Active clinical trials for "Ventricular Remodeling"

A prospective, multi-center, single-arm study. This study will enroll a maximum of 35 subjects treated with the Revivent TC System.

This longitudinal cohort study evaluates the relationship of myocardial tissue markers characteristics assessed by cardiac MRI, with clinical measures of symptoms and functions in adults with primary mitral regurgitation. Participants are followed conservatively or may choose to undergo surgical repair at the discretion of their clinical team.

role of different risk scores in acute coronary syndrome to predict left ventricular remodeling

The pathogenesis of cardiomyopathies is complex and a simple approach cannot describe the whole picture. Different etiologies are reported in pediatric age and heart failure onset can lead to poor prognosis in term of need of heart transplantation and ventricular assist device implantation. Based on hypothesis that heart failure development is related to heart inability to meet metabolic demands of the body, our study will focus to evaluate cardiac metabolism as one of the most critical factors and the accompanying changes of metabolic and echocardiographic profiles at different stages of heart failure. The heart is a unique organ working continuously as a pump supplying blood to the body. To meet this requirement, the myocardium utilizes fatty acids to generate 70-90% of the adenosine triphospate, with the rest being produced by oxidation of glucose, lactate, ketone bodies, aminoacids. Utilization of fatty acids is reduced in the failing heart and there is a metabolic shift to generation of adenosine triphospate from glucose. In patients with advanced cardiomyopathies, the heart is unable to utilize either metabolite and thus "runs out of fuel". It is reported that the adenosine triphospate level is approximately 30% lower in failing human hearts compared with non-failing hearts. In addition to this premise about the metabolic profile of the failing heart, recent advances in the field of metabolomics have indicated that several metabolites and/or metabolic pathways have a role in heart failure. Metabolism of lipids, glycolysis, fructolysis, aminoacids, and ketone oxidation have been found to be altered in non-ischemic cardiomyopathy in adult population. Also in adult heart failure patients some metabolic profiles resulted pronounced perturbated. Taking advantage of the high throughput, metabolomics is a platform for identifying metabolic signatures in children at each stages of heart failure (from pre clinical heart failure to end stage forms). We also will determine whether metabolomic analysis provides sensitive evaluation of heart failure in terms of remodelling at different stages and in disease regression after therapeutic interventions. Study desing is conceived in two parts. The first part is retrospective and we will analyze all echocardiograms in all children affected by cardiomyopathies. The second part is a cross sectional study in which will evaluate untargeted metabolomics in children at any stage of heart failure (A,B, C, D) and in control group. We will evaluate the clinical applicability and significance of plasma metabolomic analysis in the diagnosis and prognosis of heart failure in pediatric ages.

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. The recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI. As a leading cause of heart failure, postinfarction LV remodeling represents an important target for therapeutic interventions. Within the ventricular mass, size, shape, connections and orientation in a three-dimensional space of every single constituent determine its functional behavior. The complex architecture of the ventricular mass creates multiple inhomogeneities of electrical and mechanical loads at the cellular and the microscopic tissue level, that cause cardiac function to be 'stochastic in nature'. The myocardial infarction will altered the ventricular shape and functional inhomogeneities carrying the morphodynamic advantages such as impaired suction for diastole after diminishing recoil relaxation with decreased twisting strain in systole. The alteration in contractile mechanics interacts with the intraventricular fluid dynamic filed that influence the regional myocardial shearing stress. Altered LV transmural wall strains have been proposed to cause infarct extension and may have an important role in propagating LV remodeling.

Pregnancy is a physiological situation that produces transient preload and afterload changes. The heart is subjected to reversible morphological remodelings and hemodynamic and functional adaptations. The characterization and understanding of maternal cardiac function during normal pregnancy by echocardiography 2D is of clinical importance for the opportune recognition of cardiac pathology. This study aims to investigate pregnancy-induced changes in ventricular strain in healthy pregnant women by echocardiography.