Inhibition of angiotensin II signaling and recurrence of atrial fibrillation in AFFIRM

Murray, Katherine T.; Rottman, Jeffrey N.; Arbogast, Patrick G.; Shemanski, Lynn; Primm, R.Kirby; Wb, Campbell; Solomon, Allen J.; Olgin, Jeffrey E.; Wilson, M.; DiMarco, John P.; Beckman, Karen J.; Dennish, George W.; Naccarelli, Gerald V.; Ray, Wayne A.

doi:10.1016/j.hrthm.2004.08.008

Cited by 65 publications

(36 citation statements)

References 26 publications

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“…21 Murray et al 22 investigated whether inhibition of endogenous angiotensin II signaling reduces the recurrence rate of AF in patients enrolled in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study. His analysis provides evidence that ACEI use may be beneficial in some patients with AF.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Chen¹,

Bing²,

He³

et al. 2009

Clinical Cardiology

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Background: Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) has been proved to have anti-inflammatory effects and is implicated as a molecular pathway involved in many cardiovascular diseases, such as hypertension. The correlation between PPARγ inflammation and AF is still unknown. Methods: Using a case-control study design, 57 patients with hypertensive AF (persistent AF: 32, paroxysmal AF: 25) were included into the study groups. A total of 32 age-matched patients with hypertension, but without AF were selected as the control group. The expressions of PPARγ, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA in monocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods. Results: The PPARγ mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 ± 0.0702 vs 0.564 ± 0.0436, P<0.01). TNF-α mRNA, IL-6 mRNA, and IL-1 were increased in patients with hypertensive AF compared to the non-AF group and it was even higher in persistent AF than in paroxysmal AF (0.721 ± 0.0541 vs 0.530 ± 0.0496, 0.567 ± 0.044 vs 0.457 ± 0. 0505, 325.61 ± 88.10 vs 190.65 ± 59.38, respectively, P<0.01). TNF-α, IL-6, and IL-1 were in negative correlation with PPARγ, the correlation coefficient was −0.854, −0.769, and −0.702, respectively (P<0.01). Conclusions: In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARγ may be involved in the pathogenesis of AF by regulation of inflammation.

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Section: Discussionmentioning

confidence: 99%

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Chen¹,

Bing²,

He³

et al. 2009

Clinical Cardiology

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“…10 However, in addition to this suppression of new-onset AF, the AFFIRM study demonstrated that ACEI treatment suppressed AF relapse in patients with congestive heart failure among patients who had been randomized to rhythm control. 20 Furthermore, previous clinical studies demonstrated that patients who had been treated with amiodarone plus ACEI or ARB had a lower rate of recurrence of AF than patients treated with amiodarone alone after electrical cardioversion in patients with persistent AF. 21 In addition, Zaman et al demonstrated abbreviated signal-averaged P-wave duration, reflecting improved atrial conduction abnormality, after successful electrical cardioversion in AF patients on long-term (6-12 months) ACEI therapy.…”

Section: Angii Blockade and Af Reverse-remodelingmentioning

confidence: 99%

Reverse-Remodeling Effects of Angiotensin II Type 1 Receptor Blocker in a Canine Atrial Fibrillation Model

