Active clinical trials for "Heart Diseases"

The purpose of this study is to test the expression of microRNAs related to the syndromes after the intervention of Tongguan capsule,preliminarily to investigate the mechanism of the effects of Tongguan capsule, and provide the biological foundation of curative effect of Tongguan capsule.

The aims of the present study are to measure dynamic changes over time in the plasma level of SDF-1α in patients with confirmed diagnoses of AMI, AF and CHF and in so doing: Monitor the plasma level of SDF-1α at the diagnosis, during and after the long term treatment of AMI, AF and CHF. The SDF-1α level of patients is expected to decrease during treatment of the aforementioned conditions. Correlate the plasma level of SDF-1α in relation to clinical, biochemical characteristics of Acute Myocardial Infarction(AMI), Atrial Fibrillation(AF) and Congestive Heart Failure (CHF). In so doing, the investigators expect that SDF-1α will correlate with the severity of heart disease. Study the dynamic of SDF-1α pertaining to its property as prognostic indicator for the long term follow up risk of readmission and mortality of patients diagnosed with AMI, AF or CHF.

In a prospective observational study during the six-month duration, coronary artery bypass graft surgery (CABG) and valve repair surgery (mitral, mitral, and aortic valve and/or tricuspid valve) patients were investigated for hepatic dysfunction. All patients were divided into two groups as with or without hyperbilirubinemia, and this was defined by the occurrence of a plasma total bilirubin concentration of more than 34 µmol/L (2 mg/dL) in any measurement during the postoperative period. Our goal was to determine the risk factors associated with hepatic dysfunction in patients undergoing open-heart surgery with cardiopulmonary bypass. The collected parameters include; alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL), and gamma-glutamyl transpeptidase (GGT) and albumin preoperatively and on postoperative days 1, 3 and 7. Possible preoperative, intraoperative, and postoperative risk factors were investigated. Logistic regression analysis was done to identify the risk factors for postoperative hyperbilirubinemia.

The purpose of this research is to prospectively test and validate the single-lead Low EF algorithm in outpatients in order to test the performance of a single-lead ECG based algorithm to identify people with decreased left ventricular EF.

Monocentric study for the evaluation of a whole body CZT scintigraphy system.

Microcirculatory disturbance occurs most seriously during cardiopulmonary bypass (CPB) in cardiac surgery. If microvascular reactivity compensates for microcirculatory disturbance during CPB, tissue hypoxemia may be minimized. On the other hand, tissue hypoxemia may develop and lead to poor clinical outcomes. The primary aim of this study was to assess whether microvascular reactivity during CPB can predict major adverse events (MAE) within 30 days after cardiac surgery. This prospective, observational, single-center study was conducted on 115 patients who underwent elective on-pump cardiac surgery. The vascular occlusion test (VOT) with near-infrared spectroscopy was performed five times for each patient, before the induction of general anesthesia (baseline, T0), 30 min after the induction of general anesthesia (T1), 30 min after applying CPB (T2), 10 min after injection of protamine (T3), and after sternal closure (T4). Sequential Organ Failure Assessment (SOFA) and Acute Physiologic and Chronic Health Evaluation (APACHE) II scores and the length of ventilator care, intensive care unit stay, and hospital stay were recorded. Postoperative MAE within 30 days after surgery was also recorded.

In a randomized, sham-controlled crossover trial the investigators will test whether supplemental oxygen given during cardiopulmonary exercise testing will improve exercise performance and physiological parameters in patients with grown-up congenital heart disease.

Participants aged 80 years or over, who attend Castle Hill Hospital with either stable angina or an acute coronary syndrome will be invited to participate in the study. After induction into the study, these participants will be assessed for frailty and quality of life (QoL) using predetermined assessment tools. Quality of life (QoL) will be assessed using the standardised SF-12 questionnaire proforma. Frailty assessment will be based on the use of the Fried Frailty Phenotype criteria and the Edmonton Frailty Scale. Patients will be reassessed at 3,9 and 24 months for their clinical outcomes, repeat frailty assessment and quality of life.

Metabolites of dietary phosphatidylcholine- choline and trimethylamine N-oxide (TMAO)- were recently identified as being associated with myocardial infarction in a case-control study. The latter TMAO is a gut-microflora-derived choline metabolite that has been shown to be a potent risk factor for cardiovascular disease (CVD). This pilot study seeks to use information derived from a dietary questionnaire in children to test the association of dietary choline intake to plasma levels of TMAO as well as the relationship between plasma choline levels and components of atherogenic dyslipidemia (increased triglycerides and small LDL, and reduced HDL cholesterol). An ancillary goal of this study is to build on existing programs of community outreach to local Oakland/Berkeley minority communities, and to develop an infrastructure for family-based and community participation in clinical research across the full age spectrum and among diverse populations. This pilot study will examine the association of dietary choline intake assessed by food frequency questionnaires to biomarkers of CVD risk in 40 children (> 7 years of age) and their parents as there is no information regarding this relationship in children. The results of this pilot study will form the basis for a proposal to carry out a randomized intervention trial to directly test the effects of dietary choline intake on plasma TMAO and lipoprotein levels. Ultimately, better understanding of the relationship between dietary choline intake and CVD risk factors may facilitate the formulation of appropriate dietary choline recommendations in children and adults.

Endostatin, a 20-kDa cleavage product of collagen XVIII, is a component of the extracellular matrix expressed in the basement membrane. As a potent inhibitor of angiogenesis, endostatin induces endothelial cell apoptosis and diminishes cell migration, adhesion and proliferation. Endostatin may stop the progression of atherosclerosis. Atherosclerotic heart disease involves unwanted tissue growth. By cutting off the blood supply from a plaque the likelihood of plaque rupture may eventually be reduced. Recent data indicates that the loss of collagen XVIII/endostatin is related to the enhancement of neo-vascularization and vascular permeability in atherosclerosis. Plaque neo-vascularization strongly correlates with the regional content of inflammatory cells. Furthermore, increased vascular permeability enhances lipid accumulation in the vessel walls, hence increasing foam cells. Therapeutic angiogenesis is a most promising strategy for the treatment of myocardial infarction. However, it remains unknown if and how endogenous angiogenesis inhibitors, such as endostatin, regulate angiogenesis in myocardial infarction. Rat models showed that after myocardial infarction endostatin neutralization displayed adverse left ventricular remodeling and severe heart failure compared with controls. Although angiogenesis was increased, tissue remodeling and interstitial fibrosis were further exaggerated in post-myocardial infarction hearts by endostatin neutralization. However, several studies suggest that endostatin may locally modulate coronary collateral formation by inhibiting collateral vessel formation in patients with ischemic heart disease. During treadmill exercise tests in healthy volunteers a significant increase in circulating endostatin levels can be observed. Exercise induces angiogenesis in cardiac and skeletal muscles by decreasing endostatin in the muscle tissues to increase blood flow to these metabolically active tissues. Thereby endostatin is released into the general circulation. In summary, endostatin might be a new weapon to fight against atherosclerotic progression by inhibiting neo-vascularization of atherosclerotic plaques.