Determining Optimal Intervals for In-Person Visits During Video-Based Telemedicine Among Patients With Hypertension: Cluster Randomized Controlled Trial.

BACKGROUND: Introducing telemedicine in outpatient treatment may improve patient satisfaction and convenience. However, the optimal in-person visit interval for video-based telemedicine among patients with hypertension remains unreported in Japan. OBJECTIVE: We determined the optimal in-person visit interval for video-based telemedicine among patients with hypertension. METHODS: This was a cluster randomized controlled noninferiority trial. The target sites were 8 clinics in Japan that had a telemedicine system, and the target patients were individuals with essential hypertension. Among patients receiving video-based telemedicine, those who underwent in-person visits at 6-month intervals were included in the intervention group, and those who underwent in-person visits at 3-month intervals were included in the control group. The follow-up period of the participants was 6 months. The primary end point of the study was the change in systolic blood pressure, and the secondary end points were the rate of treatment continuation after 6 months, patient satisfaction, health economic evaluation, and safety evaluation. RESULTS: Overall, 64 patients were enrolled. Their mean age was 54.5 (SD 10.3) years, and 60.9% (39/64) of patients were male. For the primary end point, the odds ratio for the estimated difference in the change in systolic blood pressure between the 2 groups was 1.18 (90% CI -3.68 to 6.04). Notably, the criteria for noninferiority were met. Patient satisfaction was higher in the intervention group than in the control group. Furthermore, the indirect costs indicated that lost productivity was significantly lesser in the intervention group than in the control group. Moreover, the treatment continuation rate did not differ between the intervention and control groups, and there were no adverse events in either group. CONCLUSIONS: Blood pressure control status and safety did not differ between the intervention and control groups. In-person visits at 6-month intervals may cause a societal cost reduction and improve patient satisfaction during video-based telemedicine. TRIAL REGISTRATION: UMIN Clinical Trials Registry (UMIN-CTR) UMIN000040953; https://tinyurl.com/2p8devm9.

Efficacy and safety of empagliflozin in Japanese patients with type 2 diabetes mellitus: A sub-analysis by body mass index and age of pooled data from three clinical trials.

AIMS: To investigate the efficacy and safety of empagliflozin in subgroups based on body mass index (BMI) and age, using a pooled data set from Japanese patients with type 2 diabetes mellitus (T2DM). METHODS: Pooled data from 1403 patients treated with empagliflozin at 10mg/day or 25mg/day in three clinical studies (≥52week treatment) were stratified by baseline BMI (<22, 22 to <25 and ≥25kg/m2) and baseline age (<50, 50 to <65 and ≥65years). RESULTS: Empagliflozin at 10mg/day and 25mg/day reduced mean glycated hemoglobin (HbA1c) (-0.77 to -0.87% and -0.76 to -0.97%, respectively), mean fasting plasma glucose (FPG) (-20.79 to -27.06mg/dL and -26.08 to -29.60mg/dL) and mean body weight (-3.4 to -4.7% and -3.7 to -4.7%) in all subgroups of baseline BMI and age, regardless of age and degree of obesity. Adverse events were observed in approximately 70-80% patients in BMI and age subgroups of both empagliflozin groups. No hypoglycemia requiring assistance was observed. Neither UTI nor genital infection rates differed markedly among the BMI and age subgroups. Volume depletion was increased in patients ≥65years of age as compared to younger patients. CONCLUSIONS: Empagliflozin was well tolerated and improved HbA1c, FPG and body weight in all BMI and age subgroups of Japanese patients with T2DM, regardless of age and degree of obesity. Empagliflozin is considered to be effective and well tolerated for treating a wide range of Japanese patients with T2DM. TRIAL REGISTRATION: Study 1 (NCT01193218), Study 2 (NCT01289990) and Study 3 (NCT01368081).

Sunitinib, a small-molecule receptor tyrosine kinase inhibitor, suppresses neointimal hyperplasia in balloon-injured rat carotid artery.

The migration and proliferation of vascular smooth muscle cells (VSMCs) induced by growth factors play a critical role in in-stent stenosis after percutaneous coronary intervention (PCI). The present study tested the hypothesis that sunitinib malate (sunitinib), a tyrosine kinase inhibitor of multiple receptors for growth factors, can reduce neointimal formation after arterial injury in vivo and sought to reveal the underlying mechanism in vitro. Male Wistar rats with balloon-injured carotid arteries were administered either sunitinib or a vehicle orally for 2 weeks. Sunitinib significantly inhibited neointimal hyperplasia relative to control by reducing active cell proliferation. In cultured human aortic smooth muscle cells (HASMCs), sunitinib significantly inhibited platelet-derived growth factor (PDGF)-induced increases of DNA synthesis, cell proliferation, and migration relative to controls as evaluated by [(3)H] thymidine incorporation, cell number, and the Boyden chamber assay, respectively. Immunoblot analyses showed that sunitinib suppressed phosphorylation of PDGF-BB inducible extracellular signal-regulated kinase and autophosphorylation of PDGF ß-receptor, which are the key signaling steps involved in HASMC activation. These results indicate that sunitinib inhibits neointimal formation after arterial injury by suppressing VSMC proliferation and migration presumably through inactivation of PDGF signaling. As such, it may be a potential therapeutic agent, which targets arterial restenosis after PCI.

Adiponectin inhibits macrophage tissue factor, a key trigger of thrombosis in disrupted atherosclerotic plaques.

OBJECTIVE: Adiponectin (APN) is an adipocytokine with anti-atherogenic and anti-inflammatory properties. Hypoadiponectinemia may associate with increased risk for coronary artery disease (CAD) and acute coronary syndrome (ACS). Tissue factor (TF) initiates thrombus formation and facilitates luminal occlusion after plaque rupture, a common cause of fatal ACS. This study tested the hypothesis that APN influences TF expression by macrophages (MΦ), inflammatory cells found in atheromatous plaques. METHODS: Human monocyte-derived MΦ or RAW 264.7 cells transfected with TF promoter construct, pretreated with a physiological range of recombinant APN (1-10 µg/ml), received LPS stimulation. TF mRNA and protein levels were quantified by real-time RT-PCR and ELISA. TF pro-coagulant activity was evaluated by one-step clotting assay. TF promoter activity was determined by a dual-luciferase reporter assay. Immunoblot analyses assessed intracellular signaling pathways. RESULTS: APN treatment suppressed TF mRNA expression and protein production in LPS-stimulated human MΦ, compared to vehicle controls. APN treatment also significantly reduced TF pro-coagulant activity in lysates of LPS-stimulated human MΦ, compared to vehicle controls. Moreover, APN suppressed TF promoter activity in LPS-stimulated MΦ compared to controls. APN suppressed phosphorylation and degradation of IκB-α in LPS-stimulated MΦ. CONCLUSIONS: APN reduces thrombogenic potential of MΦ by inhibiting TF expression and activity. These observations provide a potential mechanistic link between low APN levels and the thrombotic complications of atherosclerosis.