Abstract 15132: Amiodarone Treatments Improve the Inflammation in Heart Failure
Introduction: Inflammation is deeply involved in heart failure (HF). In vitro studies showed that amiodarone blocked cytokine production from human mononuclear cells stimulated with LPS. In addition, the randomised trial showed that the low-dose amiodarone improved the mortality in severe congestive heart failure.
Hypothesis: Amiodarone treatments improve the inflammation in HF.
Methods/Results: Twenty-nine patients with HF (Age:57.1±16.9, Men:58.6%, LVEF:43.9±9.6%, NYHA2.0±0.9) including DCM, HCM, ARVC, ICM, and Valvular CM patients were studied, and compared with 64 normotensive healthy controls (Cont). BNP, hsCRP levels were higher in HF than Cont (P<0.001 and P<0.00001). In addition, inflammatory T cell cytokine, IL-6, IFNγ, and IL17, were increased in HF by CBA kit (P<0.001, P<0.05, and P<0.001, respectively). After amiodarone treatments for 1 month, the levels of IL-6, hsCRP, and BNP were significantly improved in HF patients. To investigate the beneficial amiodarone effects for inflammation in HF, we examine the memory T cell subsets by FACS. In HF, CD45RA−CCR7− effecter memory T cells and CD45RA+CCR7− effecter T cells were increased by FACS. To investigate the effector function of T cells in HF, we examine T cell phenotype. IFNγ+CD4+ T cells, IFNγ+CD8+ T cells, IL17+CD8+ T cells, and granzyme+CD8+ T cells were increased in HF. Finally, 10μM amiodarone treatments for 24h in vitro decreased INFγ+ CD4+ T cells, IFNγ+ CD8+ T cells, IL17+ CD4+ T cells, and IL17+ CD8+ T cells (P<0.01, P<0.01, P<0.01, and P<0.01, respectively), but not granzyme+CD8+T cells.
Conclusions: The effecter memory T cells and effecter T cells were elevated in HF patients. Amiodarone treatments might have an important role for improving the effector memory function of T cells and the outcome of HF patients.
Author Disclosures: Y. Tanigaito: None. K. Sato: None. K. Kitamura: None. A. Suzuki: None. A. Futase: None. T. Shiga: None. N. Hagiwara: None.
- © 2014 by American Heart Association, Inc.