Related Experiment Video
Updated: Aug 6, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
Published on: December 11, 2017
Anti-inflammatory effect of cardiac resynchronization therapy
Knut T Lappegård1, Hanne Bjørnstad
1Department of Medicine, Nordland Hospital, Bodø, Norway. knut.lappegard@nlsh.no
Background:
Congestive heart failure (CHF) is associated with persistent immune activation. Medical therapy has been shown to exert only limited anti-inflammatory effects. Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in a subset of patients with heart failure, but it is not known whether this treatment affects the immune system as well. To test this hypothesis, eight patients with heart failure scheduled for CRT were investigated for immune activation before and 6 months after CRT treatment.
Methods And Results:
After 6 months, all patients had improved in NYHA-class and LVEF, and there was a statistically significant reduction in serum N-terminal pro brain natriuretic peptide (BNP). Furthermore, there was a statistically significant reduction in plasma levels of the chemokines monocyte chemoattractant protein 1 (MCP-1) and interleukin 8 (IL-8) and the cytokine interleukin 6 (IL-6). We observed no changes in the levels of interleukin 1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), interleukin 10 (IL-10), or complement activation products. There was a significant correlation between changes in BNP and IL-6 (r = 0.74, P = 0.037).
Conclusion:
Although based upon a limited number of patients, this report indicates that CRT reduces peripheral markers of immune activation in patients with CHF. Further large scale studies are warranted to verify these findings.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Rheumatic Heart Disease I: Introduction
Myocarditis I: Introduction
Cardiomyopathy IV: Restrictive Cardiomyopathy
Myocarditis III: Medical Management
Heart Failure Drugs: Inotropic Agents

