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Objective
Efficacy of atrial fibrillation ablation in rheumatic mitral valve disease has been regarded inferior to that in nonrheumatic diseases. This study aimed to evaluate net clinical benefits by the addition of concomitant atrial fibrillation ablation in rheumatic mitral valve surgery.Methods
Among 1229 consecutive patients with atrial fibrillation from 1997 to 2016 (54.4 ± 11.7 years; 68.2% were female), 812 (66.1%) received concomitant ablation of atrial fibrillation (ablation group), and 417 (33.9%) underwent valve surgery alone (no ablation group). Death and thromboembolic events were compared between these groups. Mortality was regarded as a competing risk to evaluate thromboembolic outcomes. To reduce selection bias, inverse probability of treatment weighting methods were performed.Results
Freedom from atrial fibrillation occurrence at 5 years was 76.5% ± 1.8% and 5.3% ± 1.1% in the ablation and no ablation groups, respectively (P < .001). The ablation group had significantly lower risks for death (hazard ratio [HR], 0.69; 95% confidence interval [CI], 0.52-0.93) and thromboembolic events (HR, 0.49; 95% CI, 0.32-0.76) than the no ablation group. Time-varying Cox analysis revealed that the occurrence of stroke after surgery was significantly associated with death (HR, 3.97; 95% CI, 2.36-6.69). In subgroup analyses, the reduction in the composite risk of death and thromboembolic events was observed in all mechanical (n = 829; HR, 0.53; 95% CI, 0.39-0.73), bioprosthetic replacement (n = 239; HR, 0.67; 95% CI, 0.41-1.08), and repair (n = 161; HR, 0.17; 95% CI, 0.06-0.52) subgroups (P for interaction = .47).Conclusions
Surgical atrial fibrillation ablation during rheumatic mitral valve surgery was associated with a lower risk of long-term mortality and thromboembolic events. Therefore, atrial fibrillation ablation for rheumatic mitral valve disease may be a reasonable option. 相似文献The effects of the endogenous antioxidant α-lipoic acid on guinea pig colon smooth muscle contraction (Gpcc) induced by hydrogen peroxide were examined. Having previously shown that the histone deacetylase (HDAC) benzamide inhibitor MGCD0103 inhibits guinea-pig smooth muscle contraction, as do various sulfur-containing antioxidants, we asked whether hybrid compounds possessing both α-lipoic acid-derived antioxidant properties and HDAC inhibitory activity could inhibit Gpcc.
Materials and methodsGuinea pig colon (Gpc) was incubated at 37°C with Krebs buffer; the four stimulants—hydrogen peroxide, carbachol, histamine, and sodium fluoride—were added independently. The response to each stimulant alone was compared with that in the presence of each of the test compounds: MGCD0103, α-lipoic acid, and two of their hybrids, UCL M084 and UCL M109.
ResultsNaF (10 mM), carbachol (0.05 μM), histamine (0.1 μM), and hydrogen peroxide (1 μM) produced Gpcc of about 50–60% above basal level. With the exception of MGCD0103 against hydrogen peroxide, all four test compounds at 1 μM—MGCD0103, α-lipoic acid, UCL M084, and UCL M109—produced a significant inhibition of 35–60% of Gpcc induced by hydrogen peroxide, NaF, and carbachol, although none reduced histamine or ovalbumin-induced Gpcc. Benzalkonium chloride (Bcl), a G-protein inhibitor, reduced the hydrogen peroxide-induced Gpcc by 35%.
ConclusionsContraction by stimulants used to induce Gpcc is known to involve G-proteins. All four test compounds—MGCD0103, α-lipoic acid and two of their hybrids, UCL M084 and UCL M109—reduced Gpcc induced by NaF and carbachol, suggesting that G-protein pathway involvement is relevant to the action of the test compounds, as is also indicated by the Bcl-induced inhibition of hydrogen peroxide-induced contractions. Additionally, α-lipoic acid and the two hybrids showed >30% inhibition of hydrogen peroxide-induced contractions, consistent with the antioxidant properties of the 1,2-dithiolane ring.
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