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Lower heart rate variability predicts increased level of C‐reactive protein 4 years later in healthy, nonsmoking adults
Author(s) -
Jarczok M. N.,
Koenig J.,
Mauss D.,
Fischer J. E.,
Thayer J. F.
Publication year - 2014
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12295
Subject(s) - medicine , heart rate variability , c reactive protein , prospective cohort study , heart rate , body mass index , ambulatory , cardiology , endocrinology , inflammation , physiology , blood pressure
Abstract Background Inflammation and vagally mediated heart rate variability (vmHRV) have been implicated in a number of conditions including diabetes and cardiovascular disease. Consistent with the inflammatory reflex termed the ‘cholinergic anti‐inflammatory pathway’, numerous cross‐sectional studies have demonstrated negative associations between vmHRV and inflammatory markers such as C‐reactive protein (CRP). The only prospective study, however, showed the opposite: higher CRP at baseline predicted higher high‐frequency heart rate variability (HF‐HRV) at follow‐up. Thus, additional studies are needed to examine the prospective association between vmHRV and CRP. Methods Healthy employees participated in a voluntary on‐site health assessment. Blood samples and ambulatory heart rate recordings were obtained, and night‐time HF‐HRV was calculated. Useable heart rate data were available in 2007 for 106 nonsmoking employees (9% women; age 44.4 ± 8 years), all of whom returned for an identical follow‐up health assessment in 2011. Bootstrapped (500 replications) bivariate ( r ) and partial Pearson's correlations (ppc) adjusting for sex, age and body mass index at baseline (2007) were calculated. Results Zero‐order correlations indicated that higher HF‐HRV was associated with lower levels of CRP at both time‐points (2007: r = −0.19, P < 0.05; 2011: r = −0.34, P < 0.001). After adjustment, HF‐HRV remained a significant predictor of CRP (ppc = −0.20, P < 0.05). Conclusion In this study, we have provided in vivo support for the cholinergic anti‐inflammatory pathway in humans. Cardiac vagal modulation at baseline predicts level of CRP 4 years later. Our findings have important implications for the role of vmHRV as a risk factor for cardiovascular disease morbidity and mortality. Interventions targeted at vmHRV might be useful in the prevention of diseases associated with elevated systemic inflammation.