The role of flow-mediated dilatation and high sensitive C-reactive protein in paroxysmal atrial fibrillation

被引:1
作者
Wafa, Ahmed A. [1 ]
Daoud, Eid M. [1 ]
Gomaa, Gamal F. [1 ]
机构
[1] Mansoura Univ, Specialized Med Hosp, Fac Med, Dept Cardiol, Mansoura City, Egypt
关键词
Paroxysmal atrial fibrillation; Brachial flow-mediated dilatation; C-reactive protein;
D O I
10.1016/j.ehj.2012.05.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Atrial fibrillation (AF) is the most common type of arrhythmia and recognized as a risk factor for thromboembolism. Endothelial damage or dysfunction may contribute to increase the risk of thromboembolism via the mediation of a prothrombotic or hypercoagulable state. Objectives: The aim of the current study is to investigate endothelial dysfunction (represented by brachial flow-mediated dilatation "FMD'') and inflammation (represented by hs-CRP) in patients with paroxysmal atrial fibrillation. Subjects and methods: Forty-two patients with AF taken from the Cardiology Department and Outpatients Clinic, Specialized Medical Hospital, Mansoura University, in the period between February 2011 and May 2011 were enrolled in our study, the patients were then subsequently divided according to the clinical type of AF into Group I: comprised 20 patients with paroxysmal AF (PAF) with mean age 57.35y. Group II: comprised 22 patients with chronic AF (CAF) with mean age 57.68y. Twenty control subjects without AF were enrolled in this study (Group III). Patients and control groups were subjected to clinical evaluation, electrocardiography (ECG), echo-cardiography and brachial FMD (using external brachial ultrasonography. Serum level of hs-CRP was assessed in all subjects. The diameter change induced by FMD was expressed as the percent change relative to that at the initial scan (FMD%) according to the following equation: FMD% = Maximum diameter - baseline diameter / Baseline diameter x 100. Results: Left atrial diameter was significantly increased when compared either GI or GII with control group (3.96 +/- 0.27; 4.7 +/- 0.48 vs 3.05 +/- 0.35 cm) (P < 0.001). Brachial flow-mediated dilatation difference and percentage change of FMD were significantly lower in groups I and II in comparison to group III (0.09 +/- 0.05; 0.09 +/- 0.04 vs 0.79 +/- 0.07 mm) and (1.96 +/- 0.98; 1.99 +/- 0.89 vs 18.3 +/- 3.26) (P < 0.001). High sensitive CRP was significantly higher when compared either group I or group II with control group. Also hs-CRP has significantly increased when compared GII with group I (8.35 +/- 1.55; 10.58 +/- 1.75 vs 3.61 +/- 0.61 mg/L) (P < 0.001). Conclusion: Patients with PAF are comparable in the degree of endothelial dysfunction (reflected as impaired brachial artery FMD) and inflammatory element (reflected as a higher serum hs-CRP) to CAF. This may explain why the risk of thromboembolism in PAF is comparable with that in CAF patients. (C) 2012 Egyptian Society of Cardiology. Production and hosting by Elsevier B. V. All rights reserved.
引用
收藏
页码:211 / 217
页数:7
相关论文
共 30 条
[1]   PROTHROMBIN FRAGMENT F1+2 AND THROMBIN ANTITHROMBIN-III COMPLEX ARE USEFUL MARKERS OF THE HYPERCOAGULABLE STATE IN ATRIAL-FIBRILLATION [J].
ASAKURA, H ;
HIFUMI, S ;
JOKAJI, H ;
SAITO, M ;
KUMABASHIRI, I ;
UOTANI, C ;
MORISHITA, E ;
YAMAZAKI, M ;
SHIBATA, K ;
MIZUHASHI, K ;
MIFUNE, J ;
MATSUDA, T .
BLOOD COAGULATION & FIBRINOLYSIS, 1992, 3 (04) :469-473
[2]   C-reactive protein and other inflammatory risk markers in acute coronary syndromes [J].
Blake, GJ ;
Ridker, PM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2003, 41 (04) :37S-42S
[3]   Is atrial fibrillation an inflammatory disorder? [J].
Boos, CJ ;
Anderson, RA ;
Lip, GYH .
EUROPEAN HEART JOURNAL, 2006, 27 (02) :136-149
[4]   Atrial fibrillation and the hypercoagulable state: From basic science to clinical practice [J].
Choudhury, A ;
Lip, GYH .
PATHOPHYSIOLOGY OF HAEMOSTASIS AND THROMBOSIS, 2003, 33 (5-6) :282-289
[5]   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
[6]  
CONLAN MG, 1993, THROMB HAEMOSTASIS, V70, P380
[7]  
Davi G, 1998, CIRCULATION, V97, P953
[8]   Relationship between C-reactive protein concentrations during glucocorticoid therapy and recurrent atrial fibrillation [J].
Dernellis, J ;
Panaretou, M .
EUROPEAN HEART JOURNAL, 2004, 25 (13) :1100-1107
[9]   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
[10]   Inflammation in the genesis and perpetuation of atrial fibrillation [J].
Engelmann, MDM ;
Svendsen, JH .
EUROPEAN HEART JOURNAL, 2005, 26 (20) :2083-2092