Prevention of atrial fibrillation in patients with symptomatic chronic heart failure by candesartan in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program

Ducharme, Anique; Swedberg, Karl; Pfeffer, Marc A.; Cohen‐Solal, Alain; Granger, Christopher B.; Maggioni, Aldo P.; Michelson, Eric L.; McMurray, John J.V.; Olsson, Lars; Rouleau, Jean L.; Young, James B.; Olofsson, Bertil; Puu, Margareta; Yusuf, Salim

doi:10.1016/j.ahj.2005.06.036

Cited by 275 publications

(205 citation statements)

References 38 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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“…His analysis provides evidence that ACEI use may be beneficial in some patients with AF. It has revealed in the CHARM program 23 that treatment with the angiotensin receptor blocker candesartan, reduced the incidence of AF in a large, broadly-based, population of patients with symptomatic chronic heart failure, which provided the opportunity to prospectively determine the effect of candesartan on the incidence of new AF in this CHF population. Madrid et al 24 found that patients treated with amiodarone plus irbesartan had a lower rate of recurrence of atrial fibrillation than did with amiodarone alone.…”

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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“…To zmniejszenie zapadalności na AF jest mniejsze u pacjentów z HFpEF [239], natomiast nie obserwuje się go u pacjentów bez niewydolności serca [240][241][242]. Nie wydaje się, aby hamowanie neprilizyny zwiększało ten efekt [224].…”

Section: Prewencja Migotania Przedsionków U Pacjentów Z Niewydolnościunclassified

“…Wydaje się, że inhibitory ACE i ARB zapobiegają nowemu AF u pacjentów z dysfunkcją lewej komory oraz u pacjentów z nadciśnieniem tętniczym i przerostem lewej komory [219,236,237,239,246,250,686]. Hamowanie neprilizyny wymaga dalszych badań, ale nie wydaje się zwięk-szać tego efektu [224].…”

Section: Antyarytmiczne Działanie Leków Nieantyarytmicznychunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

2,319

4,163

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Prevention of atrial fibrillation in patients with symptomatic chronic heart failure by candesartan in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program

Cited by 275 publications

References 38 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

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

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

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