The effect of atrial dilatation on the genesis of atrial arrhythmias

Solti, F; Vecsey, T; Kékesi, Violetta; Juhász‐Nagy, Alexander

doi:10.1093/cvr/23.10.882

Cited by 189 publications

(98 citation statements)

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“…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. To our knowledge, 2 trials have studied RAS inhibition and risk of AF post‐AMI.…”

Section: Discussionsupporting

confidence: 81%

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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: 81%

“…Also, ACEIs and ARBs have, in previous studies, shown to have antiarrhythmic properties by restraining the structural and electrical remodeling associated with atrial fibrillation (AF) 6, 7, 8, 9, 10…”

Section: Introductionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

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“…6,22,24 In a canine model of progressive heart failure, interstitial fibrosis and heterogeneous conduction were considered important determinants of the substrate for AF. 14 In human studies as well, atrial dilatation and impaired conduction were correlated with atrial arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Development of a Substrate of Atrial Fibrillation During Chronic Atrioventricular Block in the Goat

et al. 2005

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Background-Atrial dilatation is an important risk factor for atrial fibrillation (AF). In the present study, we monitored the electrophysiological changes during progressive atrial dilatation in chronically instrumented goats. Methods and Results-In 8 goats, 2 screw-in leads with piezoelectric crystals were implanted transvenously in the right atrium. After 2 weeks, atrial diameter and effective refractory period were measured. AF paroxysms were induced by burst pacing to determine the baseline AF cycle length and stability of AF. After His-bundle ablation, the above measurements were repeated once a week. After 4 weeks of complete AV block, the free wall of the right atrium was mapped and the atrium was fixed in formalin for histological analysis. After His-bundle ablation, the ventricular rate decreased from 113.8Ϯ4.8 to 44.6Ϯ2.5 bpm. Right atrial diameter increased gradually by 13.5Ϯ3.9% during 4 weeks of AV block (PϽ0.01). The duration of induced AF paroxysms increased from 4.6 seconds to 6.4 minutes (PϽ0.05). Atrial effective refractory period and AF cycle length remained constant. Spontaneous paroxysms of AF were not observed. Atrial mapping during rapid pacing revealed that slow conduction (Ͻ30 cm/s) was present in 3.7Ϯ1.0% of the mapped area (control, 0.9Ϯ0.5%, PϽ0.05). Histological analysis showed hypertrophy without atrial fibrosis. Connexin40 and connexin43 expression was unchanged. Conclusions-Chronic

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“…23 Atrial stretch induced by increased atrial pressure may be involved in the initiation and pathogenesis of AF through shortening of refractory period and lengthening of intra-atrial conduction time. 24,25 Because ACEi cause a decline in both left atrial 26 and LV end-diastolic pressures in patients with HF, 9 it is possible that these agents may decrease the susceptibility to AF simply by lowering atrial pressure and wall stress and consequently by attenuating left atrial enlargement. This hypothesis, however, seems less probable, since Li and colleagues 9 have shown experimentally a reduction in atrial fibrosis only with enalapril despite a similar decrease in left atrial pressure with hydralazine/isosorbide.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2003

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Background— Atrial fibrillation (AF) is frequently encountered in patients with heart failure (HF) and is also a predictor of morbidity and mortality in this population. Recent experimental studies have shown electrical and structural atrial remodeling with increased fibrosis in animals with HF and have suggested a preventive effect of ACE inhibitors (ACEi) on the development of AF. To verify the hypothesis that ACEi prevent the development of AF in patients with HF, we conducted a retrospective analysis of the patients from the Montreal Heart Institute (MHI) included in the Studies Of Left Ventricular Dysfunction (SOLVD). Methods and Results— Clinical charts were reviewed and serial ECGs interpreted by a single cardiologist blinded to drug allocation. Patients with AF or flutter on the baseline ECG were excluded. Baseline characteristics were obtained from the SOLVD databases. The mean follow-up was 2.9±1.0 years. Of the 391 patients randomly assigned at MHI, 374 were in sinus rhythm at the time of random assignment, with 186 taking enalapril and 188 taking placebo. Baseline characteristics were similar in the two groups except for a higher incidence of previous myocardial infarction in the enalapril group. Fifty-five patients had AF during the follow-up: 10 (5.4%) in the enalapril group and 45 (24%) in the placebo group ( P <0.0001). By Cox multivariate analysis, enalapril was the most powerful predictor for risk reduction of AF (hazard ratio, 0.22; 95% CI, 0.11 to 0.44; P <0.0001). Conclusions— Treatment with the ACEi enalapril markedly reduces the risk of development of atrial fibrillation in patients with left ventricular dysfunction.

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The effect of atrial dilatation on the genesis of atrial arrhythmias

Cited by 189 publications

References 0 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

Development of a Substrate of Atrial Fibrillation During Chronic Atrioventricular Block in the Goat

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

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