Article

Markers of inflammation before and after curative ablation of atrial flutter

Division of Cardiology, Electrophysiology Section, University of California, San Francisco, San Francisco, California 94143-1354, USA.
Heart Rhythm (Impact Factor: 4.92). 03/2008; 5(2):215-21. DOI: 10.1016/j.hrthm.2007.10.007
Source: PubMed

ABSTRACT Atrial arrhythmias are associated with inflammation. The cause and effect of the association are unknown.
The purpose of this study was to test the hypothesis that atrial tachyarrhythmias contribute to inflammation.
We performed a prospective observational study wherein C-reactive protein (CRP) and interleukin-6 (IL-6) levels from the femoral vein and coronary sinus (CS) were compared before curative ablation for atrial flutter (AFL; n = 59) and paroxysmal supraventricular tachycardia (SVT; n = 110). Follow-up levels were obtained at 1 and 6 months.
Peripheral levels of both biomarkers were significantly higher in the AFL group. After multivariate adjustment, only those in the AFL group who presented in AFL or atrial fibrillation (AF) had significantly elevated CRP levels (odds ratio 1.26; P = .033). Levels of each marker were similar in the CS and peripheral blood in the SVT group; in the AFL group, both CRP and IL-6 were significantly lower in the CS than in the periphery (P = .0076 and P = .0021, respectively). CRP was significantly lower a median of 47 days after AFL ablation (from a median of 6.28 mg/L to a median of 2.92 mg/L; P = .028) and remained reduced at second follow-up. IL-6 decreased across three time points after AFL ablation (P = .002). No reduction in inflammatory biomarkers was observed after SVT ablation.
CRP and IL-6 levels are elevated in patients presenting in AFL. Given the lower CS values in these patients, their origin appears to be systemic rather than cardiac. Because these levels significantly fall after ablation of AFL, the atrial tachyarrhythmia appears to be the cause (not the effect) of the inflammation.

1 Follower
 · 
86 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is the most common sustained arrhythmia and a challenging clinical problem encountered in daily clinical practice. There is an increasing body of evidence linking inflammation to a broad spectrum of cardiovascular conditions including AF. Historical evidence supports an association between AF and inflammation and is consistent with the association of AF with inflammatory conditions of the heart, such as myocarditis and pericarditis. AF has been associated with myocardial oxidative stress, and antioxidant agents have demonstrated antiarrhythmic benefit in humans. Increased plasma interleukin (IL)-6, C-reactive protein (CRP), and plasma viscosity support the existence of an inflammatory state among "typical" populations with chronic AF. These indexes of inflammation are related to the prothrombotic state and may be linked to the clinical characteristics of the patients (underlying vascular disease and comorbidities), rather than simply to the presence of AF itself. It has been suggested that inflammation may have a role in the development of atrial arrhythmias after cardiac surgery, and that a genetic predisposition to develop postoperative complications exists. Cytokines can have a prognostic significance; IL-6 levels, CRP, and other cytokines may have prognostic value in AF. Cytokine lowering therapies, statins, angiotensin converting enzyme inhibitors and other anti-inflammatory agents may have a role in the treatment of AF. The present article provides an overview of the evidence linking inflammatory cytokines to AF and their therapeutic and prognostic implications.
    Journal of Inflammation Research 08/2010; 3:75-97. DOI:10.2147/JIR.S10095
  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is the most common cardiac arrhythmia, contributing to increased morbidity and reduced survival through its associations with stroke and heart failure. AF contributes to a four- to fivefold increase in the risk of stroke in the general population and is responsible for 10-15 % of all ischemic strokes. Diagnosis and treatment of AF require considerable health care resources. Current therapies to restore sinus rhythm in AF are suboptimal and are limited either by their pro-arrhythmic effects or by their procedure-related complications. These limitations have necessitated identification of newer therapeutic targets to expand the treatment options. There has been a considerable amount of research interest in investigating the mechanisms of initiation and propagation of AF. Despite extensive research focused on the pathogenesis of AF, a thorough understanding of various pathways mediating initiation and propagation of AF still remains limited. Research efforts focused on the identification of these pathways and molecular mediators have generated a great degree of interest for developing more targeted therapies. This review discusses the potential therapeutic targets and the results from experimental and clinical research investigating these targets.
    American Journal of Cardiovascular Drugs 08/2014; 14(6). DOI:10.1007/s40256-014-0085-0 · 2.20 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: There are two FDA approved catheters (THERMOCOOL RF and Arctic Front Advance cryoballoon) for the treatment of drug refractory and symptomatic paroxysmal atrial fibrillation (AF). Each tool is used to ablate the area surrounding the pulmonary veins (PVs). However, no study has described and quantified the ablated surface area after the application of cryoablation lesions with the second generation cryoballoon. Objective: This study was conducted to determine the area of ablation during cryoballoon PV isolation. Methods: 43 patients had a pre]procedural computed tomography angiography (CTA) of the LA to accurately access spatial chamber dimensions. Before and after the ablation procedure, a detailed 3 dimensional electroanatomical map (3D EAM) of the LA was collected and overlaid with the CTA to improve the accuracy of the data recordings. Results: The LA posterior wall had a mean surface area of 31.1 +/- 1.6 cm2 (SEM). Left- and right-sided antral PV surface areas of cryoballoon ablation were not statistically different (P = 0.935), which measured 11.4 +/- 0.8 cm2 (SEM) and 11.3 +/- 0.8 cm2 (SEM), respectively. In total, 27% of the posterior LA wall remained un]ablated, electrically functional, and homogenous with regard to voltage conductivity. This ablation strategy resulted in a 95.3% freedom from AF at 6 months. Conclusions: The area of LA posterior wall ablation with the cryoballoon catheter is wide and antral, and the resulting LA posterior wall de]bulking could be a part of the cryoballoon efficacy beyond discrete PV isolation.
    Heart Rhythm 11/2014; 12(2). DOI:10.1016/j.hrthm.2014.11.012 · 4.92 Impact Factor