Effect of the cation structure on cellulose dissolution in aqueous solutions of organic onium hydroxides.

The solubility of cellulose was systematically assessed in organic onium/inium hydroxide aqueous solutions (OHAS) having assorted cations, such as phosphonium, ammonium, piperidinium, morpholinium, pyrrolidinium, and cholinium. From a dissolution test of cellulose in OHAS, it was confirmed that the single most important factor in the dissolution is the high concentration of OHAS. In addition, having a weaker hydrogen bond network around OH and H2O was found to be important to facilitate the cellulose dissolution. In NMR analysis, the OHAS with an excellent cellulose solubility, such as tetrabutylphosphonium hydroxide ([P4444]OH), exhibited a chemical shift of water (δH2O) integrated with that of OH in the low frequency region (∼4.9 ppm), while choline hydroxide ([Ch]OH) with poor cellulose solubility showed δH2O higher than 5.2 ppm. A higher δH2O means that the protons are deshielded due to a stronger hydrogen bond network around H2O and OH, which indicates a strong self-associating property of OHAS that is unfavourable for the cellulose dissolution. Assuming that the strong self-associating property can be reduced by improving the hydrophobicity of organic cations, the methyl group in N-butyl-N-methylmorpholinium hydroxide ([Mor14]OH) was replaced by a butyl chain to shield the positive charge. While [Mor14]OH dissolved only 5 wt% of cellulose, the solubility in the synthesised OHAS, N,N-dibutylmorpholinium hydroxide ([Mor44]OH), was successfully improved to 20 wt%. In the present paper, cellulose solubility was also analysed in relation to the Kamlet-Taft parameters.

Right ventricular dysfunction is associated with exercise intolerance and poor prognosis in ischemic heart disease.

Right ventricular (RV) function is a prognostic factor in ischemic heart disease (IHD) patients, although its correlations with exercise capacity and cardiac rehabilitation (CR) efficacy are unknown. We aimed to clarify how RV function was associated with exercise tolerance and efficacy of phase II CR in IHD patients. We retrospectively analyzed 301 consecutive IHD patients who underwent phase II CR. We defined RV dysfunction using a combination of RV fractional area change < 35%, tricuspid annular plane systolic excursion < 1.6 cm, and systolic velocity < 10 cm/s. Exercise capacity was assessed using cardiopulmonary testing. The relation between RV function and exercise capacity was analyzed. The all-cause death and major adverse cardiac events (MACE) were evaluated by survival curve. The RV dysfunction group (n = 121) showed impaired left ventricular (LV) systolic and diastolic function before CR contrary to the normal RV function group (n = 180). The presence of RV dysfunction significantly reduced %AT by 4% and %Peak[Formula: see text] by 9% before CR, but increases the degree of improvement in %Peak[Formula: see text] with CR, independent of LV systolic and diastolic function. Univariate analysis demonstrated that previous coronary artery bypass grafting (CABG) was negatively associated with all-cause deaths and MACE. Adjusted for previous CABG, poor prognosis correlated with coexisting LV and RV dysfunction (hazard ratio [HR] 3.91, 95% confidence interval [CI] 1.13-13.53, P = 0.03) and RV dysfunction alone (HR 3.08, 95% CI 1.01-9.37, P = 0.05). In IHD patients, RV dysfunction is associated with exercise intolerance before CR and increased MACE risk, independent of LV function. The CR was effective in patients with RV dysfunction.

Cardiac Sarcoidosis Diagnosed by Incidental Lymph Node Biopsy.

Cardiac involvement in systemic sarcoidosis sometimes provokes life-threatening ventricular tachyarrhythmia. Steroid administration is one of the fundamental anti-arrhythmia therapies. For an indication of steroid therapy, a definitive diagnosis of sarcoidosis is required.1) However, cases that are clearly suspected of cardiac sarcoidosis based on their clinical courses sometimes do not meet the current diagnostic criteria and result in the loss of an appropriate opportunity to perform steroid therapy.Here we report a case that was diagnosed as sarcoidosis by incidental biopsy of an inguinal lymph node during cardiac resuscitation for cardiac tamponade.2) While the inguinal lymph node was not swollen on computed tomography, a specimen obtained from an incidental biopsy during the exposure of a femoral vessel for the establishment of extracorporeal cardio-pulmonary resuscitation showed a non-caseating granuloma.This findings suggest a non-swelling lymph node biopsy might be an alternative strategy for the diagnosis for sarcoidosis if other standard strategies do not result in a diagnosis of sarcoidosis.

Early Appearance of Principal Symptoms of Kawasaki Disease is a Risk Factor for Intravenous Immunoglobulin Resistance.

