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

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. 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. 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), echocardiography 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 diameterBaseline diameter×100. 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). 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.