View clinical trials related to Cardiomyopathies.
Filter by:The study is designed to assess the safety and efficacy of allogeneic human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) with injectable collagen scaffold transplanted into patients with chronic ischemic cardiomyopathy.
First, investigators must determine the physiological standards across age classes of myocardial stiffness estimated by Elastography in ultrafast (estimated right ventricular stiffness [VD] and left ventricular [LV]). This will be done in groups of children without heart condition, age group (10 children per group, four age groups [0-1mois, 1 month-1 year 1 year-5 years, 5 years-15years]). Secondly, investigators will evaluate myocardial stiffness Elastography (RV and LV) on different groups of children (same age group) with cardiomyopathy and examine correlations with the conventional parameters of systolic and diastolic function of both ventricles and with myocardial strain values. The total population of the study will be 120 children (40 healthy, 80 patients).
Pathophysiology of acromegaly cardiomyopathy is yet unclear and a specific treatment have not been indicated. It was already demonstrated the positive impact of phosphodiesterase type 5A (PDE5A) inhibition in several models of cardiomyopathy and in a model of endocrine cardiomyopathy due to type 2 diabetes mellitus. In this patients with diabetic cardiomyopathy it was demonstrated an improvement in cardiac kinetic, geometry and performance parameters and reduction of the ambulatory measurement of waist circumference. This represents the first study that evaluate heart remodeling and performance changes and metabolic/immunological/molecular parameters after 5-months of Tadalafil 20 mg in Acromegaly cardiomyopathy. The proposed research will test whether phosphodiesterase 5A inhibition could become a new target for antiremodeling drugs and to discover molecular pathways affected by this class of drugs and a network of circulating markers (miRNA) for the early diagnosis of acromegaly cardiomyopathy. We hypothesize that: - the signal molecules cGMP and cAMP could underlie the hypertrophic/profibrotic triggers related to this model of endocrine cardiomyopathy and that chronic inhibition of PDE5, activating cGMP signaling pathways, could improve cardiac remodeling due to acromegaly - PDE5 inhibition could have a role in lipolytic regulation; - neuroendocrine (e.g. natriuretic peptides) and metabolic markers and chemokines (e.g. MCP-1, TGF-ß) might relate with left ventricular (LV) remodeling in Acromegaly; - there are neuroendocrine (e.g. natriuretic peptides), metabolic markers and chemokines (e.g. MCP-1, TGF-ß) related to cardiac disease in Acromegaly; - miRNA expression [miR-208a, 499, 1, 133, 126, 29, 233, 222, 4454] might relate with LV remodeling in Acromegaly.
Pathophysiology of Cushing's Syndrome (CS) cardiomyopathy is yet unclear and a specific treatment have not been indicated. It was already demonstrated the positive impact of phosphodiesterase type 5A (PDE5A) inhibition in several models of cardiomyopathy and in a model of endocrine cardiomyopathy due to type 2 diabetes mellitus. In this patients with diabetic cardiomyopathy it was demonstrated an improvement in cardiac kinetic, geometry and performance parameters and reduction of the ambulatory measurement of waist circumference. This represents the first study that evaluate heart remodeling and performance changes and metabolic/immunological/molecular parameters after 5-months of Tadalafil 20 mg in Cushing's Syndrome cardiomyopathy. The proposed research will test whether phosphodiesterase 5A inhibition could become a new target for anti-remodeling drugs and to discover molecular pathways affected by this class of drugs and a network of circulating markers (miRNA) for the early diagnosis of Cushing's Syndrome cardiomyopathy. The investigators hypothesize that: - the signal molecules cGMP and cAMP could underlie the hypertrophic/profibrotic triggers related to this model of endocrine cardiomyopathy and that chronic inhibition of PDE5, activating cGMP signaling pathways, could improve cardiac remodeling due to CS; - PDE5 inhibition could have a role in lipolytic regulation; - neuroendocrine (e.g. natriuretic peptides) and metabolic markers and chemokines (e.g. MCP-1, TGF-ß) might relate with left ventricular remodeling in CS; - there are neuroendocrine (e.g. natriuretic peptides), metabolic markers and chemokines (e.g. MCP-1, TGF-ß) related to cardiac disease in CS; - miRNA expression [miR-208a, 499, 1, 133, 126, 29, 233, 222, 4454] might relate with left ventricular remodeling in CS;
This research study includes patients ages 1 to 25 years old with Lamin A/C related muscular dystrophy (LMNA-MD). The goal of this study is to evaluate how the heart is affected in children and teens with LMNA-MD. The evaluation includes an echocardiogram, an electrocardiogram, an electrophysiological study and the implantation of a subcutaneous ECG holter monitor.
Hypertrophic cardiomyopathy (HCM) is the most frequent genetic cardiac disease characterized by an asymmetric hypertrophic. In two third of patients, an obstruction to blood ejection is observed within the left ventricle which is named left ventricular outflow tract obstruction (LVOTO). This phenomenon can occur at rest or during exercise and is associated with symptoms such as dyspnea, dizziness or chest pain that can significantly limit day life adaptation. To now, medical or interventional treatments such as betablocacker, calcium blockers or septal alcoholisation or surgery present with a limited efficiency. Recent studies from investigators group revealed new concepts about the role of venous return to the LVOTO. Therefore the investigators hypothesis that BX1514M generating a venous vascular constriction, could improve symptoms of HCM patients by reducing LVOTO.
Peripartum cardiomyopathy (PPCM) is a rare, but significant heart disease affecting young women in the puerperal period. Thus far, no specific treatment has been approved to treat this disease. PPCM has a wide spectrum of clinical manifestations ranging from mild heart failure to severe cardiomyopathy, cardiogenic shock and death. A significant proportion of survivors have persistent chronic heart failure leading to disabling symptoms and decreased quality of life. Animal studies have suggested that prolactin is central to the development of PPCM. Prolactin has pro-inflammatory and anti-angiogenic effects that may promote PPCM. Bromocriptine, a central dopamine agonist known to decrease prolactin levels, might thwart its deleterious effects in women suffering from PPCM. Following this rationale, bromocriptine should improve myocardial function in women suffering from PPCM and thus, improve cardiovascular outcomes and healthcare outcomes.
This study will collect clinical, echocardiographic, nuclear imaging and hemodynamic data in a group of patients with end stage ischemic cardiomyopathy undergoing left ventricular assist device (LVAD) implantation to investigate the incidence of recovery of myocardial function when supported with LVADs, and to study the association between hibernating myocardium and myocardial recovery in this population.
The main objective of this randomized controlled trial is to test the association between standard cardiac risk factors, biomarkers and parameters of echocardiography, electrocardiography, and cardiac magnetic resonance imaging, (predictors) and subsequent occurrence, frequency and severity of clinical or subclinical cardiotoxicity (outcome) within and between-groups, before start of chemotherapy, during treatment and at 1, 5, and 10 years after the completion of the chemotherapy among women with early breast cancer.
The purpose of the present study is to evaluate the safety and exploratory efficacy of the umbilical cord mesenchymal stem cells for patients with ischemic heart diseases.