View clinical trials related to Cardiomyopathies.
Filter by:The purpose of this study is to determine whether using an echocardiogram (a painless test where ultrasound is used to see your heart) while using mild electrical stimulation from your own CRT-D device to stimulate the ventricles (the lower chambers of the heart) to squeeze one slightly earlier than the other will show a sustained increase your heart's productivity (Cardiac Output (CO)), following implantation of a Cardiac Resynchronization Device (CRT-D). We believe that squeezing some parts of the heart earlier than others may make the heart a stronger pump.
Nesiritide is a rapid vasodilator that mimics the action of an endogenous hormone - human B-type natriuretic peptide (BNP). BNP is produced naturally in the ventricles of the heart in response to stretch. Nesiritide decreases systemic vascular resistance (SVR), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), and mean pulmonary arterial pressure. Nesiritide does not affect the heart rate, but does increase the stroke volume and consequently cardiac output, resulting in a decrease in the symptoms of decompensated heart failure. It is generally well tolerated, with the major negative side effect being hypotension. When compared to standard therapy consisting of dobutamine and nitroglycerin, nesiritide had similar vasodilatory effects, but showed a lower incidence of arrhythmia. Nesiritide has been approved for IV treatment of patients with acutely decompensated congestive heart failure. Although studies have tested the effectiveness and safety of nesiritide in adult CHF patients, this has not been done in children. Subjects enrolled in this study will be pediatric (<21 years) patients carrying a diagnosis of dilated cardiomyopathy with decompensated congestive heart failure. The standard of care for these patients is to undergo cardiac catheterization with placement of a Swan-Ganz catheter for hemodynamic monitoring. Subjects will be randomly assigned to receive either Nesiritide or placebo (5% Dextrose). The infusion will then be continued for a total of twenty-four hours. During this one day period, measurements of systemic blood pressure, central venous pressure (right atrial pressure), pulmonary capillary wedge pressure, cardiac output, mixed venous saturation, pulmonary vascular resistance, and systemic vascular resistance will be measured at regularly scheduled intervals. The Swan-Ganz catheter will remain in place for 2 hours after the discontinuation of study drug, and then removed. The objectives of this study are: 1. To assess the efficacy of Nesiritide therapy in decreasing the pulmonary capillary wedge pressure, right atrial pressure, and systemic vascular resistance in children with dilated cardiomyopathy. 2. To assess the efficacy of Nesiritide in decreasing pulmonary edema and increasing cardiac index in the above mentioned population. 3. To assess the safety of both bolus administration and continuous infusion of Nesiritide in children with dilated cardiomyopathy. 4. To assess the pharmacokinetics of Nesiritide in this population.
The purpose of this study is to see if taking a cholesterol lowering drug Lipitor (Atorvastatin Calcium)will increase the number of endothelial progenitor cells (EPC's) circulating in the blood of heart failure patients taking this cholesterol-lowering drug, and if this will also show an improvement in the damaged areas of the patient's hearts as documented by MRI scans.
Heart failure affects over 5.3 million Americans and, while other cardiovascular diseases have enjoyed a reduction in mortality rates over the last decade, the mortality from heart failure continues to rise[1]. Thus, identifying novel therapies that can reduce heart failure development and/or progression are warranted. Unifying to most cardiomyopathic processes is an impaired handling of reactive oxygen species (ROS)[2-4]. Reactive oxygen species are generated as byproducts of inflammation and oxidative stress that occur in the setting of normal myocardial aerobic metabolism. Metallothionein, glutathione reductase, and superoxide dismutase are major antioxidants in the myocardium that help combat oxidative stress and prevent myocardial damage. In certain clinical settings, including cardiac ischemia, diabetes, and heavy metal excess (copper, iron), myocardial oxidative stress levels are greatly increased. When pro-oxidant levels exceed myocardial antioxidant capabilities, ROS-induced membrane, protein, and DNA inactivation can lead to the development of cardiac dysfunction. One means of preventing the development or progression of cardiomyopathy is to reduce oxidative stress through up-regulation of intramyocardial antioxidants. Murine studies of cardiomyopathy have shown that oral administration of zinc acetate may succeed as an indirect myocardial anti-oxidant because zinc sufficiently up-regulates the intramyocardial production of superoxide dismutase (a zinc-dependant anti-oxidant enzyme) and metallothionein (a "super antioxidant") [5-8]. Zinc also directly reduces prooxidant Cu levels by reducing gastrointestinal zinc absorption. However, to date, no studies have examined the impact of zinc acetate supplementation in subjects with cardiomyopathy and systolic failure on antioxidant capacity and remodeling. The hypothesis of this pilot study is that administration of oral zinc acetate to humans with cardiomyopathy will lead to an up-regulation of myocardial anti-oxidant capabilities,leading to a favorable reduction in oxidative stress. This study will provide preliminary data to support a randomized, placebo-controlled trial of zinc therapy in heart failure as a means of improving or preventing the progression of systolic dysfunction in subjects with mild-moderate heart failure.
