Relationship between C-reactive protein concentrations during glucocorticoid therapy and recurrent atrial fibrillation

被引:245
作者
Dernellis, J [1 ]
Panaretou, M [1 ]
机构
[1] Vostanion Hosp, Dept Cardiol, Mitilini, Greece
关键词
inflammation; C-reactive protein; atrial fibrillation; glucocorticoid;
D O I
10.1016/j.ehj.2004.04.025
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background Little direct information is available on the effect of C-Reactive Protein (CRP) lowering on the reduction of recurrent atrial. fibrillation (AF). Methods and Results We compared tow-dose glucocorticoid therapy (16 mg methylprednisolone for 4 weeks tapered to 4 mg for 4 months) and placebo in 104 patients who had experienced persistent AF with a median concentration of CRP 1.14 mg/dL (min = 0.01, max = 2.58). Methy[prednisolone reduced recurrent AF (primary end-point) from 50% in the placebo group to 9.6% in the glucocorticoid group and permanent AF (expanded end-point) from 29% in the placebo group to 2% in the glucocorticoid group. Survival distributions for methylprednisolone were significantly different (for both primary and expanded end-point, P < 0.001). In multivariate Cox analysis, average CRP concentrations during follow-up were significant predictors of the primary end-point, with a relative risk 6.72 (P = 0.006) and the expanded end-point, with a relative risk of 11.67 (P = 0.0006). Conclusions CRP concentration is a risk factor for recurrent and permanent AF. Methylprednisolone successfully prevents recurrent and permanent AF. (C) 2004 Published by Elsevier Ltd on behalf of The European Society of Cardiology.
引用
收藏
页码:1100 / 1107
页数:8
相关论文
共 27 条
[1]  
[Anonymous], 2001, CIRCULATION, V104, P2118
[2]  
ARMITAGE P, 1994, STAT METHODS MED RES, P450
[3]   Inflammation as a risk factor for atrial fibrillation [J].
Aviles, RJ ;
Martin, DO ;
Apperson-Hansen, C ;
Houghtaling, PL ;
Rautaharju, P ;
Kronmal, RA ;
Tracy, RP ;
Van Wagoner, DR ;
Psaty, BM ;
Lauer, MS ;
Chung, MK .
CIRCULATION, 2003, 108 (24) :3006-3010
[4]  
BAUDNER S, 1996, J LAB MED, V20, P145
[5]  
Bruins P, 1997, CIRCULATION, V96, P3542
[6]   C-reactive protein elevation in patients with atrial arrhythmias - Inflammatory mechanisms and persistence of atrial fibrillation [J].
Chung, MK ;
Martin, DO ;
Sprecher, D ;
Wazni, O ;
Kanderian, A ;
Carnes, CA ;
Bauer, JA ;
Tchou, PJ ;
Niebauer, MJ ;
Natale, A ;
Van Wagoner, DR .
CIRCULATION, 2001, 104 (24) :2886-2891
[7]   Conversion of recent onset paroxysmal atrial fibrillation to normal sinus rhythm: the effect of no treatment and high-dose amiodarone - A randomized, placebo-controlled study [J].
Cotter, G ;
Blatt, A ;
Kaluski, E ;
Metzkor-Cotter, E ;
Koren, M ;
Litinski, I ;
Simantov, R ;
Moshkovitz, Y ;
Zaidenstein, R ;
Peleg, E ;
Vered, Z ;
Golik, A .
EUROPEAN HEART JOURNAL, 1999, 20 (24) :1833-1842
[8]   CARDIAC ANAPHYLAXIS - COMPLEMENT ACTIVATION AS AN AMPLIFICATION SYSTEM [J].
DELBALZO, U ;
POLLEY, MJ ;
LEVI, R .
CIRCULATION RESEARCH, 1989, 65 (03) :847-857
[9]  
DELBALZO UH, 1985, P NATL ACAD SCI USA, V82, P886
[10]   C-reactive protein and paroxysmal atrial fibrillation: evidence of the implication of an inflammatory process in paroxysmal atrial fibrillation [J].
Dernellis, J ;
Panaretou, M .
ACTA CARDIOLOGICA, 2001, 56 (06) :375-380