病床あたりの循環器内科医数が急性心不全の院内死亡に与える影響

Background Little evidence is available about the number of cardiologists required for appropriate treatment of heart failure (HF). Our objective was to determine the association between the number of cardiologists per cardiology beds for treating patients with acute HF and in-hospital mortality. Methods and Results This was a cross-sectional study, and we used the Japanese Registry of All Cardiac and Vascular Diseases Diagnosis Procedure Combination discharge database. The data of patients with HF on emergency admission from April 1, 2012, to March 31, 2014, were extracted. The patients were categorized into 4 groups by the quartiles of the numbers of cardiologists per 50 cardiovascular beds (first group: median, 4.4 [interquartile range, 3.5-5.0]; second group: median, 6.7 [interquartile range, 6.5-7.5]; third group: median, 9.7 [interquartile range, 8.8-10.1]; and fourth group: median, 16.7 [interquartile range, 14.0-23.8]). Using multilevel mixed-effect logistics regression, we determined adjusted odds ratios for in-hospital mortality. We identified 154 290 patients with HF on emergency admissions. There were 29 626, 36 587, 46 451, and 41 626 patients in the first, second, third, and fourth groups, respectively. HF severity, on the basis of New York Heart Association classification, was similar in the 3 groups. Adjusted odds ratios (95% CIs) for in-hospital mortality were 0.92 (0.82-1.04; P=0.20), 0.82 (0.72-0.92; P<0.001), and 0.70 (0.61-0.80; P<0.001) for the second, third, and fourth groups, respectively. The proportion of medication used, including angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, β blockers, and mineralocorticoid receptor antagonists, was positively correlated to the number of cardiologists. Conclusions Patients hospitalized for HF in hospitals with larger numbers of cardiologists per cardiovascular beds had lower 30-day mortality.博士（医学）・甲第776号・令和3年3月15日Copyright © 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License(https://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes

たこつぼ症候群におけるカテコラミンと機械的サポートの効果

Objective: This study aimed to reveal the clinical characteristics of patients with severe Takotsubo syndrome (TTS) who needed catecholamine support (CS) or mechanical support (MS) and to identify factors associated with serious illness and in-hospital mortality. Methods: This was a nationwide retrospective study that used claims data from the Japanese registry of all cardiac and vascular diseases and the diagnosis procedure combination registry, from April 2012 to March 2016. The patients with TTS were divided into severe TTS and mild TTS groups. The severe group was defined as patients who needed CS and/or MS. Results: Among 6169 patients with TTS, 1148 (18.6%) had severe TTS. No significant difference in age was found between the two groups; however, the number of female patients was significantly lower in the severe group than in the mild group. Among 130 patients who underwent MS, 22 and 108 patients required MS alone and both MS and CS, respectively. The 30-day mortality rate was significantly higher in the severe group than in the mild group (11.4% vs 2.6%, p<0.01) and increased with age. Of the patients with severe TTS, 65.6% died within 7 days. Multivariable analysis showed that male sex (OR 1.22, p=0.03), higher Charlson scores (OR 1.11, p<0.01), comorbid pneumonia (OR 1.68, p<0.01), comorbid sepsis (OR 6.02, p<0.01) and ambulance use (OR 2.01, p<0.01) were associated with severe TTS. Conclusions: The rate of severe TTS was 18.6% among 6169 patients registered in the Japanese nationwide database, and the 30-day mortality was higher in patients with severe TTS than in those with mild TTS (11.4% vs 2.6%).博士（医学）・甲第822号・令和4年3月15日© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.This article has been accepted for publication in Heart, 2022 following peer review, and the Version of Record can be accessed online at http://dx.doi.org/10.1136/heartjnl-2021-319904.発行元が定める登録猶予期間終了の後、本文を登録予定（2023.01

高脂血症を合併する急性心筋梗塞における冠動脈血管修復過程に及ぼす多価不飽和脂肪酸の追加投与効果に関する研究

BACKGROUND Vascular healing response associated with adjunctive n-3 polyunsaturated fatty acid therapy therapy in patients receiving strong statin therapy remains unclear. The aim of this study was to evaluate the effect of polyunsaturated fatty acid therapy with eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) in addition to strong statin therapy on coronary atherosclerotic plaques using optical coherence tomography. METHODS AND RESULTS This prospective multicenter randomized controlled trial included 130 patients with acute coronary syndrome treated with strong statins. They were assigned to either statin only (control group, n=42), statin+high-dose EPA (1800 mg/day) (EPA group, n=40), statin+EPA (930 mg/day)+DHA (750 mg/day) (EPA+DHA group, n=48). Optical coherence tomography was performed at baseline and at the 8-month follow-up. The target for optical coherence tomography analysis was a nonculprit lesion with a lipid plaque. Between baseline and the 8-month follow-up, fibrous cap thickness (FCT) significantly increased in all 3 groups. There were no significant differences in the percent change for minimum FCT between the EPA or EPA+DHA group and the control group. In patients with FCT <120 µm (median value), the percent change for minimum FCT was significantly higher in the EPA or EPA+DHA group compared with the control group. CONCLUSIONS EPA or EPA+DHA therapy in addition to strong statin therapy did not significantly increase FCT in nonculprit plaques compared with strong statin therapy alone, but significantly increased FCT in patients with thinner FCT. Registration URL: https://www.umin.ac.jp/ctr/; Unique identifier: UMIN 000012825.博士（医学）・乙第1477号・令和2年12月24日Copyright © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes

PE859, a novel tau aggregation inhibitor, reduces aggregated tau and prevents onset and progression of neural dysfunction in vivo.

In tauopathies, a neural microtubule-associated protein tau (MAPT) is abnormally aggregated and forms neurofibrillary tangle. Therefore, inhibition of the tau aggregation is one of the key approaches for the treatment of these diseases. Here, we have identified a novel tau aggregation inhibitor, PE859. An oral administration of PE859 resulted in the significant reduction of sarkosyl-insoluble aggregated tau along with the prevention of onset and progression of the motor dysfunction in JNPL3 P301L-mutated human tau transgenic mice. These results suggest that PE859 is useful for the treatment of tauopathies