Open-label, multicenter, international, single-treatment study designed to determine TTR stabilization as well as Fx-1006A safety and tolerability, and its effects on clinical outcomes in patients with V122I or wild-type TTR amyloid cardiomyopathy. The study will be conducted in two parts. Part 1 will include a six-week dosing period during which all enrolled patients will self-administer oral Fx-1006A 20 mg soft gelatin capsules once daily for six weeks. At Week 6, blood samples will be collected from each patient to determine TTR stabilization. Patients who complete the Week 6 visit will continue taking daily oral Fx 1006A 20 mg for up to a total of 12 months during Part 2 of this study. If it is determined that a patient is not stabilized at Week 6 (based on TTR stabilization data), the patient will be discontinued from the study. Safety and clinical outcomes will be evaluated during Part 2 of this study. Two whole blood samples for pharmacodynamic assessments (TTR stabilization) and pharmacokinetic assessments (Fx-1006A concentrations as well as calculated steady-state parameters) will be collected at Baseline and Week 6. At Months 6 and 12, two whole blood samples will be collected for pharmacodynamic assessments, and four whole blood samples (two samples per time point) will be collected for pharmacokinetic assessments to be utilized in population pharmacokinetic modeling. Echocardiography, chest x-ray, cardiac MRI, and 24-hour Holter monitoring will be conducted at Baseline, and Months 6 and 12. Six-minute walk test and quality of life utilizing the Patient Global Assessment, KCCQ, and SF-36 will be assessed at Baseline, and Months 3, 6, and 12. NYHA Classification will be assessed at Baseline, Week 6, and Months 3, 6, and 12. Serum markers of troponin I and T, and NT-pro-BNP levels will be assessed at each study visit. Safety and tolerability will be assessed throughout the study. Vital signs, 12-lead ECG, blood and urine samples for clinical laboratory tests (serum chemistry, hematology, coagulation panel, and urinalysis), AEs, and concomitant medications (including diuretic usage) will be assessed at each study visit. Abbreviated physical examinations will be conducted at Baseline, Weeks 2 and 6, and Months 3 and 6, and a complete physical examination will be conducted at Month 12. Clinic visits will be conducted during Screening (Days -30 to -1) and Baseline (Day 0); procedures scheduled for the Baseline visit may be conducted over a period of one week to accommodate patient scheduling. All Baseline procedures must be completed prior to the first self-administered dose on Day 1. Day 1 will be defined as administration of the first dose of study medication, which patients will self-administer at home. During treatment, clinic visits will be conducted at Week 2 (± 2 days), Week 6 (± 1 week), Month 3 (± 1 week), Month 6 (± 2 weeks), and Month 12 (± 2 weeks). Procedures scheduled for the Month 6 and 12 visits may occur over one week during the visit window to accommodate patient scheduling. Monthly telephone contacts (± 1 week of the scheduled date) will be made during months in which no clinical site visits are scheduled (Months 4, 5, 7, 8, 9, 10, and 11) for assessment of AEs and concomitant medications. A final telephone contact to assess AEs and concomitant medication usage will be made 30 days after the last dose of study medication for each patient. Patients who discontinue from the study at any time will have a final visit performed, including all safety assessments, at the time of discontinuation. Any patient discontinuing after the Month 6 visit will also have all exploratory assessments performed.
Coronary artery disease (CAD) is caused by a narrowing of the blood vessels that supply blood and oxygen to the heart. Balloon angioplasty and stent placement are two treatment options for people with reduced heart function caused by CAD. This study will use magnetic resonance imaging (MRI) procedures to evaluate heart function over time in people with CAD who have undergone a balloon angioplasty or stent placement procedure.
This study investigates whether symptom-limited exercise capacity in ischemic cardiomyopathy patients with angina is deleteriously affected by treatment with CK-1827452.
The purpose of this study is to compare cardiac output results obtained using the thermodilution push technique with the Pulmonary Arterial Catheter (PAC) to the predicted cardiac output results obtained from the non-invasive FloWave™ 1000 device.
The aim of the study is to compare clinical benefits of the cardiac resynchronisation (CRT) achieved by the PEA optimised pacing configuration and a CRT optimised by standard clinical procedure. PEA optimised configuration (PEA-CRT) is obtained, during patient's follow-up, using the Peak Endocardial Acceleration sensor features onboard the device.
Several hormones involved in body weight regulation increase the subject's ability to burn fat for energy. The purpose of this study is to investigate how burning fat for energy may affect those hormones and body weight in children. The study will also determine if eating a diet higher in protein alters the amount of fat you burn and how these hormones control body weight.