879 Clinical Trials for Various Conditions
The goal of this clinical trial is to evaluate a novel imaging approach that combines hyperpolarized 13C pyruvate magnetic resonance imaging (HP-13C-MRI) and \[¹⁸F\]Fluorodeoxyglucose positron emission tomography (FDG-PET) in a single exam to improve the prognostic assessment of ischemic cardiomyopathy. The main questions this study aims to answer are: Primary Hypothesis: Can the simultaneous acquisition of HP-13C-MRI and FDG-PET data improve the metabolic, viability, and mechanical function assessment in ischemic cardiomyopathy? Primary Outcome Measure: To determine whether the combined HP-13C-MRI/FDG-PET approach provides better prognostic value for ischemic cardiomyopathy compared to current separate imaging modalities. Secondary Outcome Measures: Baseline metabolic and viability profiles in healthy individuals. Correlation of metabolic imaging with clinical outcomes in preoperative patients with low left ventricular ejection fraction (LVEF). Longitudinal changes in myocardial metabolism post-surgery. Study Design: This is a prospective, non-blinded, single-center study utilizing a hybrid PET-MR scanner for simultaneous imaging. Participants will be divided into three groups: Healthy subjects (n=6) with normal LVEF for baseline reference. Preoperative patients (n=6) with low LVEF due to ischemic cardiomyopathy undergoing coronary artery bypass grafting (CABG). Post-CABG patients (n=6 at 4-6 months, n=6 at 10-12 months) to evaluate post-surgical changes. Procedures: Undergo HP-13C-MRI and FDG-PET imaging in a single session. Blood samples for metabolic biomarkers (lactate, pyruvate, triglycerides, insulin, glucose). Standard clinical cardiac imaging (Echocardiography, SPECT Myocardial Perfusion Imaging).
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.
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.
This is a prospective, single-arm clinical trial in which participants with dilated cardiomyopathy will invite their first degree relatives to undergo mobile cardiac, electrocardiogram screening.
This study will examine the clinical effectiveness of Tafamidis in patients with Mixed Phenotype Transthyretin Amyloidosis using data that already exist in patients' medical records
This is a multicenter, non-interventional study to observe the natural progression of the disease and to study the prevalence of pre-existing antibodies to AAV9 used for gene therapy in a population of patients with PKP2 gene-associated ARVC. Participation from all patients is encouraged regardless of interest in or eligibility for gene therapy.
The goal of this clinical trial is to test IC14 (atibuclimab) in patients with arrhythmogenic cardiomyopathy (ACM) and who have an implantable cardoverter/defibrillator in place. ACM is also called arrhythmogenic right ventricular dysplasia (ARV) or arrhythmogenic right ventricular cardiomyopathy (ARVC). The main questions the study aims to answer are the effect of treatment on blood markers of inflammation, safety, and pharmacokinetics. There will also be measurements of myocardial imaging of C-C chemokine receptor type 2 (CCR2+) immune cells (optional), monitoring of cardiac arrhythmias using the patient's pre-existing intracardiac cardioverter/defibrillator (ICD) and a Holter monitor, electrocardiogram (ECG), echocardiogram (ECHO), and blood tests. Results will be compared to baseline; there is no inactive placebo treatment group. Participants will be asked to undergo screening and baseline testing, then receive 4 intravenous infusions with blood measurements before and after the infusion (including 24, 48, and 72 hours and 7, 14, and 28 days). Participants will be offered specialized scanning of the heart muscle, and will be asked to provide recordings from their ICD, undergo Holter monitoring twice, and have electrocardiograms (ECG), echocardiograms (ECHO) and blood tests.
This is a Phase IIA, randomized, double blind, placebo controlled, multicenter study designed to assess the safety, feasibility, and efficacy of umbilical cord derived mesenchymal stromal cells (UC MSCs), administered intravenously (IV) as a single dose or repeated doses, in patients with ischemic cardiomyopathy (ICM).
The purpose of this study is to evaluate the mavacamten impact on myocardial structure with cardiac magnetic resonance imaging (CMR) in adult participants with symptomatic obstructive hypertrophic cardiomyopathy (oHCM) \[New York Heart Association (NYHA) Functional Class II or III\].
This is an observational, retrospective non-inferiority study with a study sample from a large national database. A machine learning (ML) model will use a national database to predict the clinical diagnosis of ATTRwt-CM among HF patients. This study will include HF patients ≥50 years old.
