Short-term amiodarone treatment attenuates the production of monocyte cytokines and chemokines by C-reactive protein and improves cardiac function in patients with idiopathic dilated cardiomyopathy and ventricular tachycardia.

BACKGROUND: Increased expression of cytokines and chemokines has been observed in chronic heart failure (CHF). Amiodarone reduces circulating cytokine levels, so it may attenuate the production of monocyte cytokines and chemokines by C-reactive protein (CRP) and thus improve the left ventricular ejection fraction (LVEF) in dilated cardiomyopathy (DCM) patients with ventricular tachycardia (VT). METHODS AND
RESULTS: Peripheral blood mononuclear cells (PBMCs) were stimulated by 25 microg/ml CRP in 23 patients with DCM, who were divided into 2 groups based on whether or not amiodarone was included in their treatment (Amiodarone group n=8; No amiodarone group n=15). Tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein (MCP)-1 on monocytes at baseline and after 4 weeks of treatment was measured by ELISA and expressed as mean+/-SD (pg.ml(-1)x10(-6) PBMCs). The LVEF and the CRP-induced monocyte cytokine and chemokine production were unchanged in the No amiodarone group after 4 weeks; however, LVEF in the Amiodarone group was increased (32.7+/-6.9 to 39.2+/-6.9%; P=0.005), and TNF-alpha and MCP-1 production in the Amiodarone group were decreased (P=0.012, respectively).
CONCLUSIONS: Amiodarone attenuates the production of monocyte cytokines and chemokines by CRP, and improves LVEF in CHF patients with VT.