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Resumen de Lower heart rate variability predicts increased level of C-reactive protein 4 years later in healthy, nonsmoking adults

M.N. Jarczok, J. Koenig, D. Mauss, J. E. Fischer, J.F. Thayer

  • 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.


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