The purpose of this study is to learn about the natural progression of DCM (dilated cardiomyopathy) caused by BAG3 gene mutations. DCM is a condition as the heart muscle is weakened and the heart becomes enlarged. This makes it hard for the heart to pump enough blood for the body. The study is seeking up to about 35 participants who have: * BAG3 mutation (change in the gene) that causes or is likely to cause dilated cardiomyopathy * NYHA (New York Heart Association) Class I-IV at screening (Stage B-D) * Left Ventricular Ejection Fraction less than or equal to 50% (meaning reduced heart function) All participants in this study will receive their usual treatment. The investigators will observe the natural progression of people who have BAG3 DCM. This will help the investigators better understand the disease and aid in future research. Participants will take part in this study for one year. During this time, participants will visit the site at least 4 times (about every 3 months). Participants will undergo study procedures and give information about their health. These procedures will include a physical exam, cardiac magnetic resonance imaging, echocardiography, ECG monitoring, activity monitoring, cardiopulmonary exercise testing, and blood tests. Participants will answer questions about health and quality of life. The study team will also call participants about 1 time over the phone.
The Canadian CABG or PCI in Patients With Ischemic Cardiomyopathy (STICH3C) trial is a prospective, unblinded, international multi-center randomized trial of 754 subjects enrolled in approximately 45 centers comparing revascularization by percutaneous coronary intervention (PCI) vs. coronary artery bypass grafting (CABG) in patients with multivessel/left main (LM) coronary artery disease (CAD) and reduced left ventricular ejection fraction (LVEF). The primary objective is to determine whether CABG compared to PCI is associated with a reduction in all-cause death, stroke, spontaneous myocardial infarction (MI), urgent repeat revascularization (RR), or heart failure (HF) readmission over a median follow-up of 5 years in patients with multivessel/LM CAD and ischemic left ventricular dysfunction (iLVSD). Eligible patients are considered by the local Heart Team appropriate and amenable for non-emergent revascularization by both modes of revascularization. The secondary objectives are to describe the early risks of both procedures, and a comprehensive set of patient-reported outcomes longitudinally.
The purpose of this study is to test the safety and preliminary efficacy of AAVrh.10hFXN to treat the cardiomyopathy associated with Friedreich's ataxia (FA). AAVrh.10hFXN is a serotype rh.10 adeno-associated virus gene transfer vector coding for Frataxin (FXN). The drug is administered intravenously. This is a phase 1, open label, dose escalation study with a total of 25 participants.
The purpose of this study is to improve the cardiovascular care of adult cancer survivors. The goal is to obtain the data necessary to plan and develop a nation-wide network of a screening program that can help provide cost-effective and long-term monitoring.
In Fabry disease (FD), α-galactosidase A deficiency leads to the accumulation of globotriaosylceramide (Lyso-Gb3 and Gb3), triggering a pathologic cascade that causes progressive damage to multiple organs, including the heart. The heart is one of the organs that is very sensitive to the deficiency of α-galactosidase A. There is a subgroup of patients with significant residual α-galactosidase activity and a phenotype with primary cardiac involvement, occasionally referred as "cardiac variant." The manifestations of cardiac involvement in FD are left ventricular hypertrophy (LVH), diastolic dysfunction, microvascular angina. Cardiac hypertrophy is the most common cardiac pathology and cause of death in patients with FD. The elevation of the inflammatory markers strongly demonstrates that chronic inflammation drives the cardiovascular pathophysiology in FD. Moreover, plasma TNF, TNFR2, Il-6 specifically elevated in FD patients with cardio hypertrophy. The chronic inflammation in combination with elevated Lyso-Gb3 further drives the FD progression even under therapy. The expression of the endothelial-cardiomyocyte growth factors will change in response to chronic inflammation during the development of cardiac hypertrophy. This is a clinical observational study designed to identify the role of inflammatory signaling markers and secreted growth factors in the progression of cardiac pathology in FD
Background: HCM is a genetic heart disease. It can cause fatigue, chest pain, or even death. For more than 50 years, a surgery called septal myectomy has been used to help people with this disease. Dr. Andrew G. Morrow originated the surgery and performed it more than 200 times at NIH starting in 1960. Researchers want to learn the long-term success of this surgery. Objective: To determine long-term survival at least 35 years after surgical myectomy at NIH and examine data for people who are confirmed to be deceased or alive. Eligibility: People who had surgical myectomy by Dr. Morrow from 1960 to 1983. Design: This study uses images and data that were obtained in the past. Many of the participants are deceased. Most of the others are no longer being followed at the NIH. The medical records of people treated by Dr. Morrow were microfiched. These records can be accessed at the NIH. The records will be searched for keywords to find participants for this study. Participants clinical data, such as lab testing and imaging, will be used. Other data collected as part of the original study will also be used. Researchers will use participants name, date of birth, and Social Security number to learn if they are alive or deceased. If they are deceased, researchers will try to find the age of death. Online databases and search engines will also be used. Survival data will be compared to data from the general U.S. population for the same time period. Data will be stored in a database that is password protected. The study will last about 1 year.
This study is designed to determine the efficacy and safety of colchicine in patients with chronic kidney disease.
A study to assess the safety and preliminary efficacy of serial intravenous dose of Allogeneic Mesenchymal Bone Marrow Cells in subjects with heart failure and implanted left ventricular assist devices.
