Angiotensin II receptor blockers in the prevention of atrial fibrillation

Barra, Silvia; Silvestri, Nunzia; Vitagliano, Giancarlo; Madrid, Alfredo; Gaeta, Giovanni Battista

doi:10.1517/14656560902973736

Cited by 4 publications

(4 citation statements)

References 97 publications

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“…These factors are in turn induced by, or associated with, hypertension, heart failure, or coronary artery disease 110-113. Studies of drugs designed to directly or indirectly mitigate these precipitating factors, such as ACE inhibitors, angiotensin II receptor blockers (ARBs), omega-3 polyunsaturated fatty acids, and statins, have yielded variable results 110,111,114-117. The precise value of upstream therapy in the treatment of AF varies substantially by AF pathology 111,116-118.…”

Section: Upstream Therapymentioning

confidence: 99%

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New developments in atrial antiarrhythmic drug therapy

Burashnikov

Antzelevitch

2010

Nat Rev Cardiol

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Atrial fibrillation (AF) is a growing clinical problem associated with increased morbidity and mortality. Currently available antiarrhythmic drugs (AADs), although highly effective in acute cardioversion of paroxysmal AF, are generally only moderately successful in long-term maintenance of sinus rhythm. The use of AADs is often associated with an increased risk of ventricular proarrhythmia, extracardiac toxicity, and exacerbation of concomitant diseases such as heart failure. AF is commonly associated with intracardiac and extracardiac disease, which can modulate the efficacy and safety of AAD therapy. In light of the multifactorial intracardiac and extracardiac causes of AF generation, current development of anti-AF agents is focused on modulation of ion channel activity as well as on upstream therapies that reduce structural substrates. The available data indicate that multiple ion channel blockers exhibiting potent inhibition of peak INa with relatively rapid unbinding kinetics, as well as inhibition of late INa and IKr, may be preferable for the management of AF when considering both safety and efficacy.

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Section: Upstream Therapymentioning

confidence: 99%

“…Most of the current clinical data on upstream AF therapy are, however, derived from observational studies that were not sufficiently powered, and these findings do not warrant rejection or widespread use of any of the approaches 111,115-117. The results of several large randomized placebo-controlled trials are now available.…”

Section: Upstream Therapymentioning

confidence: 99%

New developments in atrial antiarrhythmic drug therapy

Burashnikov

Antzelevitch

2010

Nat Rev Cardiol

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“…Indeed, there is an increasing body of experimental evidence that the use of angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) may have a corollary beneficial effect in AF [205][206][207][208][209][210][211][212][213][214]. Interestingly, polymorphisms in AngII-related genes have been shown to affect the risk of AF [215].…”

Section: Renin Amgiotensin Alsosterone System (Raas) Blockersmentioning

confidence: 99%

“…Several authors reviewed published clinical studies to assess the role of RAAS inhibitors in preventing AF [92,93,213,253]. Unfortunately, data mining and across-trial comparisons are challenging and somewhat controversial because of relevant limitations: "there are multiple challenges to examining existing clinical trial data" [43].…”

Section: Renin Amgiotensin Alsosterone System (Raas) Blockersmentioning

confidence: 99%

Targeting the Arrhythmogenic Substrate in Atrial Fibrillation: Focus on Structural Remodeling

Raschi¹,

Boriani²,

Ponti³

2011

CDT

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Atrial fibrillation (AF) is an emerging clinical problem with multifaceted issues: current and expected prevalence, significant morbidity, potentially fatal outcome (e.g., stroke) and gaps in therapeutic approaches. Current anti-arrhythmic strategies not only fail to guarantee effective rhythm control, but also cause "on target" (i.e., pro-arrhythmia, namely torsade de pointes) and "off target" (i.e., extra-cardiac toxicities) side effects. Although a number of drugs have just come out of the pipeline with promising results (e.g., dronedarone), the question arises whether channel-targeted drugs represent the only viable approach. A body of evidence has emerged supporting structural remodeling as the main arrhythmogenic substrate perpetuating AF. Fibrosis, inflammation and oxidative stress appear strongly interconnected in the pathogenesis of remodeling-induced abnormalities. Moreover, insights into extracellular matrix network strongly suggested an active cross-talk within the cardiac microenvironment, which should be further investigated as promising "anti-remodeling" approach. Therefore, pharmacological modulation of non-ionic targets (the so called "upstream" therapy) has gained interest as a preventive strategy in AF. At the present state of knowledge, renin-angiotensin-aldosterone system blockers and statins offer evidence for potential clinical exploitation, while several remodeling-targeted therapies have been tested only experimentally or failed when studied for human validation. Fascinating and innovative strategies have been proposed (e.g., miRNAs modulation), but the actual benefit is debated. This review will provide mechanistic insights into structural remodeling and highlight emerging upstream strategies in AF management.

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Aliskiren protecting atrial structural remodeling from rapid atrial pacing in a canine model

Zhao

Chen

Liu

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

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Atrial fibrillation (AF) contributing to the increasing mortality risk is the most common disease in clinical practice. Owing to the side effects and relative inefficacy of current antiarrhythmic drugs, some research focuses on renin-angiotensin-aldosterone system (RAS) for finding out the new treatment of AF. The purpose of this study is to confirm whether aliskiren as a proximal inhibitor of renin, which completely inhibits RAS, has beneficial effects on atrial structural remodeling in AF. In this study, rapid atrial pacing was induced at 500 beats per minute for 2 weeks in a canine model. A different dose of aliskiren was given orally for 2 weeks before rapid atrial pacing. HE staining and Masson's staining were used for analysis of myocardial fibrosis. TGF-β1, signal pathways, and pro-inflammatory cytokines were shown for the mechanism of structural remodeling after the treatment of aliskiren. Serious atrial fibrosis was induced by rapid atrial pacing, followed by the elevated TGF-β1, upregulated MEK and ERK1/2, and increased inflammatory factors. Aliskiren could apparently improve myocardial fibrosis by reducing the expression of TGF-β1, inhibiting MEK and ERK1/2 signal pathways, and decreasing IL-18 and TLR4 in both serum and atrial tissue. In conclusion, aliskiren could prevent atrial structural remodeling from rapid atrial pacing for 2 weeks. Aliskiren may play a potential beneficial role in the treatment of AF induced by rapid atrial pacing.

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Angiotensin II receptor blockers in the prevention of atrial fibrillation

Cited by 4 publications

References 97 publications

New developments in atrial antiarrhythmic drug therapy

New developments in atrial antiarrhythmic drug therapy

Targeting the Arrhythmogenic Substrate in Atrial Fibrillation: Focus on Structural Remodeling

Aliskiren protecting atrial structural remodeling from rapid atrial pacing in a canine model

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