Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation
| Autor: | Keijiro Saku, Hidenori Urata, Naoki Gondo, Koichiro Kumagai, Hideko Nakashima, Kikuo Arakawa |
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| Rok vydání: | 2003 |
| Předmět: |
Male
medicine.medical_specialty Time Factors medicine.drug_class Refractory period Hemodynamics Tetrazoles Angiotensin Receptor Antagonists Random Allocation Dogs Heart Conduction System Internal medicine Atrial Fibrillation Medicine Animals Ventricular remodeling Antihypertensive Agents Receptors Angiotensin Ventricular Remodeling business.industry Biphenyl Compounds Antagonist Cardiac Pacing Artificial Atrial fibrillation Receptor antagonist medicine.disease Angiotensin II Electrophysiology Candesartan Disease Models Animal Endocrinology Chronic Disease Cardiology Benzimidazoles Female Cardiology and Cardiovascular Medicine business medicine.drug |
| Zdroj: | Journal of the American College of Cardiology. 41(12) |
| ISSN: | 0735-1097 |
| Popis: | ObjectivesThe purpose of the present study was to evaluate the effect of angiotensin II type 1 receptor (AT1R) antagonist on chronic structural remodeling in atrial fibrillation (AF).BackgroundWe previously reported that an AT1R antagonist, candesartan, prevents acute electrical remodeling in a rapid pacing model. However, the effect of candesartan on chronic structural remodeling in AF is unclear.MethodsSustained AF was induced in 20 dogs (10 in a control group and 10 in a candesartan group) by rapid pacing of the right atrium (RA) at 400 beats/min for five weeks. Candesartan was administered orally (10 mg/kg/day) for one week before rapid pacing and was continued for five weeks. The AF duration, atrial effective refractory period (AERP) at four sites in the RA, and intra-atrial conduction time (CT) from the RA appendage to the other three sites were measured every week.ResultsThe mean AF duration in the control group after five weeks was significantly longer than that with candesartan (1,333 ± 725 vs. 411 ± 301 s, p < 0.01). The degree of AERP shortening after five weeks was not significantly different between the two groups. The CT from the RA appendage to the low RA after five weeks with candesartan was significantly shorter than that in the control (43 ± 14 vs. 68 ± 10 ms, p < 0.05). The candesartan group had a significantly lower percentage of interstitial fibrosis than the control group (7 ± 2% vs. 16 ± 1% at the RA appendage, p < 0.001).ConclusionsCandesartan can prevent the promotion of AF by suppressing the development of structural remodeling. |
| Databáze: | OpenAIRE |
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