A proposal for new clinical concepts in the management of atrial fibrillation

Al‐Khatib, Sana M.; Calkins, Hugh; Halperin, Jonathan L.; Kirchhof, Paulus; Lip, Gregory Y.H.; Nattel, Stanley; Ruskin, Jeremy N.; Banerjee, Amitava; Blendea, Dan; Guasch, Eduard; Needleman, Matthew; Savelieva, Irina; Viles-González, Juan F.; Williams, Eric S.

doi:10.1016/j.ahj.2012.05.017

Cited by 43 publications

(32 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11 Further progression occurs at increasing rates, with 35% to 40% of patients with persistent AF developing permanent AF <1 year. 4 The progression rate is lowest in young patients without associated heart disease (lone AF), amounting to 1% to 3% per year. 16 However, there exists a wide variability in AF progression among patients.…”

Section: Conceptual Framework Af As a Progressive Diseasementioning

confidence: 99%

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Heijman

Voigt

Nattel

et al. 2014

Circulation Research

Self Cite

557

603

View full text Add to dashboard Cite

Atrial fibrillation (AF) is the most common clinically relevant arrhythmia and is associated with increased morbidity and mortality. The incidence of AF is expected to continue to rise with the aging of the population. AF is generally considered to be a progressive condition, occurring first in a paroxysmal form, then in persistent, and then long-standing persistent (chronic or permanent) forms. However, not all patients go through every phase, and the time spent in each can vary widely. Research over the past decades has identified a multitude of pathophysiological processes contributing to the initiation, maintenance, and progression of AF. However, many aspects of AF pathophysiology remain incompletely understood. In this review, we discuss the cellular and molecular electrophysiology of AF initiation, maintenance, and progression, predominantly based on recent data obtained in human tissue and animal models. The central role of Ca 2+ -handling abnormalities in both focal ectopic activity and AF substrate progression is discussed, along with the underlying molecular basis. We also deal with the ionic determinants that govern AF initiation and maintenance, as well as the structural remodeling that stabilizes AF-maintaining re-entrant mechanisms and finally makes the arrhythmia refractory to therapy. In addition, we highlight important gaps in our current understanding, particularly with respect to the translation of these concepts to the clinical setting. Ultimately, a comprehensive understanding of AF pathophysiology is expected to foster the development of improved pharmacological and nonpharmacological therapeutic approaches and to greatly improve clinical management.

show abstract

Section: Conceptual Framework Af As a Progressive Diseasementioning

confidence: 99%

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Heijman

Voigt

Nattel

et al. 2014

Circulation Research

Self Cite

557

603

View full text Add to dashboard Cite

show abstract

“…3 Predisposing factors for all 3 mechanisms include cardiac aging, genotype, ischemic heart disease, and hyperthyroidism. 4 …”

Section: The Pathogenesis Of Atrial Fibrillationmentioning

confidence: 99%

Inflammation and C-Reactive Protein in Atrial Fibrillation: Cause or Effect?

Galea¹,

Cardillo²,

Caroli³

et al. 2014

Texas Heart Institute Journal

View full text Add to dashboard Cite

show abstract

“…Stroke risk was assessed using the CHADS 2 16,17 The R 2 CHADS 2 score incorporated the components of the CHADS 2 score and also gave 2 points for renal dysfunction defined as eGFR <60 mL/min. 12 eGFR was calculated using the Cockroft-Gault equation: (140-age)×weight (kg)×(0.85 if female)/72×serum creatinine (mg/dL).…”

Section: Patients and Risk Scoresmentioning

confidence: 99%

“…1,2 Major complications occur between 3.9% and 5.1% and can include thromboembolic complications in 1%. [3][4][5][6] Although the thromboembolic risk seems to be increased after ablation, there is the suggestion of a reduction in thromboembolic event (TE) rates during long-term follow-up.…”

mentioning

confidence: 99%

“…Although previous studies suggest that both the CHADS 2 and CHA 2 DS 2 -VASc scores, as well as renal dysfunction, are useful predictors for thromboembolic complications after ablation, they are hampered by small sample sizes, inclusion of few high-risk patients, incomplete follow-up, and an unknown number of patients on anticoagulation with possible underuse. 4,10,11 Renal dysfunction was incorporated in the R 2 CHADS 2 risk score by adding 2 additional points for estimated glomerular filtration rate (eGFR) <60 mL/min per 1.73 m 2 as an additional risk factor to the CHADS 2 score and demonstrated marginal additive predictive power over the CHADS 2 score in predicting TE in a selected anticoagulated trial patient cohort with nonvalvular AF, 12 whereas in real-world cohorts, renal impairment did not independently add to stroke risk scores to improve their predictive value. 13,14 Despite this controversy, this score has not been evaluated in patients with AF after catheter ablation.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Renal Dysfunction, Stroke Risk Scores (CHADS ₂ , CHA ₂ DS ₂ -VASc, and R ₂ CHADS ₂ ), and the Risk of Thromboembolic Events After Catheter Ablation of Atrial Fibrillation

Kornej

Hindricks

Kosiuk

et al. 2013

Circ: Arrhythmia and Electrophysiology

Self Cite

View full text Add to dashboard Cite

Background-There are limited data on the predictive value of stroke risk scores for thromboembolic events (TEs) after catheter ablation of atrial fibrillation (AF). Our objectives were to report the incidence of TEs after AF ablation in a large contemporary AF ablation cohort and to investigate the impact of renal dysfunction and the value of stroke risk stratification scores (CHADS 2 , CHA 2 DS 2 -VASc, and R 2 CHADS 2 ) for predicting TE after AF ablation. Methods and Results-Using

show abstract

A proposal for new clinical concepts in the management of atrial fibrillation

Cited by 43 publications

References 60 publications

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Inflammation and C-Reactive Protein in Atrial Fibrillation: Cause or Effect?

Renal Dysfunction, Stroke Risk Scores (CHADS ₂ , CHA ₂ DS ₂ -VASc, and R ₂ CHADS ₂ ), and the Risk of Thromboembolic Events After Catheter Ablation of Atrial Fibrillation

Contact Info

Product

Resources

About

A proposal for new clinical concepts in the management of atrial fibrillation

Cited by 43 publications

References 60 publications

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Cellular and Molecular Electrophysiology of Atrial Fibrillation Initiation, Maintenance, and Progression

Inflammation and C-Reactive Protein in Atrial Fibrillation: Cause or Effect?

Renal Dysfunction, Stroke Risk Scores (CHADS 2 , CHA 2 DS 2 -VASc, and R 2 CHADS 2 ), and the Risk of Thromboembolic Events After Catheter Ablation of Atrial Fibrillation

Contact Info

Product

Resources

About

Renal Dysfunction, Stroke Risk Scores (CHADS ₂ , CHA ₂ DS ₂ -VASc, and R ₂ CHADS ₂ ), and the Risk of Thromboembolic Events After Catheter Ablation of Atrial Fibrillation