Inflammation and Atrial Fibrillation

Dr. Weeks’ Comment: So many people (my 93 year old mother included) have arrhythmia,  but ask yourself,  how many of them (or their doctors) know how important it is to remedy the inflammation?  Did you know that all cardiac ailments are driven (amplified / made worse) by inflammation?  Get your inflammation markers tested (hs-CRP, ESR, fibrinogen, homocysteine) and get your blood anti-inflamed using organic non-GMO anti-inflammatory seeds. Now, here is the astonishing research!

Inflammation as a Risk Factor for Atrial Fibrillation

Ronnier J. Avileset al

Circulation. 2003; 108:3006–3010


Background— The presence of systemic inflammation determined by elevations in C-reactive protein (CRP) has been associated with persistence of atrial fibrillation (AF). The relationship between CRP and prediction of AF has not been studied in a large population-based cohort.

Methods and Results— CRP measurement and cardiovascular assessment were performed at baseline in 5806 subjects enrolled in the Cardiovascular Health Study. Patients were followed up for a mean of 6.9±1.6 (median 7.8) years. AF was identified by self-reported history and ECGs at baseline and by ECGs and hospital discharge diagnoses at follow-up. Univariate and multivariate analyses were used to assess CRP as a predictor of baseline and future development of AF. At baseline, 315 subjects (5%) had AF. Compared with subjects in the first CRP quartile (<0.97 mg/L), subjects in the fourth quartile (>3.41 mg/L) had more AF (7.4% versus 3.7%, adjusted OR 1.8, 95% CI 1.2 to 2.5; P=0.002). Of 5491 subjects without AF at baseline, 897 (16%) developed AF during follow-up. Baseline CRP predicted higher risk for developing future AF (fourth versus first quartile adjusted hazard ratio 1.31, 95% CI 1.08 to 1.58; P=0.005). When treated as a continuous variable, elevated CRP predicted increased risk for developing future AF (adjusted hazard ratio for 1-SD increase, 1.24; 95% CI 1.11 to 1.40; P<0.001).

Conclusions— CRP is not only associated with the presence of AF but may also predict patients at increased risk for future development of AF.


Journal of the American College of Cardiology

Volume 60, Issue 22, December 2012

Inflammation in Atrial Fibrillation

Yutao Guo, et al 


Atrial fibrillation (AF) is associated with increased risk for stroke and systemic embolism. There is plausible evidence linking inflammation to the initiation and perpetuation of AF and AF-related thrombosis. Various inflammatory markers (C-reactive protein, tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-8) have been associated with AF. Proposed mechanisms linking inflammation and the prothrombotic AF state include endothelial activation/damage, production of tissue factor from monocytes, increased platelet activation, and increased expression of fibrinogen. The present review aims to provide an update on the association of inflammation and AF, including the impact of inflammatory markers on clinical presentation and outcome of AF patients.


Is atrial fibrillation an inflammatory disorder? 

Christopher J. BoosRichard A. AndersonGregory Y.H. Lip

European Heart Journal, Volume 27, Issue 2, January 2006, Pages 136–149,


There is mounting evidence to support the influence of inflammation in the pathogenesis of atrial fibrillation (AF). Indeed, AF is associated with increased levels of known inflammatory markers, even after adjustment for confounding factors. The renin–angiotensin–aldosterone system (RAAS) appears to play a key role in this process. Atrial biopsies from patients with AF have also confirmed the presence of inflammation. Furthermore, there is preliminary evidence to support a number of drug therapies that have the potential to reduce the clinical burden of AF. In this review, we present an overview of the evidence supporting a link between inflammation and AF, and some of the drug therapies, such as the angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, steroids, fish oils, and vitamin C, that might be efficacious in the prevention of AF by modulating inflammatory pathways.


