Introduction: Studies suggest that cardiac resynchronization therapy (CRT) can induce a decrease in brain natriuretic peptide (BNP) and systemic inflammation, which may be associated with CRT-response. However, the evidence is inconclusive. We examined levels of BNP and inflammatory markers from pre-CRT implantation to 14. months follow-up in CRT-responders and nonresponders, defined by two response criteria. Methods: We studied 105 heart failure patients implanted with a CRT-defibrillator (68% men; age = 65.4. ± 10.1. years). The objective CRT-response was defined as a reduction of ≥15% in left ventricular end systolic volume; subjective CRT-response was defined as an improvement of ≥10 points in patient-reported health status assessed with the Kansas City Cardiomyopathy Questionnaire. Plasma BNP and markers of inflammation (CRP, IL-6, TNFα, sTNFr1 and sTNFr2) were measured at three time points. Results: Pre-implantation concentrations of TNFα were significantly lower for subjective responders compared to nonresponders (p = .05), but there was no difference in BNP and the other inflammatory markers at baseline. Objective CRT-response was significantly associated with lower BNP levels over time (F = 27.31, p. < .001), and subjective CRT-response with lower TNFα levels (F = 5.67, p = .019). Conclusion: Objective and subjective response to CRT was associated with lower levels of BNP and TNFα, respectively, but not with other markers of inflammation. This indicates that response to CRT is not automatically related to a stronger overall decrease in inflammation. Large-scale studies are warranted that further examine the relation between the clinical effects of CRT on inflammatory markers, as the latter have been associated with poor prognosis in heart failure.

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Brain, Behavior, and Immunity
Department of Cardiology

Brouwers, C., Versteeg, H., Meine, M., Heijnen, C., Kavelaars, A., Pedersen, S., & Mommersteeg, P. (2014). Association between brain natriuretic peptide, markers of inflammation and the objective and subjective response to cardiac resynchronization therapy. Brain, Behavior, and Immunity, 40, 211–218. doi:10.1016/j.bbi.2014.03.017