Phase 3 efficacy and safety study to evaluate acoramidis (AG10) HCl 800 mg administered orally twice a day compared to placebo in subjects with symptomatic Transthyretin Amyloid Cardiomyopathy (ATTR-CM).
This study evaluates mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy, in comparison to patients with well-understood arrhythmogenic substrate (ischemic cardiomyopathy), as well as to individuals free from arrhythmogenic substrate
The goal of this protocol is to obtain information from individuals with cardiomyopathy and from their families in order to elucidate the molecular genetics of this disorder. This will provide the basis for future genetic counseling as well as contribute to elucidating the biology of normal and abnormal cardiac function.
The purpose of this study is to use cardiac magnetic resonance imaging (CMR) and echocardiographic tissue Doppler imaging to demonstrate a unique restrictive cardiomyopathy of sickle cell disease. The investigators will characterize its frequency and how it might change (e.g., presence/absence and severity) over a 2-year period.
To determine the safety profile of CAP-1002 administered by multi-vessel intracoronary infusion in subjects with DCM. The study will further explore safety and exploratory efficacy endpoints of CAP-1002.
The primary objective of this study was to evaluate the effect of eleclazine (GS-6615) on exercise capacity as measured by Peak oxygen uptake (VO2) achieved during cardiopulmonary exercise testing (CPET), in participants with symptomatic hypertrophic cardiomyopathy (HCM).
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.
This study proposes to describe how children s hypertrophic cardiomyopathy (HCM) risk status affects family functioning, behaviors, and relationships. HCM is the most common inherited cardiovascular single-gene disorder. Individuals with HCM may experience shortness of breath, chest pain, palpitations, dizziness, syncope, heart failure, and arrhythmias predisposing to sudden cardiac death at any age. Notably, HCM is the most common cause of sudden cardiac death in people under 30 years of age. Genetic testing can identify at-risk individuals; however, the impact of potentially life-altering genetic information on families remains largely unexplored. Increasingly, health care providers are providing the testing in children for conditions like HCM that are life-threatening and medically manageable without the benefit of understanding the psychological consequences. The few studies that have been conducted suggest that genetic testing in children may result in changes to family relationships, parental emotional wellbeing, parenting behaviors, and child functioning in a subset of children. One synthesis of these studies suggests that children as a group show little evidence for maladjustment to risk information, but that parents are affected by the carrier status of their children. The proposed study intends to further this body of knowledge by exploring the impact of children s risk status on families with HCM. Health care providers and researchers can inform their work with HCM families by better understanding the potential impact of genetic risk as an important component of families adaptation to the life-threatening information about their children. The families targeted for this exploratory study will be purposively sampled from those that have been aware of the children s risk status or not at-risk status for HCM for at least 3 months. The cross-sectional design is composed of semi-structured interviews with a parent and, separately, with his/her 13 to 23 year-old child who is either a carrier for HCM, a non-carrier, or at 50% risk for being a carrier. The interview will target issues related to the perceived impact of the child s risk status on family functioning, parenting behaviors and relationships. Data from the parent-child dyads will be analyzed for concordance/discordance along parallel themes. The results of this study may facilitate the understanding of the perceived impact of learning children s HCM risk status, which will inform both clinical care and future research. Importantly, since predictive testing in children for adult-onset diseases is generally discouraged, very little is actually known about its impact on families. Therefore, the study of this unique subgroup of an HCM population that uses clinically indicated predictive testing in childhood offers a preliminary opportunity to learn about predictive testing of minors....
We hope to determine the importance of different genes (including B receptors) in anthracycline-induced cardiomyopathy. This has important benefits to patients exposed to anthracyclines, as this could help determine whether certain individuals have increased susceptibility to cardiac injury.
Peri-partum cardiomyopathy is a heart muscle weakness that occurs during or following pregnancy. Research suggests that many initial heart injuries including viruses, pregnancy and other unknown causes, can lead to a process of inflammation of the heart muscle which can weaken the heart and cause cardiomyopathy. Why this process occurs in women during pregnancy is not well understood and if it differs from those women who develop cardiomyopathy from a virus is unknown. This study has been proposed to look at genetic information (DNA) as well as the immune system (the body's response to fight off infections and/or viruses) to find possible causes for the heart muscle damage that occurs in peripartum cardiomyopathy.
The objective of this study is as follows: * Perform genetic analysis to define the prevalence of each of the known gene mutations in an unselected cohort of patients with focal segmental glomerulosclerosis (FSGS) * Perform a comprehensive assessment of cardiovascular status to determine the incidence of any cardiac abnormalities in patients with FSGS * Determine if patients with mutations in specific proteins are more likely to have cardiovascular abnormalities * Initiate long-term follow up in all patients to determine whether cardiac prognosis is related to any specific genetic abnormality
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.