Different association of HDL-C, apoA-I, and HDL-C/apoA-I with multiple outcomes in HFrEF patients.

Background: High-density lipoprotein-cholesterol (HDL-C) has been considered a cardioprotective factor for several decades. However, its association with outcomes in patients with heart failure with reduced ejection fraction (HFrEF) remains controversial. We aimed to investigate the association of HDL-C, apolipoprotein A-I (apoA-I), and the HDL-C/apoA-I ratio with multiple outcomes of HFrEF patients and establish prognostic models using machine learning methods.

Twelve-week high-fat diet for improving adverse ventricular remodeling post-myocardial infarction by alleviating local inflammation.

Background: Many studies have examined how to achieve better outcomes in myocardial infarction (MI) patients with mild obesity or who are overweight. However, the influence of a high-fat diet (HFD) and the underlying mechanisms by which it can affect ventricular remodeling following MI are poorly understood. This study investigated the impact of a 12-week HFD on the left ventricular (LV) remodeling of permanent MI models and immune cell involvement.

Eosinophilic granulomatosis with polyangiitis presenting with repetitive acute coronary syndrome, refractory coronary vasospasm, and spontaneous coronary dissection: a case report.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a type of eosinophilic vasculitis that is mainly limited to small- and medium-sized arteries. Cardiac involvement is the leading cause of death in patients with EGPA. Spontaneous coronary artery dissection (SCAD) is an important cause of acute coronary syndrome in middle-aged women with no or few traditional cardiovascular risk factors.

Oxidized low-density lipoprotein inhibits the degradation of cyclophilin A via the lysosome in vascular smooth muscle cells.

Background: Cyclophilin A (CyPA) plays an important role in the progression of atherosclerosis. Additionally, it has been reported that lysosomal function is markedly impaired in atherosclerosis induced by oxidized low-density lipoprotein (ox-LDL). As the CyPA degradation pathway remains to be elucidated, we aimed to uncover the role of lysosomes and ox-LDL in the degradation of CyPA.

The Release of Cyclophilin A from Rapamycin-Stimulated Vascular Smooth Muscle Cells Mediated by Myosin II Activation: Involvement of Apoptosis but Not Autophagy.

Introduction: The exocytosis of cyclophilin A (CyPA) by a vesicular pathway in response to reactive oxygen species has been determined. However, other sources of extracellular CyPA remain obscure.

Objective: The aim of this study was to determine the role of autophagy in the secretion of CyPA.

Yes-associated protein mediates angiotensin II-induced vascular smooth muscle cell phenotypic modulation and hypertensive vascular remodelling.

Objectives: Yes-associated protein (YAP) has been reported to regulate cell proliferation and differentiation. We aimed to characterize the role of YAP in angiotensin II (Ang II)-induced hypertensive vascular remodelling (HVR) and vascular smooth muscle cells (VSMCs) phenotypic modulation and to explore the underlying mechanisms.

Materials And Methods: An HVR rat model was established by continuous Ang II infusion for 2 weeks.

Prognostic Impact of Fasting Plasma Glucose on Mortality and Re-Hospitalization in Patients with Acute Heart Failure.

Background: The impact of fasting plasma glucose (FPG) on survival outcomes in patients with acute heart failure (HF) is unclear, and the relationship between intensity of glycemic control of FPG in diabetes mellitus (DM) patients and HF prognosis remains uncertain. This retrospective study aimed to evaluate the prognostic impact of FPG in patients with acute HF.

Methods: A total of 624 patients hospitalized with acute HF from October 2000 to April 2014 were enrolled in this study.

Effect of Endoplasmic Reticulum Stress and Autophagy in the Regulation of Post-infarct Cardiac Repair.

Background: Acute myocardial infarction (AMI) is reported to be accompanied by endoplasmic reticulum (ER) stress and autophagy induction. Nevertheless, the roles of ER stress and autophagy in post-infarct reparative fibrosis remain to be elucidated.

Aim: To investigate the effects of ER stress and autophagy on the regulation of post-infarct reparative fibrosis.

Honeycomb-like structure in the right coronary artery treated with a drug-eluting stent: a case report and literature review.

