View clinical trials related to Hypertrophic Cardiomyopathy.
Filter by:Objective The objective of the study is to assess the structural and functional cardiac effects of treatment with losartan in patients with hypertrophic cardiomyopathy (HCM). Design The study is a randomized, placebo‐controlled, double‐blinded trial. The follow‐up period is 12 months. 130 patients with HCM will be included in predefined subgroups. Genotype positive relatives with borderline hypertrophy (> 13 mm) will also be included. Data on individuals with borderline hypertrophy will be analysed separately from the rest of the cohort. Primary outcome Ventricular hypertrophy assessed as left ventricular mass and maximal wall thickness.
This study is being done to determine whether or not new blood test(s) can determine the severity of heart conditions. Aortic stenosis, hypertrophic cardiomyopathy, mitral regurgitation, aortic regurgitation, artificial heart valve regurgitation or stenosis, and tricuspid valve regurgitation associated with pacemaker leads are the cardiac disorders under study. The blood tests involve analysis for von Willebrand Factor antigen and activity, von Willebrand Factor multimers, and brain natriuretic peptide (BNP) levels. The results of the blood tests will be compared to the information from the clinically-indicated echocardiogram and one blood test compared to another.
The purpose of this study is to determine whether taking losartan helps people with hypertrophic nonobstructive cardiomyopathy feel better by decreasing the amount of heart muscle thickening and/or the amount of heart muscle scarring.
Biventricular Pacing has been shown an improvement of symptoms in patients with heart failure. A temporary pacing is necessary in patients after cardiac procedures. In patients with hypertrophic cardiomyopathy, a single right ventricular pacing can decrease the cardiac output and blood pressure. The investigators propose that biventricular pacing in these patients and conditions results in an improvement of symptoms instead of single right pacing.
Hypertrophic Cardiomyopathy (HCM) is the most common genetic cardiomyopathy and remains the leading cause of sudden cardiac death in young people and an important cause of heart failure symptoms and death at any age. In HCM, pathological remodeling of the left ventricle involving myocardial fibrosis is likely a major contributor to cardiac dysfunction and also a nidus for the generation of ventricular arrhythmias. Serum markers of collagen turnover have been shown to reliably reflect the magnitude of myocardial fibrosis in a variety of cardiovascular diseases. In addition, aldosterone antagonist drugs have been shown to decrease fibrous tissue formation in the myocardium in certain pathologic cardiovascular states in which aldosterone production is increased. In HCM, aldosterone production is up-regulated and has been implicated in the formation of myocardial fibrosis. Therefore, the specific aims of this proposal are to: 1. assess serum markers of collagen turnover at baseline and correlate these findings with a variety of clinical and morphologic disease parameters 2. examine the effects of a 12-month treatment with the aldosterone antagonist spironolactone on magnitude of fibrosis as measured by serum markers of collagen turnover as well as changes in clinical and morphologic disease parameters. 3. explore the effects of a 12-month treatment with aldosterone antagonist spironolactone on heart failure status, diastolic function, arrhythmic burden, and total LV mass and quantity of fibrosis by CMR. The results of this proposal will offer important insights into the clinical significance of myocardial fibrosis in this primary genetic cardiomyopathy. The demonstration that spironolactone decreases fibrosis and improves clinical course would provide the rational for a larger multicenter clinical trial evaluating this novel therapy for improving clinical outcome in patients with HCM.
Paroxysmal or chronic atrial fibrillation (AF) develops in about 20- 25% of adult patients with hypertrophic cardiomyopathy (HCM) and represents an important complication in the clinical course of the disease, with adverse long-term consequences on functional status and outcome. Therefore, aggressive therapeutic strategies are indicated to restore and maintain sinus rhythm (SR) in patients with HCM. Nevertheless, pharmacologic prevention of AF recurrence is challenging because of the limited long-term efficacy and potentially hazardous side effects of available treatment options. Currently radiofrequency catheter ablation (RFCA) of AF is successfully used in clinical practice. However, comparison of the efficacy and safety of these two therapeutic options has not been done up till now in randomized manner in this group of patients. Thus, the aim of the present study is to compare the efficacy and safety of RFCA vs. antiarrhythmic drug therapy in patients with HCM and AF.
The purpose of this study is to learn about the twisting or wringing motion of the heartbeat called Left Ventricular Torsion (LV Torsion) which can be seen on ultrasound.
Hypertrophic Cardiomyopathy (HCM) is a relatively common inherited heart muscle disease. Many patients experience symptoms of breathlessness, fatigue and chest pain. These symptoms are not always controlled with current therapies. Recently the investigators showed that a drug called Perhexiline markedly improved exercise capacity and symptoms in patients with heart failure. In this proposal the investigators wish to test whether Perhexiline improves exercise capacity and relieves symptoms in patients with HCM
This is a pilot clinical trial to assess whether the administration of diltiazem may be able to decrease the development or progression of hypertrophic cardiomyopathy (HCM). Diltiazem is a commonly used medication for the treatment of high blood pressure and studies on animals with HCM suggest that diltiazem decreases disease development. This study specifically targets individuals in the "prehypertrophic" phase of HCM-- those with documented sarcomere gene mutations without echocardiographic or EKG evidence of LVH, and therefore without a clinical diagnosis of HCM. The hypothesis of this study is that starting diltiazem administration early in life (in the prehypertrophic phase) will decrease the progression of HCM in individuals with sarcomere gene mutations. This will be assessed by looking at an improvement in the heart's ability to relax using echocardiography, as well as exploratory analyses of a broad range of features reflecting the heart's structure and function.
The purpose of this study is to determine if a drug called atorvastatin will reduce the size and stiffness of the muscle in the left ventricle of the heart.