Non‐Antiarrhythmic Drugs in Atrial Fibrillation: A Review of Non‐Antiarrhythmic Agents in Prevention of Atrial Fibrillation

Lally, James A.; Gnall, M D O Eric; Seltzer, M.B.A. Jonathan; Kowey, Peter R.

doi:10.1111/j.1540-8167.2007.00874.x

Cited by 25 publications

(14 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There seems to be increasing evidence to suggest that ACEI have the potential to prevent post-operative AF, possibly because of its ability to decrease left atrial stretching secondary to afterload reduction and atrial remodeling (37,38). However, it is important to understand that the publication of 2 metaanalyses (38,39) did not include any cardiac surgical patients and, therefore, the evidence for this potential benefit in cardiac surgery is weak.…”

Section: Discussionmentioning

confidence: 97%

Effects of Angiotensin-Converting Enzyme Inhibitor Therapy on Clinical Outcome in Patients Undergoing Coronary Artery Bypass Grafting

Miceli

Capoun

Fino

et al. 2009

Journal of the American College of Cardiology

132

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 97%

Effects of Angiotensin-Converting Enzyme Inhibitor Therapy on Clinical Outcome in Patients Undergoing Coronary Artery Bypass Grafting

Miceli

Capoun

Fino

et al. 2009

Journal of the American College of Cardiology

132

View full text Add to dashboard Cite

show abstract

“…Upstream therapy includes a variety of agents, such as those targeting the RAS (angiotensin-converting enzyme inhibitors [ACEIs] or angiotensin receptor blockers [ARBs]), HMG-CoA reductase inhibitors (statins), corticosteroids, and N-3 polyunsaturated fatty acids (PUFAs). [15] AF may be prevented or reduced by the prevention of cardiac structural remodeling through one or more of the following mechanisms: by the reduction of fibrosis, inflammation and oxidative stress; by the improvement of hemodynamics and the reduction of wall stress and atrial cell stretch due to lowering of BP and reduced left ventricular (LV) diastolic pressure; and by preventing the development of coronary atherosclerosis.…”

Section: Upstream Therapies For Af: New Treatment Approaches and Timimentioning

confidence: 99%

Non-Antiarrhythmic Drugs to Prevent Atrial Fibrillation

Moro

Hernández‐Madrid

Matía

2010

American Journal Cardiovascular Drugs

View full text Add to dashboard Cite

Atrial fibrillation (AF) is the most frequent arrhythmia found in clinical practice. The majority of patients with AF are still candidates for antiarrhythmic drug treatment, not only for acute reversion to sinus rhythm but also for long-term treatment to prevent recurrences of AF. Currently available antiarrhythmic drugs, however, are unable to provide complete efficacy in all patients, and present problematic risks of proarrhythmia. The progressively increasing prevalence of AF supports the need to develop improved therapeutic approaches for the clinical management of arrhythmia. Accordingly, new treatment techniques aimed at suppressing the origin of the arrhythmogenic foci have been developed in the last decade. However, ablative treatments are only available for selected patients. Because of these factors, and also because primary prevention of AF should be our goal, the introduction of non-antiarrhythmic agents that could prevent both new-onset AF and recurrences of AF may eventually improve patient outcomes and reduce the incidence of this epidemic disease. The potential clinical value of these non-antiarrhythmic options is currently under active investigation. There is now clinical and experimental evidence that many drugs may have beneficial effects in preventing AF through several possible mechanisms. Non-antiarrhythmic drugs, such as ACE inhibitors and angiotensin receptor blockers, HMG-CoA reductase inhibitors (statins), corticosteroids, and N-3 polyunsaturated fatty acids may have a positive effect in patients with AF or in preventing AF in patients at risk.

show abstract

“…Pharmacological interference with signal transduction pathways has been explored as non-ion channel-targeted approach to reverse structural remodeling [87][88][89][90][91][92][93]. This strategy holds the theoretical advantage of avoiding the proarrhythmic liability of traditional antiarrhythmic therapy, with an extended benefit on the underlying cardiac diseases [57].…”

Section: Atrial Structural Remodeling As a Candidate Drug Targetmentioning

confidence: 99%

“…Evidence has begun to accrue in support of the antiarrhythmic properties of drugs that cannot be classified as purely antiarrhythmics and are encompassed in the term "upstream therapies", which include a variety of agents such as renin angiotensin aldosterone system (RAAS) blockers, statins, glucocorticoids and omega-3 polyunsaturated fatty acids (PUFAs) ( Table 1) [90][91][92][93]. Because of the advantage of targeting both underlying cardiovascular diseases and the arrhythmogenic substrate, both primary and secondary prevention have been speculated as an attractive perspective in AF [202,203].…”

Section: Pharmacological Control Of Struc-tural Remodeling: Upstream mentioning

confidence: 99%

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

Raschi¹,

Boriani²,

Ponti³

2011

CDT

View full text Add to dashboard Cite

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.

show abstract

Non‐Antiarrhythmic Drugs in Atrial Fibrillation: A Review of Non‐Antiarrhythmic Agents in Prevention of Atrial Fibrillation

Cited by 25 publications

References 79 publications

Effects of Angiotensin-Converting Enzyme Inhibitor Therapy on Clinical Outcome in Patients Undergoing Coronary Artery Bypass Grafting

Effects of Angiotensin-Converting Enzyme Inhibitor Therapy on Clinical Outcome in Patients Undergoing Coronary Artery Bypass Grafting

Non-Antiarrhythmic Drugs to Prevent Atrial Fibrillation

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

Contact Info

Product

Resources

About