Irbesartan in Patients with Atrial Fibrillation

Yusuf, Salim; Healey, Jeffrey S.; Pogue, Janice; Chrolavicius, Susan; Flather, Marcus; Hart, Robert G.; Hohnloser, Stefan H.; Joyner, Campbell; Pfeffer,; Connolly, Stuart J.; Roy, Luc De

doi:10.1056/nejmoa1008816

Cited by 209 publications

(53 citation statements)

References 28 publications

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“…In comparison, post‐hoc analyzes of randomized, controlled trials in patients with CHF but without known AF have suggested that RAS inhibition might reduce the incidence of new‐onset AF 33, 34, 35. In contrast, 2 prospective, randomized trials on patients with AF did not show beneficial effects of RAS inhibition with regard to future AF burden similar to our findings 36, 37. Explanatory mechanisms for the possible antiarrhythmic property of RAS inhibition, such as restrained electrical and structural remodeling, have been proposed in preclinical studies 7, 8, 9.…”

Section: Discussionsupporting

confidence: 85%

Angiotensin‐Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers Are Associated With Improved Outcome but Do Not Prevent New‐Onset Atrial Fibrillation After Acute Myocardial Infarction

Batra

Lindhagen²,

Andell

et al. 2017

JAHA

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BackgroundTreatment with renin‐angiotensin system (RAS) inhibitors might restrain the structural/electrical remodeling associated with atrial fibrillation (AF). Limited evidence exists regarding the potential benefits of RAS inhibition post‐acute myocardial infarction (AMI) in patients with AF. This study sought to assess the association between RAS inhibition and all‐cause mortality and new‐onset AF in patients with/without congestive heart failure (CHF) post‐AMI.Methods and ResultsPatients hospitalized for AMI between 2006 and 2012 were identified in Swedish registries. Patients were stratified in 4 subgroups; patients with CHF and AF (n=11 489); patients with CHF without AF (n=31 676); patients with AF without CHF (n=10 066); and patients without both CHF and AF (n=59 417). Patients exposed to RAS inhibition were compared to nontreated. Three‐year risk of all‐cause mortality and new‐onset AF was assessed using adjusted Cox regression analyses. At discharge, 83 291 (73.9%) patients received RAS inhibition. RAS inhibition was associated with lower 3‐year risk of all‐cause mortality in CHF patients with AF, adjusted hazard ratio (HR) with 95% CI 0.75 (0.70–0.81), CHF patients without AF, HR 0.65 (0.60–0.69), AF patients without CHF, HR 0.82 (0.75–0.90), and in patients without CHF and AF, HR 0.76 (0.72–0.81), respectively. RAS inhibition was not associated with lower 3‐year risk of new‐onset AF in patients without AF but with/without CHF; HR 0.96 (0.84–1.10) and 1.12 (1.02–1.22), respectively.Conclusions RAS inhibition post‐AMI was associated with lower risk of all‐cause mortality. In patients with/without CHF, RAS inhibition was not associated with lower incidence of new‐onset AF.

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Section: Discussionsupporting

confidence: 85%

Angiotensin‐Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers Are Associated With Improved Outcome but Do Not Prevent New‐Onset Atrial Fibrillation After Acute Myocardial Infarction

Batra

Lindhagen²,

Andell

et al. 2017

JAHA

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“…The patient pool included those from two parallel trials: ACTIVE A and ACTIVE W. Irbesartan appeared to have limited benefit in the outcomes assessed by the Active I investigators; there was no change in risk of MI [83]. …”

Section: Antihypertensive Drugsmentioning

confidence: 99%

A Review of the Relationship of Atrial Fibrillation and Acute Coronary Syndrome

Kea

Alligood

Manning

et al. 2016

Curr Emerg Hosp Med Rep

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Atrial fibrillation (AF) is the most common arrhythmia encountered by clinicians. Clinical decision-making focuses on reducing ischemic stroke risk in AF patients; however, AF is also associated with an increased risk of acute coronary syndromes (ACS). Patients with ACS and concurrent AF are less likely to receive appropriate therapies and more likely to experience adverse outcomes than ACS patients in sinus rhythm (SR). Clinicians may be able to stratify ACS patients at increased risk of AF development based on clinical characteristics. Evidence supporting specific therapeutic options for prevention of ACS in AF patients or for prevention of AF in ACS patients is limited, however there is some evidence of differing effects among oral anticoagulant regimens in these populations. Investigations of the relationship of AF with the full spectrum of ACS are not well described and should be the focus of future research.