It is difficult to accurately predict treatment resistance in Kawasaki disease (KD). Patients considered to be low-risk cases often develop resistance to intravenous immunoglobulin (IVIG). We herein examined whether information from the clinical course of KD could improve the prediction accuracy of a previously reported risk score. We retrospectively reviewed the clinical records of 100 KD patients. The clinical characteristics and laboratory data were compared between IVIG-sensitive and IVIG-resistant patients and also between patients with and without coronary artery aneurysm (CAA). The total incidence of IVIG resistance and CAA development was 34 and 13 %, respectively. Multiple regression analysis identified the early appearance of principal symptoms (≤day 2 of the illness) as a risk factor for IVIG resistance (OR 2.88, 95 % CI 1.11-7.44, p = 0.0041), whereas delayed IVIG administration (≥day 6) (OR 2.23, 95 % CI 0.66-7.64, p = 0.018) and IVIG resistance (OR 9.05, 95 % CI 2.27-36.10, p = 0.015) were independent predictors for CAA development. The addition of the first appearance day of principal symptoms into a previously reported scoring system improved its prediction accuracy for IVIG resistance. KD patients who had presented with any principal symptoms within 2 days of fever onset were at a high risk for IVIG resistance regardless of previously reported risk score. A careful medical history-taking that is focused on the clinical course enables a better prediction of IVIG resistance.

IgG4-related cardiovascular disorders.

Immunoglobulin4 (IgG4)-related disease is a systemic inflammatory disease characterized by elevation of serum IgG4. It involves various organs such as the pancreas (autoimmune pancreatitis), lacrimal gland (Mikulicz's disease), retroperitoneum (retroperitoneal fibrosis), aorta (aortic aneurysm and aortitis), heart (constrictive pericarditis), and pseudotumors around the coronary arteries. These disorders often coexist in accordance with progression of the disease. Because IgG4-related cardiovascular disorder affects the patient's prognosis, early detection and treatment is important. Coronary CT imaging and echocardiography accidentally detect IgG4-related disorders and (18)FDG-PET imaging can identify active inflammation in the lesions. Measurement of serum IgG4 levels and tissue biopsy are necessary for diagnosis. Minor salivary gland biopsy is recommended even though (18)FDG uptake is not detected when it is difficult to obtain a biopsy specimen from IgG4-related cardiovascular lesions. The first-line treatment is high-dose corticosteroid therapy, however, relapse is often reported. Corticosteroids suppress the development of active inflammatory diseases such as aortitis, pericarditis, and pseudotumors, but already-developed lesions do not respond. A large developed aneurysm can rupture even during or after corticosteroid therapy, therefore, additional surgical treatment may be needed. Treatment of IgG4-related cardiovascular disorders might require higher doses of corticosteroids than IgG4-related extracardiovascular disorders. The adequate dose of corticosteroid, type and dose of immunosuppressant, and surgical intervention should be carefully considered on a case-by-case basis.

Tie2-Cre-Induced Inactivation of Non-Nuclear Estrogen Receptor-α Signaling Abrogates Estrogen Protection Against Vascular Injury.

Using the Cre-loxP system, we generated the first mouse model in which estrogen receptor-α non-nuclear signaling was inactivated in endothelial cells. Estrogen protection against mechanical vascular injury was impaired in this model. This result indicates the pivotal role of endothelial estrogen receptor-α non-nuclear signaling in the vasculoprotective effects of estrogen.

Remote Cardiac Rehabilitation With Wearable Devices.

Although cardiac rehabilitation (CR) has been shown to improve exercise tolerance and prognosis in patients with cardiovascular diseases, there remains low participation in outpatient CR. This may be attributed to the patients' busy schedules and difficulty in visiting the hospital due to distance, cost, avoidance of exercise, and severity of coronary disease. To overcome these challenges, many countries are exploring the possibility of remote CR. Specifically, there is increasing attention on the development of remote CR devices, which allow transmission of vital information to the hospital via a remote CR application linked to a wearable device for telemonitoring by dedicated hospital staff. In addition, remote CR programs can support return to work after hospitalization. Previous studies have demonstrated the effects of remote CR on exercise tolerance. However, the preventive effects of remote CR on cardiac events and mortality remain controversial. Thus, safe and effective remote CR requires exercise risk stratification for each patient, telenursing by skilled staff, and multidisciplinary interventions. Therefore, quality assurance of telenursing and multi-disciplinary interventions will be essential for remote CR. Remote CR may become an important part of cardiac management in the future. However, issues such as cost-effectiveness and insurance coverage still persist.

A large-scale cohort study of long-term cardiac rehabilitation: A prospective cross-sectional study.

