Background: The efficiency of atrial fibrillation (AF) ablation for heart failure with preserved ejection fraction (EF) (HFpEF) has not been well investigated due to the difficulty of diagnosing HFpEF. The HFA-PEFF score from the European Society of Cardiology has been introduced as a new non-invasive diagnostic system for HFpEF. Methods: We studied 101 persistent AF patients with EF≥50% who underwent first catheter ablation (age 70±10 years, 68 men). The HFA-PEFF score was calculated as a sum of points in echocardiographic functional and morphological, and biomarker (brain natriuretic peptide: BNP) domains. Based on the HFA-PEFF score, patients were divided into High-group (score of ≥5, n=34) and Low-group (score of <5, n=67). Results: The High-group had older, higher BNP levels, left atrial volume index (LAVI), and E/e' than those in the Low-group. However, after 1.1±0.3 procedures, BNP levels (335±247 to 111±95 vs. 167±107 to 90±134pg/mL) and LAVI (62±19 to 44±12 vs. 52±22 to 42±17ml/m 2 ) were significantly decreased in each (all p<0.05 by paired t-test) and reached levels that were not significantly different in both groups. In addition, during 13.9±15.6 months after the first procedure, although recurrences of AF/atrial tachycardia were observed in 28 patients, the Kaplan-Meier curve analysis revealed no significant difference in recurrence-free survival between the two groups (Log-rank p=0.944, Figure). Conclusion: These data suggest that AF catheter ablation is effective even in patients diagnosed with HFpEF by a high HFA-PEFF score in terms of maintaining sinus rhythm comparable to patients with lower scores and improvements in cardiac function.

IntroductionRupture of the ventricular septum sometimes occurs as a complication of acute myocardial infarction (AMI). Most patients require surgical intervention because the rupture site can expand abruptly, resulting in sudden hemodynamic collapse [1].We usually observe this complication in the setting of AMI associated with major coronary artery occlusion [2]. However, ventricular septal rupture associated with side branch occlusion due to coronary stenting for stable angina pectoris is uncommon.In this report, we describe a rare case of an elderly man who developed ventricular septal rupture due to major septal branch occlusion during coronary stenting of the left anterior descending artery. Case reportA 67-year-old man presented with jaw discomfort and a temporary loss of consciousness. He initially visited the neurology department and underwent brain computed tomography. Magnetic resonance imaging, carotid ultrasonography, and electroencephalography did not reveal any abnormalities. Therefore, the neurologist consulted our department.We performed coronary computed tomography angiography to investigate ischemic heart disease since the patient was suspected of having multiple coronary vessel stenoses with calcification. Coronary angiography revealed severe segmental stenosis in the proximal right coronary artery (RCA) and diffuse stenotic lesions in the left anterior descending artery (LAD); no collateral flow to A B S T R A C TA 67-year-old man underwent elective percutaneous coronary intervention (PCI) of the left anterior descending artery. The major septal branch became occluded during coronary stenting. The patient developed dyspnea 19 days later. Chest radiography revealed lung congestion and a pleural effusion. Transthoracic echocardiography revealed a basal ventricular septal rupture. Emergency coronary angiography did not reveal any in-stent restenosis, and the major septal branch remained occluded. Therefore, the patient underwent closure of the ventricular septal rupture. The postoperative period was uneventful, and he was discharged 29 days after the operation. Septal branch occlusion due to coronary stenting occasionally occurs during routine PCI for which recanalization is sometimes not attempted. However, this case demonstrates that occluded septal branches, although rare, may cause serious complications.

M:Outcome of recent thromboembolic occlusions of limb arteries treated with streptokinase. Br Med J 4: 639-644, 1970.

Defects in articular cartilage ultimately results in loss of joint function in rheumatoid arthritis. To investigate the influences of anti-rheumatoid drugs on chondrogenic differentiation of mesenchymal stem cell (MSC), in vitro and in vivo screening system were established. MSCs were collected and palleted in 4-microtube strips for chondrogenic induction. Quantification of formed micromasses was performed by three dimensional T2-weighted magnetic resonance imaging. For in vivo screening, scaffold or scaffoldless cartilaginous tissue were transplanted to NOD/ShiJic-scid mice for 2 months. The cartilaginous tissues were then explanted and the expressions of chondrogenic markers, including aggrecan and CD44, were assessed. We examined influence on inducted differentiation cartilages by methotrexate (MTX) and prednisolone (PSL). The volume of the chondrogenic spheroid in the presence of MTX was decreased in a dose-dependent manner, whereas no significant effect of PSL on chondrogenic differential potency were observed. The MSC-derived cartilaginous spheroid provides an effective screening tool to get the impact of anti-rheumatoid drugs on cartilaginous regeneration.

Mesenchymal stem cell (MSC)-based articular regeneration might be beneficial for both protecting and rebuilding cartilaginous tissues in the management of rheumatoid arthritis. However, it is unclear how current immunosuppressive strategies influence the multipotency of MSCs. The present study was undertaken to profile the direct effectiveness of major antirheumatic drugs including methotrexate, prednisolone, adalimumab, and tocilizumab on the multipotency of MSCs, with a special focus on chondrogenesis. The inhibitory effects of methotrexate on adipogenesis, osteogenesis, and chondrogenesis were observed to occur in a dose-dependent manner in an in vitro differentiation system. Prednisolone enhanced adipogenesis, but reduced alkaline phosphatase activity in osteoprogenitors and suppressed the formation of chondrospheroids. Adalimumab suppressed alkaline phosphatase activity, while tocilizumab diminished osteogenesis and chondrogenesis of MSCs in vitro. Chondrogenesis of antirheumatic drug-treated MSCs was also evaluated in vivo using a scaffolded spheroid-engrafted murine model. The biologics examined appeared to be relatively safe for cartilaginous formation, but methotrexate and prednisolone exhibited opposing influences on chondrogenesis. Taken together, these results reveal the direct efficacy of major antirheumatic agents on the multipotency of MSCs. Therefore, our findings suggest that optimization of medication protocols is further required for therapeutic approaches involving cartilaginous tissue engineering.