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“…Most of the current clinical data on upstream AF therapy are, however, derived from observational studies that were not sufficiently powered. Generally, while many clinical studies in the early - mid 2000 th were very promising, revealing a significant AF reduction with various upstream therapy agents (i.e., ACEIs, ARBs, statins, PUFAs) in a number of AF pathologies, results of the recent studies, particularly from large randomized clinical trials, have been quite sobering (Camm et al , 2010; Disertori et al , 2009; Yusuf et al , 2011; Kowey et al , 2010; Almroth et al , 2009; Schwartz et al , 2011; Bianconi et al , 2011; Savelieva et al , 2011a; Savelieva et al , 2011b). These later data indicate that PUFAs do not significantly affect the incidence of new onset AF and AF recurrence (Camm et al , 2010; Kowey et al , 2010; Bianconi et al , 2011; Savelieva et al , 2011a; Savelieva et al , 2011b).…”

Section: 0 Upstream Therapy Targets For Afmentioning

confidence: 99%

“…These later data indicate that PUFAs do not significantly affect the incidence of new onset AF and AF recurrence (Camm et al , 2010; Kowey et al , 2010; Bianconi et al , 2011; Savelieva et al , 2011a; Savelieva et al , 2011b). ACEIs and ARBs may indeed reduce new onset AF (i.e., primary prevention) but this positive effect is limited only to patients with significant systolic dysfunction and hypertension (Camm et al , 2010; Healey et al , 2005; Maggioni et al , 2009; Disertori et al , 2009; Yusuf et al , 2011; Ducharme et al , 2006). Reasonably proven anti-AF efficacy of statins is largely limited to the prevention of new-onset AF post-operatively (Savelieva et al , 2011a; Camm et al , 2010).…”

Section: 0 Upstream Therapy Targets For Afmentioning

confidence: 99%

Novel pharmacological targets for the rhythm control management of atrial fibrillation

Burashnikov

Antzelevitch

2011

Pharmacology & Therapeutics

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Atrial fibrillation (AF) is a growing clinical problem associated with increased morbidity and mortality. Development of safe and effective pharmacological treatments for AF is one of the greatest unmet medical needs facing our society. In spite of significant progress in non-pharmacological AF treatments (largely due to the use of catheter ablation techniques), anti-arrhythmic agents (AADs) remain first line therapy for rhythm control management of AF for most AF patients. When considering efficacy, safety and tolerability, currently available AADs for rhythm control of AF are less than optimal. Ion channel inhibition remains the principal strategy for termination of AF and prevention of its recurrence. Practical clinical experience indicates that multi-ion channel blockers are generally more optimal for rhythm control of AF compared to ion channel-selective blockers. Recent studies suggest that atrial-selective sodium channel block can lead to safe and effective suppression of AF and that concurrent inhibition of potassium ion channels may potentiate this effect. An important limitation of the ion channel block approach for AF treatment is that non-electrical factors (largely structural remodeling) may importantly determine the generation of AF, so that “upstream therapy”, aimed at preventing or reversing structural remodeling, may be required for effective rhythm control management. This review focuses on novel pharmacological targets for the rhythm control management of AF.

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Irbesartan in Patients with Atrial Fibrillation

Abstract: Irbesartan did not reduce cardiovascular events in patients with atrial fibrillation. (Funded by Bristol-Myers Squibb and Sanofi-Aventis; ClinicalTrials.gov number, NCT00249795.).

Cited by 209 publications

References 28 publications

Angiotensin‐Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers Are Associated With Improved Outcome but Do Not Prevent New‐Onset Atrial Fibrillation After Acute Myocardial Infarction

Angiotensin‐Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers Are Associated With Improved Outcome but Do Not Prevent New‐Onset Atrial Fibrillation After Acute Myocardial Infarction

A Review of the Relationship of Atrial Fibrillation and Acute Coronary Syndrome

Novel pharmacological targets for the rhythm control management of atrial fibrillation

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