3 research outputs found

    Efficacy of Long-term Flecainide Therapy in Patients with Paroxysmal Atrial Fibrillation —Analysis Based on Time of Onset—

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    This study sought to evaluate the efficacy of long-term flecainide therapy in maintaining sinus rhythms in patients with paroxysmal atrial fibrillation (AF. based on time of onset. Flecainide (150 mg/day. was administered as an antiarrhythmic drug to a total of 70 patients (54 men and 16 women: mean age 65 ± 10 years. after sinus rhythm was restored spontaneously or by electrical and/or pharmacological cardioversion. Paroxysmal AF was divided into three categories based on time of onset: diurnal type (N = 11), nocturnal type (N = 13), and mixed type (N = 46). The mean follow-up period was 37.7 ± 17.7 months. The duration of sinus rhythm maintenance in patients with diurnal and nocturnal paroxysmal AF was 32.4 ± 10.4 months and 20.8 ± 8.3 months, respectively; the duration of sinus rhythm maintenance in those with mixed paroxysmal AF was only 7.2 ± 2.1 months. Significant differences were observed in duration between diurnal and mixed cases (mean ± S.E., P < 0.05). Actuarial recurrence-free rates at 1, 3, 6, 9 and 12 months were 90.9%, 63.6%, 63.6%, 54.5%, and 54.5%, respectively, for diurnal cases; 84.6%, 76.9%, 53.8%, 38.5%, and 30.8%, respectively, for nocturnal cases; and 58.7%, 39.1%, 28.3%, 21.7%, and 15.2% respectively, for mixed cases. Significant differences in rates at 12 months were observed between diurnal and mixed cases (P < 0.05). These results suggest that flecainide is highly effective in preventing AF recurrence in patients with diurnal paroxysmal AF

    Long-term Efficacy of Combination Therapy with Anti-arrhythmic Agents and Pravastatin in Patients with Paroxysmal Atrial Fibrillation

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    Objective: To investigate the long-term effects of combination therapy with antiarrhythmic agents and pravastatin (10 mg/day) in maintaining sinus rhythm in patients with paroxysmal atrial fibrillation (AF) and hyperlipidemia. Method and Results: In all, 318 patients (mean age: 69 ± 12 years) with paroxysmal AF were divided into 2 groups, one receiving pravastatin for hyperlipidemia (pravastatin (+) group, N = 41) and the other not (pravastatin (−) group, N = 277). At 60 months, the survival rate for patients free from conversion to permanent AF was significantly greater in the pravastatin (+) group than in the pravastatin (−) group. The percentage of patients who eventually developed permanent AF despite anti-arrhythmic therapy was significantly lower in the pravastatin (+) group than in the pravastatin (−) group (9.8% vs. 25.3%). Left atrial dimensions were significantly increased in the pravastatin (−) group during the follow-up period (from 34.8 ± 6.6 mm to 37.6 ± 7.0 mm: p < 0.01). In contrast, in the pravastatin (+) group, left atrial dimensions remained unchanged between baseline and after treatment (34.4 ± 7.3 mm vs 35.5 ± 6.6 mm). Conclusion: In patients with paroxysmal AF and hyperlipidemia, addition of pravastatin to anti-arrhythmic agents seems to enhance the efficacy of these agents in maintaining sinus rhythm and preventing the development of structural remodeling in the myocardium

    Central Role of Core Binding Factor β2 in Mucosa-Associated Lymphoid Tissue Organogenesis in Mouse

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    Mucosa-associated lymphoid tissue (MALT) is a group of secondary and organized lymphoid tissue that develops at different mucosal surfaces. Peyer\u27s patches (PPs), nasopharynx-associated lymphoid tissue (NALT), and tear duct-associated lymphoid tissue (TALT) are representative MALT in the small intestine, nasal cavity, and lacrimal sac, respectively. A recent study has shown that transcriptional regulators of core binding factor (Cbf) β2 and promotor-1-transcribed Runt-related transcription factor 1 (P1-Runx1) are required for the differentiation of CD3-CD4+CD45+ lymphoid tissue inducer (LTi) cells, which initiate and trigger the developmental program of PPs, but the involvement of this pathway in NALT and TALT development remains to be elucidated. Here we report that Cbfβ2 plays an essential role in NALT and TALT development by regulating LTi cell trafficking to the NALT and TALT anlagens. Cbfβ2 was expressed in LTi cells in all three types of MALT examined. Indeed, similar to the previous finding for PPs, we found that Cbfβ2-/- mice lacked NALT and TALT lymphoid structures. However, in contrast to PPs, NALT and TALT developed normally in the absence of P1-Runx1 or other Runx family members such as Runx2 and Runx3. LTi cells for NALT and TALT differentiated normally but did not accumulate in the respective lymphoid tissue anlagens in Cbfβ2-/- mice. These findings demonstrate that Cbfβ2 is a central regulator of the MALT developmental program, but the dependency of Runx proteins on the lymphoid tissue development would differ among PPs, NALT, and TALT
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