Enalapril Decreases the Incidence of Atrial Fibrillation in Patients With Left Ventricular Dysfunction

Vermès, Emmanuelle; Tardif, Jean‐Claude; Bourassa, Martial G.; Racine, Normand; Lévesque, Sylvie; White, Michel; Guerra, Peter G.; Ducharme, Anique

doi:10.1161/01.cir.0000072793.81076.d4

Cited by 520 publications

(109 citation statements)

References 35 publications

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“…A similar finding was observed in patients with and without CHF at baseline. 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.…”

Section: Discussionsupporting

confidence: 83%

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: 83%

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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“…22 A clinical counterpart to this prevention aspect of therapy with angiotensin-converting enzyme inhibitors has been observed in clinical situations, in which it has been shown that these drugs seem to retard development of AF in certain patient subsets. 23,24 Nevertheless, once extensive structural remodeling (fibrosis) has occurred, substrate/structural remodeling becomes the dominant feature of the pathophysiology. Dominance of structural remodeling is manifest as inability to maintain sinus rhythm despite aggressive therapy.…”

Section: Inside the Clinician's Boxmentioning

confidence: 99%

Atrial Fibrillation: A Perspective

Wyse

Gersh

2004

Circulation

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A trial fibrillation (AF) is a common clinical problem that is increasing in prevalence 1 and is inextricably linked to another burgeoning cardiovascular problem, namely, congestive heart failure. 2 There is increasing evidence that AF, at least in some population subsets, may be part of a spectrum of atherosclerotic vascular disease, hypertension, inflammation, diastolic dysfunction, and the metabolic syndromes. AF is part of a family of atrial tachyarrhythmias (Figure 1). A panel of experts has recently characterized the definition and position of AF within this group of tachyarrhythmias. 3 Nonetheless, this family of tachyarrhythmias is closely interrelated, and the individual tachyarrhythmias often coexist in the same patient. Although the present discussion focuses on AF, many of the points made with regard to AF apply to these other tachyarrhythmias to varying degrees.Recently, international panels of experts have also created clinical practice guidelines 4 and perspectives on future research directions 5 for AF. These documents are a rich source of reference to the vast literature on AF. It is not the intention of the present article to review this literature, and, in particular, it is not intended that the reader will use the present article as a manual for managing AF. However, the perspective is intended to provide a framework for rational thinking about the management of AF. Inside the Basic Scientist's BoxA schema of how a basic scientist might currently view AF is presented in Figure 2. In this schema, modulating factors surround the basic elements of arrhythmogenesis, and the focus is on the mechanisms for initiation and perpetuation of AF. In this particular paradigm, a trigger and substrate interact to form a reentrant circuit or circuits, but provision is also provided for a trigger to lead directly to AF. The consequences of the interaction between triggers and substrate are dependent in part on the milieu created by multiple modulating factors and in particular the autonomic nervous system. The relative influence of these pathways in the pathogenesis of AF has always been controversial, and their deemed importance has waxed and waned over the years. Until recently, reentry based on the multiple wavelet hypothesis, attributed to Moe and Abildskov, 6 has held predominance, partly because of the mapping experiments of Allessie and colleagues. 7 However, the multiple wavelet hypothesis was preceded by hypotheses that invoked single or multiple rapidly firing foci and other reentry concepts (see Waldo 8 for a review). Recent observations on the initiation of AF from the area of the pulmonary veins 9 and the concepts of fibrillatory conduction and of rotors 10 have rekindled consideration of some of the older concepts, presented some new options, and lessened the dominance of the multiple wavelet hypothesis. However, the relative roles of abnormal automaticity and reentry in the pulmonary vein region for initiation and perpetuation, respectively, of AF are entirely unclear at the present time. Furth...

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“…Experimental and observational clinical data supported reninangiotensin-aldosterone blockers in AF prevention schemes 28,29 , but subsequent large randomized trials did not demonstrate a clinical benefit in patients without an established indication for these substances 30,31 . Drugs with anti-inflammatory and antioxidative properties that were tested for the prevention of AF in several settings showed mixed outcomes 23,[32][33][34][35] .…”

mentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

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Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

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Enalapril Decreases the Incidence of Atrial Fibrillation in Patients With Left Ventricular Dysfunction

Cited by 520 publications

References 35 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

Atrial Fibrillation: A Perspective

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

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