BACKGROUND: Few studies have evaluated the therapeutic effect of long-term cardiac rehabilitation (CR) and no large-scale survey of cardiovascular outcomes after long-term CR is reported. METHODS: This cohort study included 9981 patients undergoing CR from 2004 to 2015. Patients who had supervised CR were divided into three groups according to CR duration: up to acute phase (until discharge, Phase I group), up to recovery phase (≤150 days, Phase II group), and up to maintenance phase (>150 days, Phase III group). Using propensity score matching, mortality and major adverse cardiovascular events (MACE) were compared among the groups. RESULTS: Follow-up period was 4.9 ± 3.0 years. Adult patients were divided into three groups (Phase I group: n = 4649, Phase II group: n = 3271, and Phase III group: n = 731). After propensity score matching, the risk of death and MACE was extremely lower in Phase III group than in Phase I or Phase II group (death: HR 0.47, P < 0.01, HR 0.64, P < 0.01, and MACE: HR 0.48, P < 0.01, HR 0.70, P < 0.01). Most patients in Phase II group had better survival than those in Phase I group. Subpopulations of female patients and those with dyslipidemia, smoking history, coronary artery bypass graft, or heart failure had better survival in Phase III group than in Phase II group. CONCLUSIONS: Long-term supervised CR for patients with cardiovascular diseases is more effective than short-term CR.

Estrogen Receptor-α Non-Nuclear Signaling Confers Cardioprotection and Is Essential to cGMP-PDE5 Inhibition Efficacy.

Using genetically engineered mice lacking estrogen receptor-α non-nuclear signaling, this study demonstrated that estrogen receptor-α non-nuclear signaling activated myocardial cyclic guanosine monophosphate-dependent protein kinase G and conferred protection against cardiac remodeling induced by pressure overload. This pathway was indispensable to the therapeutic efficacy of cyclic guanosine monophosphate-phosphodiesterase 5 inhibition but not to that of soluble guanylate cyclase stimulation. These results might partially explain the equivocal results of phosphodiesterase 5 inhibitor efficacy and also provide the molecular basis for the advantage of using a soluble guanylate cyclase simulator as a new therapeutic option in post-menopausal women. This study also highlighted the need for female-specific therapeutic strategies for heart failure.

Computed tomography imaging to quantify the area of the endocardial subvalvular apparatus in hypertrophic cardiomyopathy - Relationship to outflow tract obstruction and symptoms.

BACKGROUND: Abnormalities of the endocardial subvalvular apparatus (SVA), which includes the papillary muscles directly attached to the mitral leaflet and left ventricular apical-basal muscle bundles, are occasionally identified in hypertrophic cardiomyopathy (HCM). Their associations with left ventricular outflow tract (LVOT) obstruction are unknown. METHODS: We retrospectively reviewed cardiac computed tomography image data sets of 107 consecutive patients with HCM [56 obstructive (HOCM) and 51 non-obstructive (HNOCM)] as well as 53 controls. We evaluated anomalies of the SVA, measured the cross-sectional area of the SVA at the level of the LVOT, and subsequently assessed its correlation with the LVOT pressure gradient with and without medication. RESULTS: The area of the SVA was greater in HOCM than in HNOCM patients and in the control group (2.5 ± 1.3 cm(2), 1.4 ± 0.8 cm(2), and 0.9 ± 0.6 cm(2), respectively; p < 0.0001). Anomalies in the SVA were more often observed in the HOCM group than in the HNOCM patients and controls (abnormal papillary muscles, 14%, 8%, and 0%, respectively; P = 0.010; LV apical-basal muscle bundles, 73%, 65%, and 45%, respectively; P = 0.0094). Among HOCM patients, logistic regression analysis demonstrated that an SVA area of 2.2 cm(2) was an independent risk factor of residual severe LVOT obstruction (≥50 mmHg) after medication (odds ratio, 10.1; 95% confidence interval, 2.05-49.80). CONCLUSION: An increased area of the endocardial subvalvular apparatus could be an independent risk factor for clinically relevant LVOT obstruction refractory to medication.

Immunoglobulin G4-related multiple systemic aneurysms and splenic aneurysm rupture during steroid therapy.

Immunoglobulin G4 (IgG4)-related disorders in various organs have recently been described, but multiple systemic aneurysms have not yet been reported. Here, we present a 68-year-old Japanese man with multiple systemic aneurysms and tumor-forming pericoronary arteritis who was undergoing low-dose corticosteroid therapy. Elevated serum IgG4 (2390 mg/dL) and IgG4-positive plasmacyte infiltration in the salivary glands led to a diagnosis of IgG4-related disease. High-dose corticosteroid therapy was initiated, whereupon the inflammatory lesions shrank. However, the large, well-developed common hepatic aneurysm and splenic aneurysm did not change. Our patient died of splenic aneurysm rupture in the sixth month of treatment. The autopsy revealed IgG4-positive plasmacyte infiltration in the coronary wall and a thinned splenic aneurysm wall. This case suggests that early high-dose corticosteroid therapy may be necessary for the treatment of IgG4-related cardiovascular disorders. A minor salivary gland biopsy might facilitate the early diagnosis of IgG4-related disease even if (18)F-fluorodeoxyglucose positron emission tomography provides no inflammatory findings.