A honeycomb-like structure (HLS) is a rare entity encountered in catheterization laboratories. The etiology of HLS remains elusive. Moreover, no treatment guideline or consensus for HLS has been proposed.

A Low-Normal Free Triiodothyronine Level Is Associated with Adverse Prognosis in Euthyroid Patients with Heart Failure Receiving Cardiac Resynchronization Therapy.

Thyroid dysfunction is prevalent in patients with heart failure (HF) and hypothyroidism is related to the adverse prognosis of HF subjects receiving cardiac resynchronization therapy (CRT). We aim to investigate whether low-normal free triiodothyronine (fT3) level is related to CRT response and the prognosis of euthyroid patients with HF after CRT implantation.One hundred and thirteen euthyroid patients who received CRT therapy without previous thyroid disease and any treatment affecting thyroid hormones were enrolled.

Oxidized Low-Density Lipoprotein-Induced Cyclophilin A Secretion Requires ROCK-Dependent Diphosphorylation of Myosin Light Chain.

Objective: Accumulation of cyclophilin A (CyPA) within atherosclerotic lesions is thought to be implicated in the progression of atherosclerosis. However, the source of CyPA within atherosclerotic lesions is still unknown. The aim of this study is to determine the role of oxidized low-density lipoproteins (ox-LDL) in vascular smooth muscle cell (VSMC)-derived CyPA secretion and the underlying mechanism.

Effect of Metabolic Syndrome on Risk Stratification for Left Atrial or Left Atrial Appendage Thrombus Formation in Patients with Nonvalvular Atrial Fibrillation.

Background: Metabolic syndrome (MS) is a risk factor for stroke and thromboembolism event. Left atrial or LA appendage (LA/LAA) thrombus is a surrogate of potential stroke. The relationship between MS and atrial thrombus remains unclear.

Role of Circulating Fibrocytes in Cardiac Fibrosis.

Objective: It is revealed that circulating fibrocytes are elevated in patients/animals with cardiac fibrosis, and this review aims to provide an introduction to circulating fibrocytes and their role in cardiac fibrosis.

Data Sources: This review is based on the data from 1994 to present obtained from PubMed. The search terms were "circulating fibrocytes " and "cardiac fibrosis ".

Knockdown of EMMPRIN improves adverse remodeling mediated by IL-18 in the post-infarcted heart.

Interleukin-18 (IL-18) exacerbates cardiac dysfunction following myocardial infarction (MI). Extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to exacerbate ventricular remodeling via induction of extracellular matrix metalloproteinase (MMP) synthesis. While up-regulation of EMMPRIN expression by IL-18 has been demonstrated in vitro, little is known regarding its in vivo effects.

Interleukin 18 and extracellular matrix metalloproteinase inducer cross-regulation: implications in acute myocardial infarction.

Circulating interleukin-18 (IL-18) is thought to promote atherosclerosis and cardiovascular complications such as plaque rupture. Atherosclerosis is also characterized by smooth muscle cell migration, a consequence of extracellular matrix (ECM) degradation regulated by metalloproteinases (MMPs). Because extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to promote plaque instability by inducing ECM degradation and MMP synthesis, we investigated whether a cross-regulatory interaction exists between IL-18 and EMMPRIN in human monocytes.

Downregulation of HDAC1 is involved in the cardiomyocyte differentiation from mesenchymal stem cells in a myocardial microenvironment.

Under myocardial microenvironment, bone marrow-derived mesenchymal stem cells (MSCs) can transdifferentiate into cardiomyocytes (CMs). However, the role of histone deacetylase 1 (HDAC1) in this directed differentiation process remains unclear. The current study is to determine the acetylation regulatory mechanisms that may be involved in the directed CM differentiation from MSCs.

Knockdown of the HDAC1 promotes the directed differentiation of bone mesenchymal stem cells into cardiomyocytes.

Failure of the directed differentiation of the transplanted stem cells into cardiomyocytes is still a major challenge of cardiac regeneration therapy. Our recent study has demonstrated that the expression of histone deacetylase 1 (HDAC1) is decreased in bone mesenchymal stem cells (BMSCs) during their differentiation into cardiomyocytes. However, the potential roles of HDAC1 in cardiac cell differentiation of BMSCs, as well as the mechanisms involved are still unclear.