View clinical trials related to Hypertrophy.
Filter by:Heart failure (HF) is the common end-stage of different medical conditions. It is the only growing cardiovascular disease and its prognosis remains worse than that of many malignancies. The lack of evidence-based treatment for patients with diastolic HF (HFpEF) exemplifies that the current "one for all" therapy has to be advanced by an individualized approach. Inherited cardiomyopathies can serve as paradigmatic examples of different HF pathogenesis. Both gain- and loss-of-function mutations of the same gene cause disease, calling for disease-specific agonism or antagonism of this gene´s function. However, mutations alone do not predict the severity of cardiomyopathies nor therapy, because their impact on cardiac myocyte function is modified by numerous factors, including the genetic context. Today, patient-specific cardiac myocytes can be evaluated by the induced pluripotent stem cell (hiPSC) technology. Yet, unfolding the true potential of this technology requires robust, quantitative, high content assays. The researchers' recently developed method to generate 3D-engineered heart tissue (EHT) from hiPSC provides an automated, high content analysis of heart muscle function and the response to stressors in the dish. The aim of this project is to make the technology a clinically applicable test. Major steps are (i) in depths clinical phenotyping and genotyping of patients with cardiomyopathies or HFpEF, (ii) follow-up of the clinical course, (iii) generation of hiPSC lines (40 patients, 40 healthy controls), and (iv) quantitative assessment of hiPSC-EHT function under basal conditions and in response to pro-arrhythmic or cardio-active drugs and chronic afterload enhancement. The product of this study is an SOP-based assay with standard values for hiPSC-EHT function/stress responses from healthy volunteers and patients with different heart diseases. The project could change clinical practice and be a step towards individualized risk prediction and therapy of HF.
The purpose of this study is to determine the effectiveness of RXI-109 in reducing the recurrence of hypertrophic scar formation following elective revision of a pre-existing hypertrophic scar.
Hypertrophic cardiomyopathy (HCM) is the most common monogenic heart disease and the most frequent cause of sudden cardiac death (SCD) in the young. It is characterized by unexplained left ventricular hypertrophy (LVH), diffuse and patchy fibrosis, and myofibrillar disarray. While the majority of patients remain asymptomatic, prognosis is poor in a subset who present with SCD or progress to heart failure (HF). Current methods to predict risk of these adverse events and to target therapy are limited. Current medical therapy does not protect against SCD, nor does it prevent development of HF. Therefore, the identification of novel risk markers would help develop therapeutic targets aimed at altering the phenotypic expression to impact the natural history, especially SCD and HF. Cardiovascular magnetic resonance (CMR) is emerging as a powerful tool for diagnosis and risk stratification in HCM including assessment of LV mass and pattern of hypertrophy. Late gadolinium enhancement by CMR is a marker of focal myocardial fibrosis which is thought to underlie the arrhythmogenic substrate as well as promote development of HF. The investigators hypothesize that HCM patients with a higher primary outcome event rate can be identified by novel CMR findings. The majority of cases of HCM are autosomal dominant and about 60% are caused by mutations in genes encoding cardiac sarcomeric proteins. However, the relationship between genetic mutation, disease phenotype, and clinical outcomes remains poorly understood. The investigators hypothesize that HCM patients with sarcomeric HCM mutations will have a higher primary outcome event rate and more marked myocardial pathology on CMR than those without. Furthermore, there may be a link between sarcomeric mutations and fibrosis, as mutation carriers with overt HCM as well as those without hypertrophy have elevated markers of collagen turnover. The investigators therefore hypothesize that serum biomarkers of collagen metabolism in HCM will predict outcomes. Thus, the Specific Aim is to develop a predictive model of cardiovascular outcomes in HCM by: 1) using exploratory data mining methods to identify demographic, clinical, and novel CMR, genetic and biomarker variables associated with the outcomes and 2) develop a score from the predictive model that can be used to assess risk given a patient's combination of risk factors, thus establishing the evidence base to enable clinical trial design to reduce morbidity and mortality in HCM in a cost-effective manner.
