Proximal Occlusion in the Right Coronary Artery Involving the Atrial Branch as a Strong Predictor of New-Onset Atrial Fibrillation in Acute Myocardial Infarction.

Although atrial ischemic damage is an atrial fibrillation (AF) risk factor, the impact of atrial branches' occlusion on AF development after acute myocardial infarction (AMI) is unclear. Therefore, this study's purpose was to identify predictors of new-onset AF with regard to atrial branches' occlusion. We retrospectively analyzed the AMI database at our single center. Consecutive patients with AMI from June 2011 to May 2017 were enrolled. Exclusion criteria were prior AF before AMI, hemodialysis, and follow-up of < 30 days. The study enrolled 204 consecutive patients (follow-up, 543 ± 469 days; age, 66 ± 12 years; male sex, 77%). All patients underwent primary percutaneous coronary intervention. Thirty-six patients (18%) had new-onset AF in the hospital after AMI. The Killip classification ≥ 3 (41% versus 7%, P < 0.001), ejection fraction ≤ 35% (19% versus 5%, P = 0.014), ischemic occlusion of atrial branches (58% versus 28%, P < 0.001), and ischemic occlusion of atrial branches originating from the right coronary artery (52% versus 18%, P < 0.001) were more frequent in patients with new-onset AF. Multivariable logistic regression analysis showed that Killip classification ≥ 3 (odds ratio, 6.97; 95% confidence interval [CI], 2.77-17.52; P < 0.001), and ischemic occlusion of the atrial branch of the right coronary artery (odds ratio, 4.35; 95% confidence interval, 1.91-9.93; P < 0.001) were independent predictors of new-onset AF. Altogether, proximal occlusion in the right coronary artery involving the atrial branch is a strong predictor of new-onset AF after AMI.

Multicenter research of bleeding risk between prasugrel and clopidogrel in Japanese patients with coronary artery disease undergoing percutaneous coronary intervention.

Although it has been reported that prasugrel achieves stronger antiplatelet effect and fewer cardiovascular events compared to clopidogrel in Japanese patients, there are limited data comparing the safety between the 2 dose regimens. Data from 1031 consecutive patients with coronary artery disease undergoing PCI at 5 institutions from May 2014 to April 2016, who received aspirin plus either clopidogrel (619 patients) or prasugrel (412 patients), were retrospectively analyzed. The choice of clopidogrel or prasugrel was left to the operator's discretion. Adverse events were defined as a composite of bleeding, hepatopathy, leukopenia, thrombopenia, exanthema, and major adverse cardiovascular events (MACE). MACE was defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal ischemic stroke. The average follow-up period was 143 days in the prasugrel group and 263 days in the clopidogrel group. Adverse events occurred in 34.5% of patients in the prasugrel group and in 28.6% in the clopidogrel group. Although the Kaplan-Meier curves showed lower survival rates from MACE, all-bleeding, major bleeding, minor bleeding, and adverse events, in the prasugrel group compared to the clopidogrel group (log rank test p = 0.009, p = 0.001, p = 0.012, p = 0.018, and p < 0.001, respectively), multivariate Cox-regression analyses determined prasugrel as a significant risk factor for all-bleeding, minor bleeding, and adverse events, but not for MACE and major bleeding events. Dual antiplatelet therapy with prasugrel was independently associated with minor bleeding events, but not with MACE and major bleeding events, compared to clopidogrel, after PCI in common clinical settings.

Different effects of two types of H2-receptor antagonists, famotidine and roxatidine, on the mucus barrier of rat gastric mucosa.

Compared with the aggressive factors, little attention has been paid to the mucosal defensive factors in ulcer therapy, and the role of the H2-receptor antagonists in gastric mucosal protection has not been well characterized. In the present study, the effects of different types of H2-receptor antagonists (famotidine and roxatidine) on rat gastric mucus cells were investigated using both biochemical and histological methods. Each drug (famotidine, 3 mg/kg; roxatidine, 100 mg/kg) was orally administered to rats by gavage once daily for 7 days. The biosynthesis and tissue content of mucin were compared in the gastric mucosa treated with each drug. Using anti-mucin monoclonal antibodies, the mucin content and immunohistochemical localization were also compared. Both the biosynthesis and the accumulation of gastric mucin were significantly decreased in the famotidine-treated rats, but not in the roxatidine. Both the content and the immunoreactivity of surface mucus cell-derived mucin were reduced by famotidine, while they were maintained in roxatidine-treated rat stomachs. There was no difference between the groups in the content and immunoreactivity of mucous neck cell-derived mucin. H2-receptor antagonists should be classified in relation to gastric surface mucus cell function, raising the possibility of more effective ulcer therapy.

