Comparison of the electrophysiological properties of the pulmonary veins between paroxysmal and persistent atrial fibrillation.

Background: The role of the pulmonary veins (PVs) as triggers in atrial fibrillation (AF) is well-known; however, their detailed electrophysiological properties have not been thoroughly examined.

Objective: This study aimed to investigate the electrophysiological properties of the PVs between paroxysmal AF (pAF) and persistent AF (perAF).

Methods: Prior to catheter ablation in patients with pAF ( = 51) and perAF ( = 41), a voltage map of the left atrium and PVs was created under sinus rhythm, and the area of the myocardial sleeves in the PVs and their electrophysiological characteristics, including the pacing threshold and effective refractory period (ERP), were compared between the two groups.

Reactive Oxygen Species in the Aorta and Perivascular Adipose Tissue Precedes Endothelial Dysfunction in the Aorta of Mice with a High-Fat High-Sucrose Diet and Additional Factors.

Metabolic syndrome (Mets) is the major contributor to the onset of metabolic complications, such as hypertension, type 2 diabetes mellitus (DM), dyslipidemia, and non-alcoholic fatty liver disease, resulting in cardiovascular diseases. C57BL/6 mice on a high-fat and high-sucrose diet (HFHSD) are a well-established model of Mets but have minor endothelial dysfunction in isolated aortas without perivascular adipose tissue (PVAT). The purpose of this study was to evaluate the effects of additional factors such as DM, dyslipidemia, and steatohepatitis on endothelial dysfunction in aortas without PVAT.

Endothelial Extracellular Signal-Regulated Kinase/Thromboxane A2/Prostanoid Receptor Pathway Aggravates Endothelial Dysfunction and Insulin Resistance in a Mouse Model of Metabolic Syndrome.

Background Metabolic syndrome is characterized by insulin resistance, which impairs intracellular signaling pathways and endothelial NO bioactivity, leading to cardiovascular complications. Extracellular signal-regulated kinase (ERK) is a major component of insulin signaling cascades that can be activated by many vasoactive peptides, hormones, and cytokines that are elevated in metabolic syndrome. The aim of this study was to clarify the role of endothelial ERK2 in vivo on NO bioactivity and insulin resistance in a mouse model of metabolic syndrome.

Metabolic Remodeling with Hepatosteatosis Induced Vascular Oxidative Stress in Hepatic ERK2 Deficiency Mice with High Fat Diets.

We previously demonstrated the marked hepatosteatosis and endothelial dysfunction in hepatocyte-specific ERK2 knockout mice (LE2KO) with a high-fat/high-sucrose diet (HFHSD), but detailed metabolic changes and the characteristics in insulin-sensitive organs were not tested. This study aimed to characterize metabolic remodeling with changes in insulin-sensitive organs, which could induce endothelial dysfunction in HFHSD-LE2KO. The serum glucose and fatty acid (FA) were modestly higher in HFHSD-LE2KO than HFHSD-Control.

Resistance to Obesity in SOD1 Deficient Mice with a High-Fat/High-Sucrose Diet.

Metabolic syndrome (Mets) is an important condition because it may cause stroke and heart disease in the future. Reactive oxygen species (ROSs) influence the pathogenesis of Mets; however, the types of ROSs and their localization remain largely unknown. In this study, we investigated the effects of SOD1, which localize to the cytoplasm and mitochondrial intermembrane space and metabolize superoxide anion, on Mets using SOD1 deficient mice (SOD1).

Sarco/Endoplasmic Reticulum Ca ATPase 2 Activator Ameliorates Endothelial Dysfunction; Insulin Resistance in Diabetic Mice.

Sarco/endoplasmic reticulum Ca-ATPase2 (SERCA2) is impaired in various organs in animal models of diabetes. The purpose of this study was to test the effects of an allosteric SERCA2 activator (CDN1163) on glucose intolerance, hepatosteatosis, skeletal muscle function, and endothelial dysfunction in diabetic (/) mice. Either CDN1163 or vehicle was injected intraperitoneally into 16-week-old male control and / mice for 5 consecutive days.

Artificially Created Reentry Circuit by Laser Irradiation Causes Atrial Tachycardia to Persist in Murine Atria.

Background: There is a gradual progression from paroxysmal to persistent atrial fibrillation (AF) in humans. To elucidate the mechanism involved, the creation of an artificial atrial substrate to persist AF in mice was attempted.

Methods and results: This study used wild type (WT) mice, but it is difficult to induce AF in them.

Impact of oxidative posttranslational modifications of SERCA2 on heart failure exacerbation in young patients with non-ischemic cardiomyopathy: A pilot study.

Background: Oxidative posttranslational modifications (OPTM) impair the function of Sarcoplasmic/endoplasmic reticulum (SR) calcium (Ca) ATPase (SERCA) 2 and trigger cytosolic Ca dysregulation. We investigated the extent of OPTM of SERCA2 in patients with non-ischemic cardiomyopathy (NICM).

Methods And Results: Endomyocardial biopsy (EMB) was obtained in 40 consecutive patients with NICM.

Production of adeno-associated virus vectors for in vitro and in vivo applications.

Delivering and expressing a gene of interest in cells or living animals has become a pivotal technique in biomedical research and gene therapy. Among viral delivery systems, adeno-associated viruses (AAVs) are relatively safe and demonstrate high gene transfer efficiency, low immunogenicity, stable long-term expression, and selective tissue tropism. Combined with modern gene technologies, such as cell-specific promoters, the Cre/lox system, and genome editing, AAVs represent a practical, rapid, and economical alternative to conditional knockout and transgenic mouse models.

A Rare Case of Rush Progression of Purulent Pericarditis by Escherichia coli in a Patient with Malignant Lymphoma.

Purulent pericarditis is a rare disease in the antibiotic era. The common pathogens of purulent pericarditis are gram-positive species such as Staphylococcus aureus. Streptococcus pneumoniae, Salmonella, Haemophilus, fungal pathogens/tuberculosis can also result in purulent pericarditis.

Arterial Stiffness Is Significantly Associated With Left Ventricular Diastolic Dysfunction in Patients With Cardiovascular Disease.

Left ventricular (LV) diastolic dysfunction is considered the main cause of heart failure with preserved ejection fraction (HFpEF). There have been few reports on the correlation between LV diastolic dysfunction and arterial stiffness in patients with clinical cardiovascular disease.This cross-sectional study enrolled 100 patients (67 men, 33 women; mean age, 70 years).

Usefulness of the d-ROMs test for prediction of cardiovascular events.

Background: d-ROMs test developed to determine the degree of individual oxidative stress may predict cardiovascular events.

Methods And Results: 265 patients (204 men, 61 women; age, 65±13years) who had been treated for cardiovascular disease were divided evenly by quartile of baseline d-ROMs levels, and were followed up. During the observation periods of 2.

Mechanical clot fragmentation using a Swan-Ganz catheter is useful for acute massive pulmonary thromboembolism.

Massive pulmonary thromboembolism (PE) is an acute-onset, life-threatening disease in the perioperative period. Massive PE led to severe hypoxemia and cor pulmonale in our patient who had undergone an operation for thalamic hemorrhage. Mechanical clot fragmentation using a Swan-Ganz catheter was attempted, because thrombolytic therapy was contraindicated for our patient.

The dramatic 3D IVUS imaging demonstrating a dislodged coronary stent.

A 78-year-old female underwent cardiac evaluation because she had presented with typical effort-induced chest pain. Coronary angiography revealed severe stenoses in the proximal left anterior descending coronary artery (LAD) and ostium of the diagonal branch. Then, a stent was deployed in the LAD covering the takeoff of the branch.