title: Inflammatory activation following interruption of long-term cardiac resynchronization therapy.
abstract: Previous observations suggest that cardiac resynchronization therapy (CRT) may exert an anti-inflammatory effect. The objective of this study was to evaluate the effect of temporary interruption of long-term CRT on plasma concentrations of proinflammatory cytokines and brain natriuretic peptide (BNP). The study group consisted of 54 patients (32 male and 22 female, mean age 64 years) with chronic heart failure (HF) treated with CRT. BNP, high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and neopterin were measured three times: after 26-28 weeks of continuous CRT (CRT-on), 48 h after its cessation (CRT-off), and 48 h after switching the CRT-on again. CRT interruption resulted in a significant worsening of left ventricular systolic function: reduction of cardiac output (CO), dP/dt, and left ventricular ejection fraction (LVEF), as well as deterioration of mitral regurgitation in the CRT responder group. A significant increase in serum concentrations of hs-CRP, neopterin, IL-6, and BNP was noted in this subpopulation. In CRT nonresponders, no significant changes were observed. In responders the changes in serum concentrations of hs-CRP, IL-6, neopterin, and BNP, following CRT interruption, significantly correlated with the respective changes in thoracic fluid content (TFC) and inversely correlated with LVEF changes. Even short (48 h) interruption of long-term CRT led to a significant increase of proinflammatory cytokines and BNP concentrations in responders. The changes in hs-CRP, IL-6, neopterin, and BNP concentrations correlated with the change in TFC-marker of pulmonary congestion and inversely correlated with the change in LVEF.
authors.affiliation: Department of Cardiology, Medical University of Lublin, 8 Jaczewskiego Street, Lublin, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Rubaj
authors.forename: Piotr
authors.initials: P
authors.lastname: Ruciński
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Oleszczak
authors.forename: Michał K
authors.initials: MK
authors.lastname: Trojnar
authors.forename: Maciej
authors.initials: M
authors.lastname: Wójcik
authors.forename: Andrzej
authors.initials: A
authors.lastname: Wysokiński
authors.forename: Andrzej
authors.initials: A
authors.lastname: Kutarski
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D058406:Cardiac Resynchronization Therapy; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology* / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000209:etiology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D019798:Neopterin / Q000097:blood; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D015854:Up-Regulation; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D020097:Natriuretic Peptide, Brain; D019798:Neopterin; D002097:C-Reactive Protein