Active clinical trials for "Cardiomyopathies"

Background A specific mutation in phospholamban (the PLN R14del mutation), has its origin in the northern parts of the Netherlands (Figure) and causes a severe lethal dilated and/or an arrhythmogenic cardiomyopathy. A large proportion of the population of Groningen (1:1000) carries this mutation. Until now, there is no specific treatment available for patients with PLN cardiomyopathy. Patients are treated like any other type of heart failure patients, although PLN cardiomyopathy has a different etiology from "usual" heart failure. Treatment is therefore insufficient; malignant ventricular arrhythmias and end-stage heart failure at a young age are very prevalent. To develop treatment options, the investigators aim to study the following knowledge gaps: Pathophysiology. The clinical phenotype of PLN R14del cardiomyopathy bears characteristics of both arrhythmogenic and dilated cardiomyopathy (ACM and DCM). Using an "omics" approach of plasma, cardiac and skeletal muscle of patients and controls, the investigators aim to reveal distinct pathways affected by the mutant PLN, unique to the PLN R14del cardiomyopathy. This will be related to clinical data and mutant PLN expression levels in both cardiac and skeletal muscle biopsies. Using this extensive profiling, the investigators aim to identify disease mechanisms and provide the context for future risk stratification and disease progression monitoring. Penetrance. Subjects with a heterozygous PLN R14del mutation show a wide variety in phenotype. Within the same family, patients can present either with over heart failure in their 20's or completely asymptomatic until at least their 70's. So far, no modifiers have been identified. The investigators will study cardiomyocytes derived from induced pluripotent stem cells from patients who are severely affected versus family members who are unaffected but carry the mutation. Treatment response. The investigators have identified potential treatments, and confirmed their efficacy in in vivo models of PLN cardiomyopathy. To establish their efficacy in a human setting, the investigators will generate 3D cardiac tissues of cardiomyocytes gathered from induced pluripotent stem cells of patients affected in varying degrees and subject these tissues to the treatment. Methods: For the above purposes, the investigators will collect and analyze the following data/materials: Serum and plasma of 90 PLN R14del carriers: 30 unaffected, 30 early affected and 30 end stage. Skin biopsy of 20 PLN R14del carriers: 10 unaffected, 10 end stage. Cardiac muscle biopsy (obtained during left ventricular assist device [LVAD]/ heart transplant [HTx] surgery) of 30 patients: 10 R14del, 10 arrhythmogenic cardiomyopathy, 10 dilating cardiomyopathy. Skeletal muscle biopsy of 10 patients: 5 R14del, 5 non R14del family members

There is a certain gene called sarcoplasmic reticulum gene (SERCA2a), which is found in heart muscle. This gene is also found in blood vessels and skin tissue. When active this gene builds a crucial protein inside the heart muscle called SERCA2a protein. This is responsible for regulating calcium levels inside your heart muscle. When this gene is not activated, studies have shown that it can lead to abnormal electrical currents in the heart that can lead to death. The investigators are conducting this study to prove that SERCA2a gene is inactive in patients with kidney disease. Scientists found that patient at risk for abnormal electrical currents in the heart can be tested by what they called "microvolt Twave alternans." This is a very delicate machine much more sensitive than a regular electrocardiogram that you do at the cardiology office.

Cardiac amyloidosis are related to the accumulation of fibrillar proteins in the extracellular leading to disruption of the cardiac tissue architecture. Amyloidosis in transthyretin (TTR) are the most common hereditary amyloidosis but remain poorly studied at heart. This is serious and deadly. The prevalence of TTR amyloidosis is probably underestimated in hypertrophic cardiomyopathy (HCM) often of unknown etiology because of the lack of systematic implementation of myocardial biopsy because of their side effects.

The purpose of this study is to determine whether galectin-3 binding protein plasma levels can predict adverse cardiovascular events in patients with coronary artery disease and/or heart failure.

We are performing a research study to learn more about the control of an individual's blood thinning (anticoagulation) on warfarin. Individuals from an anticoagulation clinic are being asked to participate in order to see if a lottery which provides the opportunity to win money in combination with the use of the Med-eMonitor might be useful in helping patients to achieve better control of their anticoagulation therapy. Half of the participants will be enrolled in the lottery arm and the other half will be a control group who will receive the Med-eMonitor only.

