Atrophy of the parahippocampal gyrus is prominent in heart failure patients without dementia.

Aims: The exacerbation of heart failure (HF) induces brain damage and cognitive impairment (CI), which frequently attenuates the effects of treatment. However, it is not clear whether HF patients without clinical dementia demonstrate increased risk of CI. We examined whether local atrophy in the parahippocampal gyrus, a potential predictor of CI, is prominent in HF patients without clinical dementia.

Minimizing optical losses in monolithic perovskite/c-Si tandem solar cells with a flat top cell.

In a monolithic perovskite/c-Si tandem device, the perovskite top cell has to be deposited onto a flat c-Si bottom cell without anti-reflective front side texture, to avoid fabrication issues. We use optical simulations to analyze the reflection losses that this induces. We then systematically minimize these losses by introducing surface textures in combination with a so-called burial layer to keep the perovskite top cell flat.

Significance of AT1 receptor independent activation of mineralocorticoid receptor in murine diabetic cardiomyopathy.

Background: Diabetes mellitus (DM) has deleterious influence on cardiac performance independent of coronary artery disease and hypertension. The objective of the present study was to investigate the role of the renin-angiotensin-aldosterone system, especially angiotensin II type 1a receptor (AT1aR) and mineralocorticoid receptor (MR) signaling, in left ventricular (LV) dysfunction induced by diabetes mellitus (DM).

Methods And Results: DM was induced by intraperitoneal injection of streptozotocin (200 mg/kg BW) in wild-type (WT) or AT1aR knockout (KO) male mice, and they were bred during 6 or 12 weeks.

Overexpression of human C-reactive protein exacerbates left ventricular remodeling in diabetic cardiomyopathy.

Background: C-reactive protein (CRP) is known to be a pathogenic agent in the cardiovascular system. However, the effect of CRP on heart failure has not been elucidated. The effect of human CRP on cardiac dysfunction induced by diabetes mellitus (DM) using human CRP-overexpressing transgenic mice (CRP-Tg) was examined.

C-reactive protein overexpression exacerbates pressure overload-induced cardiac remodeling through enhanced inflammatory response.

Serum C-reactive protein (CRP) elevation predicts the development of heart failure in patients with hypertension. CRP activates macrophages and enhances oxidative stress. We hypothesize that CRP itself has a pathogenic role in the development of pressure overload-induced cardiac remodeling.

Acute decompensated heart failure syndromes (ATTEND) registry. A prospective observational multicenter cohort study: rationale, design, and preliminary data.

Acute heart failure syndromes (AHFS) are likely to increase in the future, and the high readmission rate of patients with AHFS is an important issue in Western countries. However, there are very few published epidemiological studies on AHFS in the Asia Pacific region. Because AHFS are heterogeneous, the characteristics, clinical profile, and management of AHFS should be clarified in an epidemiological study.

Differential effects of carvedilol and metoprolol on renal function in patients with heart failure.

Background: The aim of the present study was to verify the effects of beta-blockers on renal function in patients with heart failure (HF).

Methods And Results: A total of 40 patients with HF (New York Heart Association class, II-III) were enrolled, who had beta-blocker therapy initiated with carvedilol (n=23) or metoprolol (n=17). The changes in renal and cardiac function were retrospectively analyzed over 16 weeks.

Elevated troponin T on discharge predicts poor outcome of decompensated heart failure.

Persistent elevation of cardiac troponin T (cTnT) predicts an adverse clinical outcome in patients with chronic heart failure (HF), but the underlying mechanisms remain to be determined. We investigated the association between predischarge cTnT elevation and coexistent pathophysiology in patients with decompensated HF. Plasma cTnT levels were determined before discharge in 170 patients with decompensated HF.

A pilot study on the role of autoantibody targeting the beta1-adrenergic receptor in the response to beta-blocker therapy for congestive heart failure.

Background: Autoantibodies directed against the beta1-adrenergic receptor exert agonist-like actions by inducing receptor uncoupling and cause myocardial damage as well as fatal ventricular arrhythmias. Previous studies have shown that beta-blockers can modulate these actions of the autoantibodies. We investigated the influence of such autoantibodies in patients with congestive heart failure (CHF) receiving beta-blocker therapy.

Elevated arterial stiffness evaluated by brachial-ankle pulse wave velocity is deleterious for the prognosis of patients with heart failure.

Background: Arterial stiffness is used as an index of arteriosclerosis. The goal of this study was to clarify whether increased arterial stiffness, evaluated by measuring the brachial-ankle pulse wave velocity (baPWV), is a risk factor for the prognosis of heart failure (HF) patients.

Methods And Results: After examination of the baPWV, as well as the levels of neurohumoral factors, the 72 enrolled HF patients were followed up for a survival study, which had a primary endpoint of re-admission because of HF.

Effects of beta-blocker therapy on high sensitivity c-reactive protein, oxidative stress, and cardiac function in patients with congestive heart failure.

Background: It is uncertain whether beta-blocker therapy affects serum C-reactive protein (CRP) level in patients with congestive heart failure (CHF). We attempted to determine if beta-blocker therapy decreases serum CRP production and to correlate the production with biomarkers and cardiac function in such patients.

Methods And Results: Fifty-two patients with mild to moderate CHF with a left ventricular ejection fraction (EF) <40% were enrolled.

Persistent cardiac aldosterone synthesis in angiotensin II type 1A receptor-knockout mice after myocardial infarction.

Background: The renin-angiotensin-aldosterone system is implicated in the pathogenesis of heart failure. Pharmacological blockade of angiotensin II (Ang II)-dependent signaling is clinically effective in reducing cardiovascular events after myocardial infarction (MI) but still fails to completely prevent remodeling. The molecular basis underlying this Ang II-independent remodeling is unclear.