Abstract:SUMMARYSeveral studies have suggested that an increased high sensitivity C-reactive protein (hsCRP) level is a strong independent predictor of increased risk for atherosclerotic cardiovascular mortality and morbidity. Reduced heart rate variability (HRV) has also been reported to predict cardiovascular events such as sudden death and myocardial infarction in apparently healthy subjects. The aim of this cross-sectional study was to test the possible correlation between variation of the R-R interval as one of th… Show more
“…Other studies have also shown an association between parasympathetic activity and inflammation (37), providing a possible mechanistic explanation for our study's results. However, treatments used in cardiac patients, such as β blockers, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, have been shown to augment parasympathetic activity and reduce inflammation as part of their beneficial mechanisms (38)(39)(40).…”
Parasympathetic activity influences long-term outcome in patients with cardiovascular disease, but the underlying mechanism(s) linking parasympathetic activity and the occurrence of major adverse cardiovascular events (MACEs) are incompletely understood. The aim of this pilot study was to evaluate the association between serum cholinesterase activities as parasympathetic biomarkers and the risk for the occurrence of MACEs. Cholinergic status was determined by measuring the cumulative capacity of serum acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) to hydrolyze the AChE substrate acetylthiocholine. Cholinergic status was evaluated in randomly selected patients undergoing cardiac catheterization. The patients were divided into two groups of 100 patients in each group, with or without occurrence of MACEs during a follow-up period of 40 months. Cox regression models adjusted for potential clinical, metabolic and inflammatory confounders served to evaluate association with clinical outcome. We found that patients with MACE presented lower cholinergic status and AChE values at catheterization (1,127 ± 422 and 359 ± 153 nmol substrate hydrolyzed per minute per milliliter, respectively) than no-MACE patients (1,760 ± 546 and 508 ± 183 nmol substrate hydrolyzed per minute per milliliter, p < 0.001 and p < 0.001, respectively), whose levels were comparable to those of matched healthy controls (1,622 ± 303 and 504 ± 126 nmol substrate hydrolyzed per minute per milliliter, respectively). In a multivariate analysis, patients with AChE or total cholinergic status values below median showed conspicuously elevated risk for MACE (hazard ratio 1.85 [95% confidence interval [CI] 1.09-3.15, p = 0.02] and 2.21 [95% CI 1.22-4.00, p = 0.009]) compared with those above median, even after adjusting for potential confounders. We conclude that parasympathetic dysfunction expressed as reduced serum AChE and AChE activities in patients compared to healthy controls can together reflect impaired parasympathetic activity. This impairment predicts the risk of MACE up to 40 months in such patients. Monitoring these parasympathetic parameters might help in the risk stratification of patients with cardiovascular disease.
“…Other studies have also shown an association between parasympathetic activity and inflammation (37), providing a possible mechanistic explanation for our study's results. However, treatments used in cardiac patients, such as β blockers, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers, have been shown to augment parasympathetic activity and reduce inflammation as part of their beneficial mechanisms (38)(39)(40).…”
Parasympathetic activity influences long-term outcome in patients with cardiovascular disease, but the underlying mechanism(s) linking parasympathetic activity and the occurrence of major adverse cardiovascular events (MACEs) are incompletely understood. The aim of this pilot study was to evaluate the association between serum cholinesterase activities as parasympathetic biomarkers and the risk for the occurrence of MACEs. Cholinergic status was determined by measuring the cumulative capacity of serum acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) to hydrolyze the AChE substrate acetylthiocholine. Cholinergic status was evaluated in randomly selected patients undergoing cardiac catheterization. The patients were divided into two groups of 100 patients in each group, with or without occurrence of MACEs during a follow-up period of 40 months. Cox regression models adjusted for potential clinical, metabolic and inflammatory confounders served to evaluate association with clinical outcome. We found that patients with MACE presented lower cholinergic status and AChE values at catheterization (1,127 ± 422 and 359 ± 153 nmol substrate hydrolyzed per minute per milliliter, respectively) than no-MACE patients (1,760 ± 546 and 508 ± 183 nmol substrate hydrolyzed per minute per milliliter, p < 0.001 and p < 0.001, respectively), whose levels were comparable to those of matched healthy controls (1,622 ± 303 and 504 ± 126 nmol substrate hydrolyzed per minute per milliliter, respectively). In a multivariate analysis, patients with AChE or total cholinergic status values below median showed conspicuously elevated risk for MACE (hazard ratio 1.85 [95% confidence interval [CI] 1.09-3.15, p = 0.02] and 2.21 [95% CI 1.22-4.00, p = 0.009]) compared with those above median, even after adjusting for potential confounders. We conclude that parasympathetic dysfunction expressed as reduced serum AChE and AChE activities in patients compared to healthy controls can together reflect impaired parasympathetic activity. This impairment predicts the risk of MACE up to 40 months in such patients. Monitoring these parasympathetic parameters might help in the risk stratification of patients with cardiovascular disease.