The goal of this study is to determine if nutritional therapy can effectively treat/prevent T2DM and its consequent cardiomyopathy.

This study will examine the relationship between certain measures of heart function and exercise capacity in patients with hypertrophic cardiomyopathy (HCM). Patients who participated in NHLBI studies 01-H-0006 ("Double Blind Placebo-Controlled Study of Pirfenidone - A Novel Anti-Fibrotic Drug - in Symptomatic Patients with Hypertrophic Cardiomyopathy Associated with Left Ventricular Diastolic Dysfunction") and 96-H-0144 ("Double Blind Placebo-Controlled Study of Long-Term Effects of Angiotensin-Converting Enzyme Inhibition (Enalapril) and Angiotensin II Receptor Blockade (Losartan) on Genetically-Induced Left Ventricular Diastolic Dysfunction") are eligible for this study. Data from echocardiograms and measures of left ventricular pressure obtained from patients in those studies will be analyzed in the current study to assess their influence on exercise capacity. No additional tests, treatments or other procedures are required. Information from this study may help in the development of improved drug treatments for HCM.

The human heart is divided into four chambers. One of the four chambers, the left ventricle, is the chamber mainly responsible for pumping blood out of the heart into circulation. Hypertrophic cardiomyopathy (HCM) is a genetically inherited disease causing an abnormal thickening of the heart muscle, especially the muscle making up the left ventricle. When the left ventricle becomes abnormally large it is called left ventricular hypertrophy (LVH). This condition can cause symptoms of chest pain, shortness of breath, fatigue, and heart beat palpitations. This study is designed to compare the ability of two drugs (enalapril and losartan) to improve symptoms and heart function of patients diagnosed with hypertrophic cardiomyopathy (HCM). Researchers have decided to compare these drugs because each one has been used to treat patients with other diseases causing thickening of the heart muscle. In these other conditions, enalapril and losartan have improved symptoms, decreased the thickness of heart muscle, improved blood flow and supply to the heart muscle, and improved the pumping action of the heart muscle. In this study researchers will compare the effectiveness of enalapril and losartan when given separately and together to patients with hypertrophic cardiomyopathy (HCM).

To ascertain the sixteen year mortality status of the 361,662 middle-aged men screened in 1973-1975 for the Multiple Risk Factor Intervention Trial (MRFIT).

The intent of the study is to show the potential benefits of angiotensin converting enzyme inhibitors in preventing anthracycline induced cardiotoxicity. This is a prospective, randomized, blinded and placebo-controlled clinical trial that will enroll patients who are to be treated with anthracycline chemotherapy (doxorubicin, epirubicin, idrarubicin, or mitoxantone) to either lisinopril or placebo group. The study will be performed at the Genesys Hurley Cancer Institute. The treating oncologist who intends to start the patient on anthracycline chemotherapeutic agent will provide the patient with a recruitment flyer and informed consent form and then referred to the research nurse. Subjects interested in participation, that do not meet any of the exclusion criteria, will be consented and enrolled by the research nurse prior to their first treatment with chemotherapy. Over a period of 1 to 3 weeks the study medication will be titrated in a stepwise fashion to a target of 20 mg daily, maintaining a systolic blood pressure greater than 90 mmHg. A baseline echocardiogram with strain and strain rate imaging will be obtained prior to initiation of anthracycline chemotherapy. Subsequent echocardiograms with strain and strain rate imaging will be performed every 3 months for a total of 12 months. Patients will be followed for a total of 12 months, starting on the day of enrollment. We intend to recruit a total of 200 patients. The primary endpoint of this study is a change in change in strain and strain rate parameters prior to, during, and after anthracycline chemotherapy compared to placebo. Study data will be collected and managed using the Ascension installation of REDCap (Research Electronic Data Capture). REDCap is a secure, web application designed to support data capture for research studies, providing user-friendly web-based case report forms, real-time data entry validation (e.g. for data types and range checks), audit trails and a de-identified data export mechanism to common statistical packages. Echocardiographic data will be stored in cine-loop format on a private, password protected echocardiogram viewing software and analyzed by a separate blinded cardiologist. Patients will be evaluated according to the standard oncologic evaluation. The treating oncologist will make decisions on their treatment based on their personal standards and clinical judgement.