43 Clinical Trials for Various Conditions
This study will look into how CDR132L (a potential new medicine) works on the structure and function of the heart in people living with heart failure. Participants will either get CDR132L or placebo (a medicine which has no effect on the body), which treatment the participants get is decided by chance. The study will last for about 60 weeks.
The objective of the proposed project is to quantify the prevalence and disparities of undiagnosed left ventricular hypertrophy (LVH) in Emergency Department (ED) patients with persistently elevated asymptomatic BP, and to measure the effect of disclosure, education, and expedited referral on 3-month outpatient follow-up and treatment rates for ED patients with newly diagnosed LVH by POCUS. Additionally, investigators will create a database of annotated clips for future development of a machine learning algorithm for LVH detection on POCUS.
The electronic health record contains vast amounts of cardiovascular data, including potential clues that an individual may have unrecognized cardiac conditions. One important example is the finding of thickened heart muscle -- known as left ventricular hypertrophy (LVH) -- on echocardiograms (heart ultrasounds). If the underlying cause of LVH is untreated, individuals are at an increased risk of developing more severe pathology. As the most common cause of LVH, hypertension and its downstream consequences account for more cardiovascular deaths than any other modifiable risk factor. Critically, many individuals have signs of cardiac damage from hypertension before it is diagnosed or treated. Despite this evidence, there are often gaps in healthcare delivery that contribute to substandard recognition and treatment. Thus, there is an urgent need to validate alternative cost-effective screening and intervention strategies. Echocardiograms are ordered by many specialties and for numerous indications. Even when LVH is reported, the finding may be underappreciated and not prompt further evaluation. Whether data from prior echocardiograms can be harnessed to improve patient care through a centralized intervention is unknown. Accordingly, the goal of this randomized pragmatic clinical trial is to study the impact of a centralized clinical support pathway on the diagnosis and treatment of hypertension and the recognition of LVH-associated diseases in individuals with evidence of thickened heart muscle on previously performed echocardiograms.
The purpose of this research study is to test whether treatment with isosorbide mononitrate will improve left ventricular hypertrophy ("thickening") which puts people at risk for developing heart failure. Once it develops, heart failure is a very serious condition and thus it is important to find ways to prevent it from happening. The investigators have reasons to believe that dilating the blood vessels with this specific medication will improve the thickening of the heart, which increases the risk of heart failure.
Individuals with kidney disease are at a higher risk for heart and vascular diseases, including heart attacks and strokes, than those with normal kidney function. The purpose of this research study is to collect information on the causes, complications and treatment of kidney disease. Patient characteristics, comorbid diseases and laboratory markers used in routine practice, as well as novel biochemical markers and genetic data will be collected to examine relationships between biochemical and genetic markers and cardiovascular risk. Information on the health history of incident hemodialysis and peritoneal dialysis patients will be captured using structured patient interviews and review of medical records. Blood and urine specimens will be collected at the time of dialysis initiation and stored in order to perform novel biochemical and genetic assays in the future. The overall goal of the CKDCS/LUCID study is improve understanding of cardiac-associated risks and to improve treatment in patients with kidney disease. A cardiac imaging substudy will be performed in a subset of patients enrolled. The goals of the substudy are to examine whether the risks of developing common cardiac-related complications (coronary artery calcification \[CAC\] and left ventricular hypertrophy \[LVH\]) are associated with certain medications taken by individuals on dialysis and whether these risks are modified by a genotypic predisposition.
The hypothesis of this trial is to assess the effect of spironolactone on heart size and mass
To compare the efficacy and safety of aliskiren in combination with losartan compared to losartan on the regression of the increased size of the left ventricle in overweight patients with high blood pressure.
Left ventricular hypertrophy (LVH) increases the risk of cardiovascular morbidity and mortality in patients with high blood pressure, compared to those without LVH. Reduction of left ventricular mass (LVM) with antihypertensive agents is associated with improved clinical outcome. This study will evaluate the effects of amlodipine/benazepril in reducing LVM in patients with high risk hypertension.
Prospective study on the structural and functional changes in the heart of adult women assessed by echocardiogram and in lipid metabolism that occur in response to physical training. Using echocardiogram we will characterize the early determinants of "athletic remodeling". We will also assess the effect of intense physical training on lipid metabolism, focus on HDL subspecies and function.
This is a non-invasive/observational study in healthy and mild HF subjects utilizing clinical and ambulatory measurements to improve detection, monitoring, and management of HF risks.
