Body Weight Measurement for Adjusting Diuretics Is Not Associated With Hospitalization and Mortality of Heart Failure Patients Under Home Medical Care.

Introduction: The post-discharge readmission rate for heart failure (HF) is high. Although some previous studies have shown the efficacy of clinic-based patient education of regular weighing in preventing readmission; however, none of these studies were conducted in home care settings.

Methods: This retrospective observational study aimed to assess whether using body weight as an indicator for treating HF with diuretics reduced hospitalization and mortality in home medical care settings.

Chronic treatment with PDGF-BB and endothelin-1 synergistically induces vascular hyperplasia and loss of contractility in organ-cultured rat tail artery.

Objective: In this study, we examined the synergistic effects of the two potent pathogenic factors, platelet-derived growth factor-BB (PDGF-BB) and endothelin-1 (ET-1) to induce vascular hyperplasia using ex vivo organ-culture system.

Methods And Results: In organ-cultured rat tail arteries, concomitant treatment with 100 ng/ml PDGF-BB and 300 nM ET-1 for 4 days induced medial hyperplasia with increased smooth muscle cell proliferation. Concomitant treatment with PDGF-BB (10-300 nM) and ET-1 (30 nM-1 μM) dose-dependently suppressed contractile responses to high K(+) and norepinephrine.

Severity of hyperlipidemia does not affect antiatherosclerotic effect of an angiotensin II receptor antagonist in apolipoprotein E-deficient mice.

The purpose of this study was to clarify whether severity of hyperlipidemia affects the antiatherosclerotic effect of angiotensin II receptor blockers (ARBs). The effect of olmesartan medoxomil, an ARB, on atherosclerotic lesion was examined in apolipoprotein E-deficient (ApoEKO) mice fed a normal diet (ND) or a high-fat-supplemented diet (FD) for 25 weeks. ApoEKO mice have high plasma cholesterol levels, which were further increased by feeding of an FD.

Fluvastatin prevents vascular hyperplasia by inhibiting phenotype modulation and proliferation through extracellular signal-regulated kinase 1 and 2 and p38 mitogen-activated protein kinase inactivation in organ-cultured artery.

Objective: We examined the inhibitory mechanisms of fluvastatin on FBS-induced vascular hypertrophy assessed by organ-cultured rat tail artery.

Methods And Results: After 5 days of culture with 10% FBS, hyperplastic morphological changes in the media layer were induced. Treatment with 1 mumol/L fluvastatin significantly inhibited these changes.