Changes in the mucus barrier of the rat during 5-fluorouracil-induced gastrointestinal mucositis.

OBJECTIVE: A frequent complication of antineoplastic chemotherapy (CT) is gastrointestinal (GI) mucositis. Although clinically this mucositis can be treated, data on the effect of CTon the mucosal defense mechanisms are scant, so the effects of 5-fluorouracil (5-FU) on mucin, one of the principal defense factors of the GI mucosa, were investigated. MATERIAL AND METHODS: 5-FU was administered orally to rats at a dose of 50 mg/kg once daily for 5 days. Using anti-mucin monoclonal antibodies, the immunoreactivity in different areas of the rats' GI tracts was compared, as well as the mucin content. Changes in the GI mucin during the process of recovery from the injury were also investigated. Immunohistochemical analysis of proliferating cell nuclear antigen (PCNA) was used to determine whether or not the effects of 5-FU on cell proliferation contributed to the changes in mucin. RESULTS: 5-FU caused significant alterations of the immunoreactivity and content of mucin in the rat GI mucosa, especially in the jejunum. The jejunal mucin content was most markedly reduced on day 1 after drug withdrawal, and increased thereafter. By day 7, the content had transiently but significantly increased approximately 1.5-fold, and returned to the basal level by day 13. The number of PCNA-positive cells strikingly decreased at day 1, but by day 7 had increased approximately 2-fold, compared with the control. CONCLUSION: The activation of mucus cells in the jejunum, if appropriately manipulated, could lead to more effective prevention of CT-induced GI mucositis.

Effects of acid antisecretory drugs on mucus barrier of the rat against 5-fluorouracil-induced gastrointestinal mucositis.

OBJECTIVE: Acid antisecretory agents are used for the prophylaxis of cancer chemotherapy (CT)-induced gastrointestinal (GI) mucositis. Although these drugs seem to be clinically beneficial, data on their effects on the GI mucosal defense during CT treatment are scant. The objective of this study was to compare the effects of omeprazole, lansoprazole, and lafutidine on mucin, a major mucus component, during 5-fluorouracil (5-FU) treatment, as a CT regimen. MATERIAL AND METHODS: Rats, weighing approximately 230 g, were divided into five groups. The control group was administered 0.5% carboxymethylcellulose orally once daily for 5 days. The second, third, fourth, and fifth groups were treated with 5-FU (50 mg/kg), 5-FU plus omeprazole (10 mg/kg), 5-FU plus lansoprazole (10 mg/kg), and 5-FU plus lafutidine (30 mg/kg) in the same way, respectively. The rats were sacrificed on the sixth day, and their stomachs and small intestines were removed. Using anti-mucin monoclonal antibodies, we compared the immunoreactivity in different areas of the rats' GI tracts as well as the mucin content. RESULTS: Body-weight decreased in rats in the 5-FU group. Lafutidine, but neither omeprazole nor lansoprazole, inhibited the 5-FU-induced weight loss. Mucosal damage and reduced mucin content in stomach and small intestine were observed in rats receiving 5-FU alone. In the stomach, all antisecretory drugs caused the protective effects against 5-FU-induced mucosal injury and alleviation of the decreased mucin accumulation. In the jejunum and ileum, lafutidine, but neither omeprazole nor lansoprazole, ameliorated the 5-FU-induced mucosal damage and decreased mucin accumulation. CONCLUSION: Lafutidine could offer the possibility of more effective prevention of CT-induced mucositis through the activation of GI mucus cells.

Biliary tuberculosis causing cicatricial stenosis after oral anti-tuberculosis therapy.

A 36-year-old Philippine woman presented with dark urine and yellow sclera. Endoscopic retrograde cholangiopancreatography (ERCP) confirmed dilatation of the intrahepatic bile ducts and also showed an irregular stricture of the common hepatic duct at the liver hilum. Histological examination of biopsies from the bile duct revealed epithelioid cell granulomas and caseous necrosis. Tubercle bacilli were then detected on polymerase chain reaction (PCR) testing of the bile, giving the diagnosis of biliary tuberculosis. Although microbiological cure was confirmed, the patient developed cicatricial stenosis of the hepatic duct. She underwent repeated treatments with endoscopic biliary drainage (EBD) tubes and percutaneous transhepatic biliary drainage (PTBD) tubes, and the stenosis was corrected after 6 years. We present a case of tuberculous biliary stricture, a condition that requires careful differentiation from the more common malignancies and needs long-term follow-up due to the risk of post-treatment cicatricial stenosis, although it is rare.

