Corline Brouwers1, Henneke Versteeg2, Mathias Meine3, Cobi J Heijnen4, Annemieke M Kavelaars4, Susanne S Pedersen5, Paula M C Mommersteeg1. 1. CoRPS - Center of Research on Psychology in Somatic Diseases, Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands. 2. CoRPS - Center of Research on Psychology in Somatic Diseases, Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands; Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands. 3. Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands. 4. Laboratory Neurodevelopmental Origins of Disease, University Medical Center Utrecht, Utrecht, The Netherlands; Neuroimmunology of Cancer-Related Symptoms (NICRS) Laboratory, Department of Symptom Research, University of Teas M.D. Anderson Cancer Center, Houston, TX, USA. 5. CoRPS - Center of Research on Psychology in Somatic Diseases, Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands; Department of Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands; Department of Cardiology, Odense University Hospital, Odense, Denmark; Institute of Psychology, University of Southern Denmark, Odense, Denmark. Electronic address: sspedersen@health.sdu.dk.
Abstract
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 14months 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±10.1years). 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.
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 14months follow-up in CRT-responders and nonresponders, defined by two response criteria. METHODS: We studied 105 heart failurepatients implanted with a CRT-defibrillator (68% men; age=65.4±10.1years). 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.
Authors: Quynh A Truong; Jackie Szymonifka; James L Januzzi; Jigar H Contractor; Roderick C Deaño; Neal A Chatterjee; Jagmeet P Singh Journal: Heart Rhythm Date: 2018-12-24 Impact factor: 6.343
Authors: Katarzyna Ptaszynska-Kopczynska; Anna Szpakowicz; Marta Marcinkiewicz-Siemion; Anna Lisowska; Ewa Waszkiewicz; Marcin Witkowski; Piotr Jakim; Bogdan Galar; Wlodzimierz J Musial; Karol A Kamiński Journal: Arch Med Sci Date: 2016-03-17 Impact factor: 3.318