Abstract

We compared plasma levels of biomarkers of inflammation (CRP) and oxidation (oxLDL), determined at study inclusion in lone atrial fibrillation (LAF) patients (48.6 ± 11.5 years; 74.0% men) and sinus rhythm controls (49.7 ± 9.3 years; 72.7% men, P > 0.05), and investigated the association of baseline CRP and oxLDL levels with the risk for vascular disease (VD) development (hypertension, cerebrovascular disease, coronary/peripheral artery disease, and pulmonary embolism) during prospective follow-up. Baseline CRP (1.2 [0.7–1.9] mg/L versus 1.1 [0.7–1.6] mg/L) and oxLDL levels (66.3 ± 21.2 U/L versus 57.1 ± 14.6 U/L) were higher in LAF patients (both P < 0.05). Following a median of 36 months, incident VD occurred in 14 (28.0%) LAF patients, all of whom developed arterial hypertension, and in 5 (11.4%) controls (hypertension, n = 4; coronary artery disease, n = 1), P < 0.05. LAF patients developed VD more frequently and at a younger age. Both CRP (HR, 2.54; 95% CI, 1.26–5.12; P = 0.009) and oxLDL (HR, 2.24; 95% CI, 1.14–4.40; P = 0.019) were multivariate predictors of incident hypertension in LAF patients, but not in the controls. Further research should clarify clinical relevance of investigated biomarkers for risk stratification and treatment of LAF patients.

Highlights

  • Lone atrial fibrillation (AF) is a term commonly used to denote AF occurring in a small subset (∼3%) of patients without identifiable cardiovascular and extracardiac comorbidities or triggering factors [1, 2]

  • We have demonstrated increased plasma levels of biomarkers of inflammation (CRP) and oxidative stress in carefully characterized lone AF patients compared to healthy controls in sinus rhythm

  • We have demonstrated that baseline plasma levels of CRP and oxLDL are associated with the risk for incident vascular disease during a median 3-year follow-up in lone AF patients, but not in healthy controls

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Summary

Introduction

Lone atrial fibrillation (AF) is a term commonly used to denote AF occurring in a small subset (∼3%) of patients without identifiable cardiovascular and extracardiac comorbidities or triggering factors [1, 2]. With growing understanding of AF pathophysiology, the existence of truly lone AF has been challenged, since emerging risk factors and evidence of subclinical vascular disease have been found in some apparently lone AF patients [2,3,4]. Determinants of future development of vascular disease in previously lone AF patients have not been broadly investigated. Current evidence indicates that chronic low-grade inflammation in association with oxidative stress could represent a link between AF and (subclinical) vascular disease [7,8,9,10]. Increased inflammatory and oxidative burden has been associated with AF recurrence and perpetuation [11], but the association of markers of inflammation and oxidative stress with the development of vascular disease in lone AF remains unknown

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