“…Findings differed across these studies. While two investigations reported a significant inverse relationship with the inflammatory markers CRP and IL-6, one study demonstrated higher CRP levels only in the group of the lowest HRV quartile (Kon et al, 2006). The remaining group tested inflammatory markers and HRV during and after a mental stress test and found no relationship between immune responses and heart rate variability (Owen and Steptoe, 2003).…”
Section: Resultsmentioning
confidence: 98%
“…The effect of vagal activity was mainly studied on Interleukin-6 (IL-6) and C-reactive peptide (CRP). Six studies reported on subjects with known or suspected coronary heart disease (CHD) (Hamaad et al, 2005; Lanza et al, 2006; Madsen et al, 2007; Nolan et al, 2007; Psychari et al, 2007; Yue et al, 2007), four studies investigated the association of HRV and inflammation in healthy population (Owen and Steptoe, 2003; Sajadieh et al, 2004; Kon et al, 2006; Sloan et al, 2007). Two papers analyzed inflammatory markers and HRV in metabolic syndrome and impaired glucose tolerance, respectively (Brunner et al, 2002; Diakakis et al, 2005).…”
Summary
Introduction
Recent evidence implicates a cholinergic anti-inflammatory pathway. Because vagus nerve activity mediates some heart rate variability (HRV), this qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans. This qualitative review examines the literature concerning circulating cytokines and HRV in cardiovascular function in humans.
Methods
Thirteen studies on HRV, inflammation, and cardiovascular function were located by electronic library search and descriptively reviewed.
Results
The relationship between HRV and inflammation was studied in healthy controls, patients with acute or stable coronary heart disease (CHD), patients with metabolic syndrome or impaired glucose tolerance and patients with kidney failure. Investigations focused mainly on lnterleukin-6 (IL-6) and C-reactive peptide (CRP). The majority of reviewed studies reported that parasympathetic nervous system tone as inferred from heart rate variability is inversely related to inflammatory markers (r values between −0.2 and −0.4). The relationships with inflammatory markers were similar whether derived from ECG signals as short as 5–30 min or from 24-h ECG readings for HRV analyses. While inflammatory markers appear to be related to HRV, it is a mistake to assume that the traditional “vagal measures” of HRV (such as high frequency heart rate variability) are the driving factors. Indeed, low frequency heart rate variability, a complex measure reflecting both parasympathetic and sympathetic activity, is the more commonly associated measure linked to inflammatory markers.
Discussion
Heart rate variability is inversely correlated with inflammatory markers in healthy individuals as well as in those with cardiovascular diseases.
“…(Int Heart J 2008; 49: 175-181) Key words: Cardiac autonomic function, Heart rate variability, Short-term, Long term, Workers HEART rate variability (HRV) is a physiological maker used to assess the autonomic nervous system (ANS) and is significantly associated with a variety of pathologies, such as cardiovascular disease and diabetes mellitus. [1][2][3][4][5][6] The HRV can be assessed over the short (usually 5-15 minutes) or long (24 hours) term. Long-term measurements reflect the overall change in the heart rate under nonspecific, changing conditions because the subjects perform their usual daily activities during the test.…”
SUMMARYHeart rate variability (HRV) is a noninvasive physiological marker used to assess autonomic nervous function and can be recorded over the short or long term. Long-term recording is a good method for assessing mortality and patient prognosis, while short-term measurement is widely used due to practical advantages and reproducibility. However, little is known about whether a short-term assessment reflects the variation in the overall heart rate of workers. This study evaluated the relationship between the 24-hour and 5-minute HRV, which was selected from a 24-hour recording. The study population was 153 male workers at the National Rail Company in Korea, who had their heart rates assessed for 24 hours. In the time and frequency domains, the correlations of the HRV between 24 hours and 5 minutes were calculated for the entire time and limited times (09:00-17:00). We found modest correlations in the time (R = 0.614-0.668) and frequency (R = 0.508-0.817) domains, but the best correlation was for the high-frequency spectra (HF; R = 0.817). Our findings suggest that the short-term HRV remains stable and may be applicable for screening the variation in the heart rate of workers, although not all of the correlations were sufficiently strong. (Int Heart J 2008; 49: 175-181) Key words: Cardiac autonomic function, Heart rate variability, Short-term, Long term, Workers HEART rate variability (HRV) is a physiological maker used to assess the autonomic nervous system (ANS) and is significantly associated with a variety of pathologies, such as cardiovascular disease and diabetes mellitus. [1][2][3][4][5][6] The HRV can be assessed over the short (usually 5-15 minutes) or long (24 hours) term. Long-term measurements reflect the overall change in the heart rate under nonspecific, changing conditions because the subjects perform their usual daily activities during the test. The long-term method has been used to assess mortality and the adverse prognosis of patients on bed rest. 7,8) This analysis is difficult and notFrom the
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