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It is still unclear whether body mass index (BMI) affects bleeding and cardiovascular events in patients requiring oral anticoagulants (OAC) for atrial fibrillation (AF) and antiplatelet agents after percutaneous coronary intervention (PCI) for coronary artery disease (CAD). The aim of this study was to evaluate the relationship between BMI and clinical events in patients who underwent PCI under OAC therapy for AF. This was a multicenter, observational cohort study conducted at 15 institutions in Japan. AF patients who underwent PCI with drug-eluting stents for CAD were retrospectively and prospectively included. Patients were divided into the Group 1 (BMI <21.3 kg/m2) and the Group 2 (BMI ≥21.3 kg/m2) according to the first-quartile value of BMI. The primary endpoint was net adverse clinical events (NACE), a composite of major adverse cardiovascular events (MACE) and major bleeding events within one year after index PCI procedure. In the 720 patients, 180 patients (25.0%) had BMI value <21.3 kg/m2. While the rates of NACE and MACE were significantly higher in the Group 1 than the counterpart (21.1% vs. 11.9%, p = 0.003 and 17.2% vs. 8.9%, p = 0.004), that of major bleeding did not differ significantly between the 2 groups (5.6% vs. 4.3%, p = 0.54). The cumulative rate of NACE and MACE was significantly higher in the Group 1 than the Group 2 (both log-rank p = 0.002), although that of major bleeding events was equivalent between the 2 groups (log-rank p = 0.41). In multivariable Cox regression analyses, while BMI value <21.3 kg/m2 was not associated with major bleeding events, that cut-off value was an independent predictor for increased NACE and MACE. Among the patients undergoing PCI for CAD and requiring OAC for AF, BMI value was a useful indicator to predict major adverse clinical events.

Abstract Background While Cutibacterium acnes is well known for its potential to cause acne vulgaris, postsurgical infections, and other human infections, few reports have described Cutibacterium modestum infections. Thus, the clinical characteristics of C. modestum as an infectious disease are not well understood. Herein, we describe the characteristics of a case of prosthetic valve infective endocarditis caused by C. modestum. Case summary An 81-year-old man was admitted to our hospital with fever, general fatigue, and appetite loss. His past medical history included aortic valve replacement surgery and coronary artery bypass grafting for aortic valve stenosis and angina pectoris. Physical examination on admission revealed a body temperature of 39.0°C, blood pressure of 97/68 mmHg, and pulse rate of 101 b.p.m. Transthoracic echocardiography showed no prosthetic valve destruction or malfunction or obvious vegetation adhesion to the prosthetic or other valves. Bacteria initially identified as C. acnes were detected in two sets of anaerobic blood culture bottles collected upon admission. However, as the samples required 111 and 118 h to become blood culture–positive, the possibility of contaminating bacteria was high. Transoesophageal echocardiography revealed vegetation in the artificial valve. Repeated blood culture revealed the same bacteria; thus, contamination was ruled out, and the diagnosis of infective endocarditis was confirmed. Finally, 16S ribosomal RNA gene sequencing identified the detected bacteria as C. modestum rather than C. acnes. Discussion Including this case, only two cases of prosthetic valve infective endocarditis caused by C. modestum have been reported, the characteristics of which are still poorly understood.

Previous intravascular ultrasound (IVUS) studies have shown coronary artery atherosclerosis even in angiographically normal reference segment. However, IVUS has not been performed in all of the three major coronary arteries. A total of 50 patients with single-vessel disease underwent IVUS evaluation in the proximal two-thirds of the three major coronary arteries. Lumen and external elastic membrane cross-sectional areas were measured at 1-mm intervals. To compensate the difference in pullback length among coronary arteries, normalized total plaque and media volume (TPV) was calculated as TPV/number of slices in pullback × median number of slices in study population. Percent plaque and media volume (PPV) was calculated as TPV/Σ external elastic membrane cross-sectional area × 100. A cross section was defined as atherosclerotic if maximum intimal thickness exceeded 0.5 mm at any point in the vessel circumference. There was no significant difference in normalized TPV, PPV, and the incidence of abnormal intimal thickness between coronary arteries with and without significant stenosis. Frequency distribution of plaque burden was similar. Atherosclerosis is ubiquitous even in coronary arteries without angiographically significant stenosis. The extent of atherosclerosis is similar between coronary arteries with and without significant stenosis.

