The role of inflammatory markers in atrial fibrillation: a review

This review is focused on the role of latent inflammation in atrial fibrillation (AF) pathogenesis. The modern views and available evidence on the association between the levels of inflammatory markers and AF development and recurrence are presented. The justification for the use of pleiotropic effects of pharmacological therapy in AF prevention and treatment is discussed.

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Atrial fibrillation ablation in heart failure

European Heart Journal Supplements ◽

10.1093/eurheartj/suaa059 ◽

2020 ◽

Vol 22 (Supplement_E) ◽

pp. E50-E53

Author(s):

Cristina Balla ◽

Riccardo Cappato

Keyword(s):

Heart Failure ◽

Atrial Fibrillation ◽

Control Strategy ◽

Rate Control ◽

Pharmacological Therapy ◽

Rhythm Control ◽

Invasive Approach ◽

Normal Cardiac Function

Abstract Atrial fibrillation (AF) and heart failure (HF) commonly coexist in the same patient and either condition predisposes to the other. Several mechanisms promote the pathophysiological relationship between AF and HF, reducing quality of life, increasing the risk of stroke, and worsening HF progression. Although restoration and maintenance of sinus rhythm would be ideal for those patients, several trials comparing rhythm and rate control failed to show a benefit of rhythm control strategy, achieved with pharmacological therapy, in terms of hospitalization for HF or death. Catheter ablation is a well-established option for symptomatic AF patients, resistant to drug therapy, with normal cardiac function. Several recent studies have shown an improvement in clinical outcomes after AF ablation in HF patients highlighting the emerging role of the invasive approach in this subset of patients. However, several concerns regarding patients’ selection and standardization of the procedure still remain to be addressed.

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Biomarkers Determining Prognosis of Atrial Fibrillation Ablation

Current Medicinal Chemistry ◽

10.2174/0929867325666180320122930 ◽

2019 ◽

Vol 26 (5) ◽

pp. 925-937 ◽

Cited By ~ 4

Author(s):

Dimitris Tsiachris ◽

George Giannopoulos ◽

Spyridon Deftereos ◽

Charis Kossyvakis ◽

Constantinos Tsioufis ◽

...

Keyword(s):

Atrial Fibrillation ◽

Catheter Ablation ◽

Inflammatory Markers ◽

Persistent Atrial Fibrillation ◽

Atrial Fibrillation Ablation ◽

Oxidative Stress Biomarkers ◽

Specific Patient ◽

Term Administration ◽

The Impact

Catheter ablation for rhythm control is recommended in specific patient populations with paroxysmal, persistent, or long-standing persistent atrial fibrillation. Pulmonary vein isolation is the cornerstone of the ablative therapy for atrial fibrillation. However, relapse is still common since the single procedure efficacy of atrial fibrillation ablation was estimated to be 60-80% in paroxysmal and 50-70% in persistent atrial fibrillation. It is important to identify predictors of successful atrial fibrillation patients ablation. In the present review, we will assess the role of available biomarkers to predict responders of an initial atrial fibrillation catheter ablation. Emphasis has been given on the role of myocardial injury biomarkers, natriuretic peptides and traditional inflammatory markers. Novel inflammatory markers, oxidative stress biomarkers and microRNAs have also been examined as predictors of a successful atrial fibrillation procedure. Notably, the impact of procedural and short-term administration of steroids, as well as the role of colchicine on preventing atrial fibrillation recurrence after ablation is thoroughly presented.

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JNK2, A Newly-Identified SERCA2 Enhancer, Augments an Arrhythmic [Ca 2+ ] SR Leak-Load Relationship

Circulation Research ◽

10.1161/circresaha.120.318409 ◽

2020 ◽

Author(s):

JiaJie Yan ◽

Dan J Bare ◽

Jaime DeSantiago ◽

Weiwei Zhao ◽

Yiming Mei ◽

...

Keyword(s):

Atrial Fibrillation ◽

Heart Function ◽

Ryanodine Receptors ◽

Specific Inhibition ◽

Increased Risk ◽

Prevention And Treatment ◽

Dual Action ◽

Stress Kinase ◽

Novel Therapeutic

Rationale: We recently discovered pivotal contributions of stress kinase JNK2 in increased risk of atrial fibrillation (AF) through enhanced diastolic sarcoplasmic reticulum (SR) Ca 2+ leak via ryanodine receptors (RyR2). However, the role of JNK2 in the function of the SR Ca 2+ -ATPase (SERCA2), essential in maintaining [Ca 2+ ] SR cycling during each heartbeat, is completely unknown. Objective: To test the hypothesis that JNK2 increases SERCA2 activity [Ca 2+ ] SR and exacerbates an arrhythmic [Ca 2+ ] SR leak-load relationship. Methods and Results: We used confocal Ca 2+ imaging in myocytes and HEK cells, biochemistry, dual Ca 2+ /voltage optical mapping in intact hearts from alcohol-exposed or aged mice (where JNK2 is activated). We found that JNK2, but not JNK1, increased SERCA2 uptake and consequently elevated [Ca 2+ ]SR load. JNK2 also associates with and phosphorylates SERCA2 proteins. JNK2 causally enhances SERCA2-ATPase activity via increased Vmax, without altering Ca 2+ affinity (Km). Unlike the CaMKII-dependent JNK2 action in SR Ca 2+ leak, JNK2-driven SERCA2 function was CaMKII-independent (not prevented by CaMKII inhibition). With CaMKII blocked, the JNK2-driven SR Ca 2+ loading alone did not significantly raise leak. However, with JNK2-CaMKII-driven SR Ca 2+ leak present, the JNK2-enhanced SR Ca 2+ uptake limited leak-induced reduction in SR Ca 2+ , normalizing Ca 2+ transient amplitude, but at a higher arrhythmogenic SR Ca 2+ leak. JNK2-specific inhibition completely normalized SR Ca 2+ handling, attenuated arrhythmic Ca 2+ activities, and alleviated AF susceptibility in aged and alcohol-exposed myocytes and intact hearts. Conclusions: We have identified a novel JNK2-induced activation of SERCA2. The dual-action of JNK2 in CaMKII-dependent arrhythmic SR Ca 2+ leak and a CaMKII-independent uptake exacerbates atrial arrhythmogenicity, while helping to maintain normal levels of Ca 2+ transients and heart function. JNK2 modulation may be a novel therapeutic target for AF prevention and treatment.

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