This research during the last decade has focused on the kinetics of the systemic and local immune response to parenteral influenza vaccine in humans. The investigators have shown that normally high numbers of influenza specific antibody secreting cells (ASC) are present in the nasal mucosa of healthy adults but upon parenteral vaccination the numbers remain stable. However, a rapid transient increase in specific ASC is observed in the tonsils and peripheral blood after parenteral vaccination. In the tonsils, this is associated with a significant decrease in both naïve/effector (CD45RA+) and memory (CD45RO+) CD4+ cells upon vaccination. In this study the investigators will extend our work to investigate the characteristics of influenza-specific T- and B-cells induced locally and systemically after intranasal vaccination in man.
The purpose of this study is to determine whether a developmental formulation is substantially equivalent to the predicate device in the treatment of hypertrophic and keloid scars.
Patients with Chronic Kidney Disease (CKD) are upto 3.5 times more likely to die from diseases of heart and blood vessels (Cardiovascular Disease-CVD). Vitamin D insufficiency is very common in CKD and associated with CVD. Animal studies have shown an improvement in heart size and function with Vitamin D therapy, although evidence in humans is lacking. The proposed study will test if oral Vitamin D treatment, in deficient CKD patients, will improve heart enlargement and function. With these proposed changes the investigators expect to reduce CVD and deaths in patients with CKD.
The clinical use of genetic testing is expanding and, as a result, the number of variants identified in patients is growing. Knowledge of the clinical impact of these variants improves over time. However, the combination of more testing and the rapid evolution of genetic knowledge make it impossible for clinicians to fully account for the latest implications of their patients' genetic profiles as patient care decisions are made. This proposed study plans to enhance and evaluate IT infrastructure developed to provide timely genetic variant updates and patient search functionality to clinicians to assist in optimizing patient care.
Most children with cancer need a central venous catheter. These catheters are typically placed on the anterior thorax, where the risk of hypertrophic scarring and keloid development is greatly enhanced. A significant part of the children who have survived childhood cancer are troubled by their scars. Topical glucocorticoid treatment is known to induce a reduction of the collagen in the connective tissue. The investigators hypothesize that treatment with topical glucocorticoids for one week before and three weeks after removal of a central venous catheter, will reduce the formation of hypertrophic scarring and keloid development in children.
In the absence of treatment, severe mitral valve regurgitation (MR) results in left atrium (LA) dilatation and hypertrophy, followed ultimately by left ventricular dysfunction and heart failure. One promising intervention for the prevention of the deleterious effects of pressure overload-induced cardiac hypertrophy and heart failure is dietary supplementation with n-3 polyunsaturated fatty acids (PUFAs). However, the molecular targets and mechanisms by which n-3 PUFAs exert their effects are not completely defined. A possible target of n-3 PUFAs is the mitochondrial membrane which has broad implications given that mitochondrial dysfunction and altered metabolism have been associated with cardiac hypertrophy and heart failure. The investigators have recently identified significant mitochondrial dysfunction in the LA of patients with severe MR, as compared to their non-hypertrophied right atrium (RA). However, the investigators have not addressed the possibility that intervention with purified n-3 PUFAs (Lovaza) could improve mitochondrial function. From a mechanistic perspective, the investigators have observed in vitro that n-3 PUFAs accumulate predominately into the mitochondrial membrane of cardiomyocytes where the investigators believe they exert their effects on the biophysical organization of the membrane. Therefore, the CENTRAL HYPOTHESIS is that administering Lovaza to patients with severe MR will reduce apoptosis and improve mitochondrial function in LA (Aim 1). This change in mitochondrial function will be driven by significant biochemical and biophysical remodeling of the mitochondrial membrane (Aim 2).
Silicone gel is a self-drying silicone polymer that forms thin film after application onto the skin. Because silicone film is a medical device, silicone gel is also regarded as a medical device. Silicone gel has been on the market for many years for the management of scar in the phase of treatment as well as in the phase of prevention. In contrast to other methods that are expensive, invasive or inconvenient, silicone gel is convenient, non-invasive and also reasonably priced. However, the number of well-designed clinicial trials for efficacy and safety are not enough to provide robust evidences in making clinical decisions for scar management options. In a prospective, multi-center, investigator-blind randomized half-split study for patients undergoing cesarean sections, the investigators attempt to provide valid information for the efficacy and safety of silicone gel in the prevention phase of scar.