Catheter ablation is currently an established treatment for symptomatic paroxysmal atrial fibrillation (AF). We focused on elderly patients with a high prevalence of AF and attempted to identify the clinical factors associated with unsuccessful ablation outcomes. Among 735 consecutive patients who underwent AF ablation procedures, 108 (14.7%, 66 men) aged !75 years were included. Of them, 80 had paroxysmal AF, and the remaining 28 non-paroxysmal AF. All patients underwent pulmonary vein (PV) isolation and occasionally additional ablation. When AF recurred, redo ablation procedures were performed if the patient so desired. The mean number of ablation procedures was 1.1 ± 0.4 times per patient. During a mean follow-up of 38.7 ± 21.7 months, sinus rhythm was maintained in 100 patients (92.6%) without any antiarrhythmic drugs, but not in the remaining 8 (7.4%). Left atrial diameter (LAD, P < 0.001), left ventricular (LV) systolic diameter (P < 0.001), LV diastolic diameter (P = 0.001), non-PV AF foci (P = 0.036), and diabetes (P = 0.045) were associated with unsuccessful ablation procedures. Multivariate logistic regression analysis revealed a large LAD and non-PV AF foci were significant independent predictors of AF recurrences, with odds ratios of 0.76 (P = 0.019) and 0.04 (P = 0.023), respectively. In a total of 124 procedures, one major (0.8%) and 11 minor (8.9%) complications occurred. In elderly AF patients, catheter ablation of AF is effective and safe. Non-PV AF foci and a large LAD were independent clinical predictors of unsuccessful AF ablation outcomes.

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Background Constitutional telomeric associations are very rare events and the mechanism underlying their development is not well understood. Case presentation We here describe a female case of Turner syndrome with a 45,X,add(22)(p11.2)[25]/45,X[5]. We reconfirmed this karyotype by FISH analysis as 45,X,dic(Y;22)(p11.3;p11.2)[28]/45,X[2].ish dic(Y;22)(SRY+,DYZ1+). A possible mechanism underlying this mosaicism was a loss of dic(Y;22) followed by a monosomy rescue of chromosome 22. However, SNP microarray analysis revealed no loss of heterozygosity (LOH) in chromosome 22, although a mosaic pattern of LOH was clearly detectable at the pseudoautosomal regions of the sex chromosomes. Conclusions Our results suggest that the separation of the dicentric chromosome at the junction resulted in a loss of chromosome Y without a loss of chromosome 22, leading to this patient’s unique mosaicism. Although telomere signals were not detected by FISH at the junction, it is likely that the original dic(Y;22) chromosome was generated by unstable telomeric associations. We propose a novel “pulled apart” mechanism as the process underlying this mosaicism.

Corticosteroid therapy may not be enough to control pneumonitis in some cases of severe drug-induced lung injury (DLI); however, an advanced treatment strategy for such cases is lacking. Here, we report the case of an 88-year-old man who presented with severe DLI, caused by Sai-rei-to. The patient visited our hospital complaining of progressive dyspnea. High-resolution computed tomography of the chest demonstrated bilateral patchy ground-glass opacities and infiltrative shadows. Nasal high-flow oxygen therapy was initiated because of severe hypoxemia. Bronchoalveolar lavage on admission revealed diffuse alveolar hemorrhage. Further, as the patient had started taking Sai-rei-to a month earlier, DLI caused by Sai-rei-to was the most likely diagnosis. Therefore, Sai-rei-to was stopped and steroid pulse therapy was initiated. However, he still required high-flow oxygen therapy. We considered an alternative diagnosis of Goodpasture syndrome or anti-neutrophil cytoplasmic antibody (ANCA) related vasculitis. We initiated the administration of cyclosporin A and therapeutic plasma exchange (TPE), but his respiratory condition did not improve satisfactorily. Therefore, we also initiated intravenous immunoglobulin (IVIG) therapy for the treatment of potential vasculitis. Subsequently, his respiratory status began to improve. Further, tests for anti-glomerular basement membrane antibody, myeloperoxidase-ANCA, and proteinase 3-ANCA revealed negative results. Drug-induced lymphocyte stimulation test performed six months after withdrawing methylprednisolone was positive for Sai-rei-to. Thus, the final diagnosis was DLI due to Sai-rei-to. Our findings demonstrate that in cases of severe acute respiratory failure due to DLI, the multi-modal therapy with plasma exchange and IVIG in addition to conventional treatment with prednisolone and immunosuppressant may be beneficial.