Nakashima

Kumagai

2007

Circ J

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trial fibrillation (AF) is one of the most common arrhythmias, but is still difficult to treat because of its complicated electrophysiological and pathological properties. 1 AF itself causes electrical and structural changes, which are called electrical and structural remodeling, and these changes are favorable for the maintenance of AF. [2][3][4][5][6] Previous studies have shown that structural abnormalities can induce conduction heterogeneity, which promotes local reentry and leads to the development of AF. 2,4,[6][7][8] Furthermore, some studies have demonstrated that although the electrical changes induced by AF rapidly recover after conversion to sinus rhythm (SR), the structural abnormalities persist and are vulnerable to AF induction. 4,9 We previously reported that an angiotensin II type 1 receptor blocker (ARB) can help prevent the promotion of AF by suppressing the development of an arrhythmogenic structural substrate. 10 However, the reverse-remodeling effect of ARB on existing AF-induced structural changes after the termination of AF is unclear. The purpose of this study was to investigate whether ARB therapy can help to reverse AFinduced structural remodeling and suppress AF after SR is restored in a canine atrial pacing model. Circulation Journal Vol.71, December 2007 Methods Animal Preparation and GroupsAll experiments were performed in accordance with the guidelines specified by the Institutional Animal Care and Use Committee, the American Heart Association Policy on Research Animal Use, and the Public Health Service Policy on the Use of Laboratory Animals.Ten mongrel dogs of either sex, weighing 24-26 kg, were randomly divided into 2 groups. In the olmesartan group (n=10), oral administration of olmesartan (3 mg·kg -1 ·day -1 [Sankyo Co Ltd, Tokyo, Japan]) was started after rapid atrial pacing was terminated, and was continued for a 4-week recovery period. The dogs in the control group (n=10) did not receive olmesartan.All dogs were anesthetized with an intravenous injection of pentobarbital (25 mg/kg), and, after intubation and mechanical ventilation, anesthesia was maintained with halothane. A tachy-pacing generator (Medtronic Co Ltd, Minneapolis, MN, USA) was implanted in a subcutaneous pocket in the neck and attached to a pacing lead in the right atrial appendage (RAA). The chest was opened through the right fourth intercostal space, and 4 electrode pairs were sutured to 4 sites in the right atrium (appendage, and high lateral, low lateral and anterior wall). When surgery was completed, the dogs were given antibiotics and then allowed to recover. Postoperative care included the administration of antibiotics and analgesics. Experimental ProtocolBaseline Electrophysiological Study One week after the operation, the dogs were re-anesthetized with pentobarbital (25 mg/kg) and ventilated with halothane. The arterial Circ J 2007; 71: 1977 -1982 (Received April 24, 2007 revised manuscript received July 11, 2007; accepted August 7, 2007 Reverse-Remodeling Effects of Angiotensin II Type 1 Recepto...

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“…122 and LV dysfunction. [120][121][122]147,148 Patients with persistent AF who were treated with amiodarone plus irbesartan had a lower rate of recurrence of AF than did patients treated with amiodarone alone . 149 A number of large clinical trials have shown a beneficial impact of ACE inhibition on AF, however, the AF was not the primary end point in these studies.…”

Section: Medical Interventions the Angiotensin Converting Enzyme Inhimentioning

confidence: 99%

Atrial Remodeling And Atrial Fibrillation: Mechanistic Interactions And Clinical Implications

Hassan¹,

Al‐Ghamdi²

2009

J.A.F.I.B

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Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. The prevalence of AF increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. Although the pathophysiological mechanism underlying the genesis of AF has been the focus of many studies, it remains only partially understood. Conventional theories focused on the presence of multiple re-entrant circuits originating in the atria that are asynchronous and conducted at various velocities through tissues with various refractory periods. Recently, rapidly firing atrial activity in the muscular sleeves at the pulmonary veins ostia or inside the pulmonary veins have been described as potential mechanism,. AF results from a complex interaction between various initiating triggers and development of abnormal atrial tissue substrate. The development of AF leads to structural and electrical changes in the atria, a process known as remodeling. To have effective surgical or catheter ablation of AF good understanding of the possible mechanism(s) is crucial.Once initiated, AF alters atrial electrical and structural properties that promote its maintenance and recurrence. The role of atrial remodeling (AR) in the development and maintenance of AF has been the subject of many animal and human studies over the past 10-15 years. This review will discuss the mechanisms of AR, the structural, electrophysiologic, and neurohormonal changes associated with AR and it is role in initiating and maintaining AF. We will also discuss briefly the role of inflammation in AR and AF initiation and maintenance, as well as, the possible therapeutic interventions to prevent AR, and hence AF, based on the current understanding of the interaction between AF and AR.

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Inhibition of angiotensin II signaling and recurrence of atrial fibrillation in AFFIRM

Cited by 65 publications

References 26 publications

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Reverse-Remodeling Effects of Angiotensin II Type 1 Receptor Blocker in a Canine Atrial Fibrillation Model

Atrial Remodeling And Atrial Fibrillation: Mechanistic Interactions And Clinical Implications

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