resting heart rate and systolic blood pressure significantly decreased after 21 days of nefazodone treatment (average dosage 413 mg/day), whereas after 10 days (average dosage 270.8 mg/day) there were no striking changes compared to the pre-treatment values. During nefazodone treatment no significant changes in parasympathetic tone occurred. Limitations: ANR was not assessed in a randomised, placebo-controlled fashion. Conclusions: (1) Patients with MD may suffer from functional disturbances in the interaction between the sympathetic and parasympathetic autonomic tree. (2) The pattern of autonomic changes during treatment suggests that nefazodone induced a dose dependent, serotonergically-mediated down-regulation of the sympathetic tone. This mechanism might be responsible for nefazodone’s properties of reducing anxiety.

Changes in arrhythmia profile and heart rate variability during abrupt withdrawal of antiepileptic drugs. Implications for sudden death

Sudden unexpected death (SUD) has been associated with low or undetectable concentrations of antiepileptic drugs in patients with epilepsy suggesting that a sudden fall in plasma levels of these drugs might be a critical factor for the occurrence of SUD. We studied the changes in arrhythmia profile and heart-rate variability, during abrupt withdrawal of carbamazepine and phenytoin treatment in 10 patients with side effects on these drugs. Continuous ECG recording and daily measurements of drug plasma concentrations were performed from the last day of steady-state treatment and the following 4 days. Three patients had a 10-fold increase in ventricular premature beats. In addition, there was a significant reduction in heart-rate variability, assessed over 24 hours, in both the time (SDNN index, P = 0.03) and frequency domains from days 1-5. In the frequency domain analysis there was a significant reduction in total power (P = 0.01), very-low-frequency power (P = 0.004) and in low-frequency (LF) power (P = 0.01). Similar reductions in heart-rate variability and increases in ventricular automaticity have been associated with increased mortality in other patient groups. Two factors that might contribute to the increased rate of SUD in patients with epilepsy have thus been identified.