The investigators' goal is to show that in hypertensive men and women with left ventricular hypertrophy (LVH) treatment with a mineralocorticoid receptor (MR) antagonist, versus a thiazide-like diuretic, will improve coronary microvascular function and cardiac efficiency, which will associate with improvements in LV structure and function. The investigators will achieve this through a randomized, controlled, basic experimental study involving humans (BESH).
The proposed mechanistic trial will test the effect of dietary sodium reduction on cardiac and vascular structure and function in those with elevated blood pressure or hypertension. Findings from this study will fill the knowledge gap on the underlying mechanisms of dietary sodium intake on cardiovascular disease risk in addition to blood pressure and could provide further evidence on sodium reduction for the prevention of cardiovascular disease.
Studying the causal roles of components of the renin-angiotensin-aldosterone system (including angiotensin-(1-7) (Ang-(1-7)), angiotensin-converting enzyme 2 (ACE2), Ang II, and ACE), uric acid, and klotho in pediatric hypertension and related target organ injury, including in the heart, kidneys, vasculature, and brain. Recruiting children with a new hypertension diagnosis over a 2-year period from the Hypertension and Pediatric Nephrology Clinics affiliated with Brenner Children's Hospital at Atrium Health Wake Forest Baptist and Atrium Health Levine Children's Hospital. Healthy control participants will be recruited from local general primary care practices. Collecting blood and urine samples to analyze components of the renin-angiotensin-aldosterone system (Ang-(1-7), ACE2, Ang II, ACE), uric acid, and klotho, and measuring blood pressure, heart structure and function, autonomic function, vascular function, and kidney function at baseline, year 1, and year 2. Objectives are to investigate phenotypic and treatment response variability and to causally infer if Ang-(1-7), ACE2, Ang II, ACE, uric acid, and klotho contribute to target organ injury due to hypertension.
This is an ongoing, prospective cohort study of children and young adults who are evaluated in the Reversing the Negative Effects of Weight on the Heart (ReNEW) Clinic at Johns Hopkins University. Demographic and clinical data of patients who agree to participate are obtained via chart review and entered into a longitudinal clinic registry.
The overall goal of this PET-MR imaging trial is to evaluate 11C-Martinostat, a histone deacetylase targeted radioligand, in patients with aortic stenosis, individuals with diabetes, and healthy volunteers.
Hereditary hypophosphatemia encompasses rare genetic conditions characterized by renal phosphate wasting. Increased circulating levels of fibroblast growth factor 23 (FGF23), a key regulator of phosphorus metabolism, are critical to the pathophysiology of these diseases, most notably in X-linked hypophosphatemia (XLH). Increased FGF23 induces hypertrophy and scarring in the heart in part via stimulating the traditional renin-angiotensin system (RAS) pathway, angiotensin-converting enzyme (ACE)/angiotensin (Ang ll), particularly in patients with chronic kidney disease, but the effect of FGF23 on the heart in patients with FGF23-related hypophosphatemic diseases is unknown. In addition, the relationship between FGF23 and the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) (Ang-(1-7) pathway of the RAS is unknown. The objective of this study is to describe the relationship between FGF23, which causes low phosphorus levels, and components of the RAS in the blood and urine to help the investigators understand why the disease occurs and how to better treat it. Subjects will be identified by querying the Electronic Medical Record according to medical diagnosis. Thirty subjects, 2-24 years of age, will be recruited from the tertiary care Pediatric Endocrinology and Pediatric Nephrology clinics at Brenner Children's Hospital. Inclusion criteria include a confirmed diagnosis of hereditary FGF23-related hypophosphatemia. Clinical data will be obtained from the Electronic Medical Record. Each subject will undergo study assessments at baseline, 6 months and 1 year that include blood work, an echocardiogram, and blood pressure measurements. The primary hypothesis is that subjects with higher Ang-(1-7) levels have lower rates of cardiac hypertrophy and thus are protected against high FGF23 levels. The secondary hypothesis is that subjects with higher Ang-(1-7) levels have lower systolic blood pressure.
