Atorvastatin and persistent atrial fibrillation following cardioversion: a randomized placebo-controlled multicentre study

Almroth, Henrik; Höglund, Niklas; Boman, Kurt; Englund, Anders; Jensen, Steen M.; Kjellman, B; Tornvall, Per; Rosenqvist, Mårten

doi:10.1093/eurheartj/ehp006

Cited by 57 publications

(52 citation statements)

References 40 publications

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“…144 Randomized control studies have not demonstrated the benefit of statins in preventing AF recurrence in patients after electrical cardioversion. 146 Meta-analyses have not resulted in consistent conclusions about the benefits of statins in the secondary prevention of AF. 147 There is only insufficient evidence in support of the use of statins for primary or secondary prevention of AF, except for postoperative AF.…”

Section: Secondary Preventionmentioning

confidence: 99%

Guidelines for Pharmacotherapy of Atrial Fibrillation (JCS 2013)

2014

Circ J

384

130

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Section: Secondary Preventionmentioning

confidence: 99%

Guidelines for Pharmacotherapy of Atrial Fibrillation (JCS 2013)

2014

Circ J

384

130

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“…A multicenter, prospective, doubleblind trial of atorvastatin in 234 patients with persistent AF for 2 weeks before cardioversion and 4 weeks afterward demonstrated only a nonsignificant improvement in AF recurrence. 100 In the statin therapy for the prevention of atrial fibrillation trial, 64 patients were randomized to atorvastatin or placebo starting 1 week before cardioversion, then continued for 12 months. 101 There was no significant reduction in AF recurrence between the groups.…”

Section: Medications For Maintenance Of Srmentioning

confidence: 99%

Atrial Fibrillation: Antiarrhythmic Therapy

Psotka¹,

Lee²

2014

Current Problems in Cardiology

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“…33 However, as shown in Figure 7, Rac1 activity was not increased in RA samples from patients with persistent AF, and atorvastatin did not cause a mevalonate-reversible reduction in superoxide production in this group, in agreement with studies indicating little or no beneficial effect of statins in the secondary prevention of AF or in disease states (eg, heart failure) associated with atrial structural remodeling. [12][13][14][15] It should be noted that our studies in human atrial tissue are limited to samples of the RA appendage. Although the similarities in the findings obtained in human and goat RA myocardium in the presence of longstanding AF suggest that the goat is a representative model of human AF, we cannot be certain that the human LA myocardium would show the same results.…”

Section: Reactive Oxygen Species and Atrial Fibrillation-induced Elecmentioning

confidence: 99%

“…[7][8][9] In humans, NOX2-containing NADPH oxidases are the main source of ROS production in both right atrial (RA) homogenates and isolated myocytes, 6 and RA NADPH-stimulated superoxide production is independently associated with an increased risk of developing AF after cardiac surgery. 10 Statins prevent AF-induced early electric remodeling in dogs 9 and reduce the occurrence of postoperative AF in patients undergoing cardiac surgery 11 but are less effective in the secondary prevention of AF [12][13][14] or in the presence of significant atrial structural remodeling (eg, in heart failure 15 ). By inhibiting HMG CoA reductase, statins prevent the isoprenylation of Rac1 and reduce ROS formation by NADPH oxidases in cardiac tissue.…”

mentioning

confidence: 99%

Atrial Sources of Reactive Oxygen Species Vary With the Duration and Substrate of Atrial Fibrillation

et al. 2011

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Background-An altered nitric oxide-redox balance has been implicated in the pathogenesis of atrial fibrillation (AF).Statins inhibit NOX2-NADPH oxidases and prevent postoperative AF but are less effective in AF secondary prevention; the mechanisms underlying these findings are poorly understood. Methods and Results-By using goat models of pacing-induced AF or of atrial structural remodeling secondary to atrioventricular block and right atrial samples from 130 patients undergoing cardiac surgery, we found that the mechanisms responsible for the NO-redox imbalance differ between atria and with the duration and substrate of AF. Rac1 and NADPH oxidase activity and the protein level of NOX2 and p22phox were significantly increased in the left atrium of goats after 2 weeks of AF and in patients who developed postoperative AF in the absence of differences in leukocytes infiltration. Conversely, in the presence of longstanding AF or atrioventricular block, uncoupled nitric oxide synthase activity (secondary to reduced BH 4 content and/or increased arginase activity) and mitochondrial oxidases accounted for the biatrial increase in reactive oxygen species. Atorvastatin caused a mevalonate-reversible inhibition of Rac1 and NOX2-NADPH oxidase activity in right atrial samples from patients who developed postoperative AF, but it did not affect reactive oxygen species, nitric oxide synthase uncoupling, or BH 4 in patients with permanent AF. Key Words: atrial fibrillation Ⅲ free radicals Ⅲ nitric oxide synthase Ⅲ oxidative stress Ⅲ statins A trial fibrillation (AF), the most common sustained cardiac arrhythmia, is associated with significantly increased morbidity and mortality. 1 A striking feature of AF is its ability to sustain itself by inducing a number of electric and structural changes in the atrial myocardium, which in turn promote AF maintenance and increase vulnerability to relapse. 2 Although the process of AF-induced atrial remodeling and its role in begetting AF have been described in great detail in animal models of atrial tachyarrhythmia and in human AF, 2 the underlying mechanisms that result in these electric and structural changes remain unclear. Emerging data indicate that an altered nitric oxide (NO)-redox balance in the atrial myocardium may be implicated in the pathogenesis of AF and AF-induced atrial remodeling. In particular, in human and experimental atrial tachyarrhythmia, increased atrial production of reactive oxygen species (ROS) and reduced NO bioavailability are associated with atrial remodeling and increased vulnerability to AF, 3-7 both of which can be prevented by agents that decrease myocardial oxidative stress and inflammation. [7][8][9] In humans, NOX2-containing NADPH oxidases are the main source of ROS production in both right atrial (RA) homogenates and isolated myocytes, 6 and RA NADPH-stimulated superoxide production is independently associated with an increased risk of developing AF after cardiac surgery. 10 Statins prevent AF-induced early electric remodeling in dogs 9 and reduce the...

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Atorvastatin and persistent atrial fibrillation following cardioversion: a randomized placebo-controlled multicentre study

Abstract: Atorvastatin was not statistically superior to placebo with regards to maintaining SR 30 days after CV in patients with persistent AF.

Cited by 57 publications

References 40 publications

Guidelines for Pharmacotherapy of Atrial Fibrillation (JCS 2013)

Guidelines for Pharmacotherapy of Atrial Fibrillation (JCS 2013)

Atrial Fibrillation: Antiarrhythmic Therapy

Atrial Sources of Reactive Oxygen Species Vary With the Duration and Substrate of Atrial Fibrillation

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