There is little information about the relationship between balloon inflation time and sirolimus-eluting stent (SES) expansion. In this randomized intravascular ultrasound (IVUS) study, 92 de novo lesions in native coronary arteries that underwent SES implantation were enrolled. Sirolimus-eluting stent was implanted using an inflation pressure of 14 atm. Stent balloon was gradually inflated until 14 atm in 10 s. In the short inflation group, it was deflated immediately after an image of the balloon inflated at 14 atm was taken. Stent balloon inflation lasted 60 s in the long inflation group. Intravascular ultrasound was then performed. The long balloon inflation resulted in a larger stent cross-sectional area (4.9 ± 1.6 mm 2 vs 4.3 ± 1.4 mm 2 , P < 0.05) and expansion (71% ± 13% vs 60% ± 13%, P < 0.001) compared to the short balloon inflation, although stent expansion was relatively low in both groups. The relatively longer balloon inflation time using an inflation pressure of 14 atm results in better SES expansion. However, in the majority of lesions, adequate stent expansion is not achieved even using long balloon inflation, if it is inflated at 14 atm.

Notch (N) is a transmembrane receptor that mediates cell–cell interactions to determine many cell-fate decisions. N contains EGF-like repeats, many of which have an O -fucose glycan modification that regulates N-ligand binding. This modification requires GDP- l -fucose as a donor of fucose. The GDP- l -fucose biosynthetic pathways are well understood, including the de novo pathway, which depends on GDP-mannose 4,6 dehydratase (Gmd) and GDP-4-keto-6-deoxy- d -mannose 3,5-epimerase/4-reductase (Gmer). However, the potential for intercellularly supplied GDP- l -fucose and the molecular basis of such transportation have not been explored in depth. To address these points, we studied the genetic effects of mutating Gmd and Gmer on fucose modifications in Drosophila . We found that these mutants functioned cell-nonautonomously, and that GDP- l -fucose was supplied intercellularly through gap junctions composed of Innexin-2. GDP- l -fucose was not supplied through body fluids from different isolated organs, indicating that the intercellular distribution of GDP- l -fucose is restricted within a given organ. Moreover, the gap junction-mediated supply of GDP- l -fucose was sufficient to support the fucosylation of N-glycans and the O-fucosylation of the N EGF-like repeats. Our results indicate that intercellular delivery is a metabolic pathway for nucleotide sugars in live animals under certain circumstances.

Notch (N) is a transmembrane receptor that mediates cell–cell interactions to determine many cell-fate decisions. N contains EGF-like repeats, many of which have an O-fucose glycan modification that regulates N-ligand binding. This modification requires GDP-l-fucose as a donor of fucose. The GDP-l-fucose biosynthetic pathways are well understood, including the de novo pathway, which depends on GDP-mannose 4,6 dehydratase (Gmd) and GDP-4-keto-6-deoxy-d-mannose 3,5-epimerase/4-reductase (Gmer). However, the potential for intercellularly supplied GDP-l-fucose and the molecular basis of such transportation have not been explored in depth. To address these points, we studied the genetic effects of mutating Gmd and Gmer on fucose modifications in Drosophila. We found that these mutants functioned cell-nonautonomously, and that GDP-l-fucose was supplied intercellularly through gap junctions composed of Innexin-2. GDP-l-fucose was not supplied through body fluids from different isolated organs, indicating that the intercellular distribution of GDP-l-fucose is restricted within a given organ. Moreover, the gap junction-mediated supply of GDP-l-fucose was sufficient to support the fucosylation of N-glycans and the O-fucosylation of the N EGF-like repeats. Our results indicate that intercellular delivery is a metabolic pathway for nucleotide sugars in live animals under certain circumstances.