Atrial fibrillation (AF) represents a genuine clinical problem in everyday practice. AF is the most common sustained arrhythmia encountered in clinical practice, affecting approximately 0.9% of the population.1–3 The prevalence of AF is strongly age-dependent, affecting approximately 1% of persons aged ≤65 years and 5% of individuals older than 65 years.4 AF is also associated with an increase in the relative risk of mortality—ranging from 1.3 to 2.34, independent of other risk factors5,6—as well as an increasing morbidity and adversely affects quality of life.7 In particular, patients who present with stroke in AF have a considerably worse outcome, defined by a higher mortality, morbidity, and longer hospital stays compared with patients who have a stroke in the absence of AF.8,9 Even patients with paroxysmal (self-terminating) and persistent AF (lasting more than 7 days or requiring cardioversion) have a risk of stroke that is similar to patients with permanent AF.10

In Western populations, hospitalizations for AF have increased by two- to three-fold in recent years.11 This is largely explained by the advent of an ageing population, the predominance of AF among the elderly, and improved survival of patients with cardiovascular disease (CVD).12 Indeed, the age-adjusted prevalence of AF among patients with ischaemic stroke has already risen by greater than 40% over the last 30 years.13 So, there is a growing need for improved primary and secondary AF prevention strategies to reduce this potentially enormous health burden.

Unfortunately, current rhythm control strategies are far from ideal. Data from five comparative studies of a primary rate control vs. rhythm control strategy for patients with a history of AF failed to show a significant superiority of rhythm control.14–18 In fact, these studies merely emphasized the limited efficacy and high side-effect profile of the currently available anti-arrhythmic drugs.19 When compared with a primary rate control strategy, rhythm control is also more expensive and leads to increased hospitalization (mainly for cardioversion) with a trend to increased mortality, without negating the need for long-term anti-coagulation.20,21 Although rhythm control may be desirable in some patients, currently available rhythm control strategies are suboptimal and there is clearly an unmet need for alternative, safer, and more effective rhythm control strategies.

There is now an increasing body of evidence linking inflammation to a broad spectrum of cardiovascular conditions, such as coronary artery disease (CAD), insulin resistance and diabetes mellitus, and hypertension.22–26 In addition, there is emerging data to support the association between inflammation and AF.27,28 This has created exciting potential opportunities to target inflammatory processes for the prevention of AF. This has lead to a paradigm shift from a more ‘electrical’ to something more ‘structural’, with the use of novel agents that can influence the inflammatory processes in AF. The aim of this article is to present an overview of the evidence linking inflammation to AF and, secondly, to highlight several pharmacological agents that have genuine potential to reduce the clinical burden of AF by modulating inflammatory pathways.


get your blood test for hs-CRP…

C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation

MK Chung, DO Martin, D Sprecher, O Wazni… – Circulation, 2001 – Am Heart Assoc

Background Atrial fibrillation (AF) may persist due to structural changes in the atria that are promoted by inflammation. C-reactive protein (CRP), a marker of systemic inflammation, predicts cardiovascular events and stroke, a common sequela of AF. 


Inflammation in the genesis and perpetuation of atrial fibrillation

MDM Engelmann, JH Svendsen – European heart journal, 2005 –

The prevalence and persistence of atrial fibrillation (AF) and the relative inefficacy of the currently available pharmacotherapy requires development of new treatment strategies. Recent findings have suggested a mechanistic link between inflammatory processes and …


C-reactive protein and atrial fibrillation

N Sata, N Hamada, T Horinouchi, S Amitani… – Japanese heart …, 2004 –

… The limitations of the study are the small patient sample size, absence of a histological examination of the atrium, and the lack of inflammatory parameters before … Because inflammationmay be caused by other factors and the other causes of atrial fibrillation remain largely …


Inflammation and the pathogenesis of atrial fibrillation

YF Hu, YJ Chen, YJ Lin, SA Chen – Nature Reviews Cardiology, 2015 –

Atrial fibrillation (AF) is the most common cardiac arrhythmia. However, the development of preventative therapies for AF has been disappointing. The infiltration of immune cells and proteins that mediate the inflammatory response in cardiac tissue and circulatory processes …


C-reactive protein and paroxysmal atrial fibrillation: evidence of the implication of an inflammatory process in paroxysmal atrial fibrillation

J Dernellis, M Panaretou – Acta cardiologica, 2001 – Taylor & Francis

Background—Detection of inflammation is best achieved by measurements of C-reactive protein (CRP). We investigated whether inflammation might promote the development of paroxysmal atrial fibrillation (PAF), and whether high levels of CRP are associated with an …


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