A case of "pure" preeclampsia with nephrotic syndrome before 15 weeks of gestation in a patient whose renal biopsy showed glomerular capillary endotheliosis.

A 35-year-old Japanese woman for whom a previous health checkup showed normal blood pressure and urinalysis results without serological abnormalities developed nephrotic syndrome with severe hypertension at 15 gestational weeks. The renal biopsy performed at 17 weeks of gestation showed severe glomerular capillary endotheliosis. By means of electron microscopy, no electron-dense deposits were observed in glomeruli, and foot-process arrangement was normal. Histological findings indicated the patient's glomerular damage was caused by the mechanisms of preeclampsia. The patient underwent an elective abortion at 18 weeks of gestation. Clinical abnormalities vanished completely within 3 months after the elective abortion, which provided additional evidence that proteinuria and hypertension were caused purely by pregnancy. In general, the term preeclampsia refers to new onset of hypertension and proteinuria after 20 weeks of gestation. When proteinuria or hypertension is newly observed before 20 weeks of gestation, they are practically associated with triploidy, trophoblastic disease, or antiphospholipid syndrome. However, our case was not associated with them. Therefore, we called this case "pure" preeclampsia. We confirm the notion for the first time that preeclampsia associated with glomerular capillary endotheliosis can occur before 20 weeks of gestation. In addition, this report describes the earliest onset of preeclampsia compared with previously published reports. We also discuss causes of preeclampsia in early gestation and refer to the issue of the application of renal biopsies during pregnancy.

Nitric oxide synthase activity in rat gastric mucosa contributes to mucin synthesis elicited by calcitonin gene-related peptide.

The majority of research for the calcitonin gene-related peptide (CGRP) in the stomach has been devoted to the submucosal blood flow, and only slight attention has been paid to its involvement in the gastric epithelial function. In this study, we examined the age-related change in the CGRP-containing nerves and its effects on the mucus metabolism. We compared the immunoreactivity for CGRP in the gastric mucosa of 7-week-old rats (young) to that of 52-week-old animals (middle-aged). The effects of CGRP on the mucin biosynthesis were compared using the stomachs from both young and middle-aged rats. The nitric oxide synthase (NOS) activity was measured in the surface and deep mucosa of the gastric corpus. The density of the CGRP nerve fibers was reduced in both the lamina propria and submucosa of the middle-aged rats compared to the young rats. CGRP stimulated the mucin biosynthesis in the cultured corpus mucosa from the 7-week-old rats, but not from the 52-week-old rats. The total NOS activity of the surface layer in the corpus mucosa was markedly reduced in the middle-aged rats compared to the young rats. These findings demonstrate the age-dependent reduction in the CGRP-induced mucin biosynthesis, as well as in the density of the CGRP fibers in the rat stomach. The decreased NOS activity in the surface layer of the oxyntic mucosa in the aged rats may also be a principal cause for the lack of regulation of the mucin biosynthesis by CGRP.

Assessment of myocardial perfusion and fatty acid metabolism in a patient with Churg-Strauss syndrome associated with eosinophilic heart disease.

Churg-Strauss syndrome is characterized by asthma, eosinophilia and systemic necrotizing vasculitis; cardiac involvement (ie, eosinophilic heart disease) is the major cause of morbidity and mortality, although there are no reports of an association between left ventricular dysfunction because of eosinophilic heart disease and myocardial blood flow or myocardial fatty acid metabolism. A patient presented with Churg-Strauss syndrome associated with eosinophilic heart disease that had progressed to dilated cardiomyopathy. Coronary angiography, thallium-201 ((201)Tl) and iodine-123 beta-methyl-iodophenyl pentadecanoic acid ((123)I BMIPP) myocardial single photon emission computed tomography (SPECT) were performed to evaluate left ventricular dysfunction. Although coronary angiography was normal and (201)Tl SPECT showed no apparent image defect, (123)I BMIPP SPECT showed diffuse decreased accumulation, excepting the apex. The left ventricular dysfunction in patients with eosinophilic heart disease is associated with impaired myocardial fatty acid metabolism rather than with impaired myocardial blood flow.