The development of symptomatic heart failure is frequently preceded by a pre-clinical period of structural remodeling in the heart. The remodeling process driving this transition, however, remains poorly understood. The investigators hypothesize that imaging the diffusion of water in the heart with MRI will allow its microstructure to be resolved. The investigators further hypothesize that the characterization of microstructural changes in the heart will help elucidate the pathogenesis of heart failure and the transition from a compensated to a decompensated state. Patients with recent myocardial infarcts and left ventricular hypertrophy, who are at risk for the development of heart failure, will be enrolled. The participants will undergo serial diffusion tensor MRI (DTI) imaging of the heart to characterize changes in myocardial microstructure over time.
This project seeks to reduce the disparity in hypertensive heart disease which exists for African-Americans who have poorly controlled hypertension (HTN), also known as blood pressure (BP). The investigators are targeting a highly vulnerable, often neglected subject population which stands to benefit tremendously from better BP control and a corresponding decrease in heart damage. HTN occurs early in life and more often in African-Americans, reducing both quality and quantity of life. Inner-city African-Americans with HTN utilize the emergency department (ED) for chronic BP management. Like cardiovascular disease, vitamin D deficiency disproportionately affects African-Americans. Vitamin D is thought to play an important role in cardiovascular health. Vitamin D replacement in those who are deficient has been thought to reduce the cardiovascular disease, especially if initiated early before irreversible damage has occurred, but this has yet to be tested in a prospective clinical trial. Accordingly, this proposal was designed to investigate the relationship between vitamin D and cardiac damage (as identified on cardiac magnetic resonance imaging) in a cohort of African-American, vitamin D deficient hypertensive patients without prior history of heart disease. The primary objective of this proposal is to evaluate the efficacy of vitamin D therapy in vitamin D deficient African-Americans with HTN. Vitamin D is an inexpensive treatment, which, if shown to be effective could improve the existing approach to a widely accessible, cost-effective option.
Heart failure with preserved ejection fraction (HFpEF) accounts for over 50% of heart failure cases in the United States, affecting a primarily elderly population. No treatment has been shown to affect mortality in HFpEF, which is more than 50% at five years a hospitalization. This project explores the underlying cardiovascular physiology of patients with HFpEF with the goal of identifying new therapeutic targets that would allow improved treatment of this devastating disease.
We will directly test the hypothesis that an initial strategy of lisinopril-based therapy will be more effective than atenolol-based therapy in causing regression of left ventricular hypertrophy (LVH) over one year in patients with hemodialysis hypertension despite similar degree of BP reduction.
To evaluate the effects of paricalcitol capsules on cardiac structure and function over 48 weeks in patients with Stage 3/4 chronic kidney disease (CKD) who had left ventricular hypertrophy (LVH).
The Dallas Heart Study (DHS-1) is a large, multi-ethnic, population-based epidemiological study designed to identify determinants of atherosclerotic heart disease (ASHD) in a representative United States (US) urban environment. This study completed enrollment in 2003. Our objective is to pinpoint factors contributing to progression: 1. from health to ASHD risk; 2. from ASHD risk to subclinical ASHD; and 3. from subclinical to clinical ASHD. Identification of the critical factors in these transitions will enable targeted implementation of appropriate therapy to interdict before clinical ASHD develops.
How high blood pressure in hemodialysis patients should be diagnosed and treated using medications or without medications is the purpose of this study.
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 the circulation. There is an inherited condition affecting the heart, passed on through genetics, hypertrophic cardiomyopathy (HCM). HCM causes the left ventricle to become abnormally enlarged (left ventricular hypertrophy LVH). Some patients with the abnormal genes that may cause HCM do not have the characteristic LVH. Approximately 20 - 40% of patients with the genetic abnormality (missense mutation of genes encoding for sarcomeric protein) actually have an enlarged left ventricle. Because of this, researchers believe there may be other factors, along with the genetic abnormality that contribute to the development of HCM. Researchers are interested in learning more about several factors they suspect may play a role in the development of HCM. Specifically, researchers plan to study levels of a hormone and the protein it attaches to, which may contribute to the development of an abnormally enlarged heart. Insulin-like growth factor (IGF-1) and insulin-like growth factor binding protein (IGFBP) work together with growth hormone (GH) in the development and maturation of many organ systems. Previous studies have suggested that these hormones affect the development and function of the heart. Patients participating in this study will undergo a variety of tests including collection of blood samples, echocardiogram of the heart, treadmill exercise test, and continuous electrical monitoring of heart activity (Holter monitor).
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 the circulation. Hypertrophic cardiomyopathy is a genetically inherited disease causing an abnormal thickening of heart muscle, especially the muscle making up the left ventricle. When the left ventricle becomes abnormally large, it is called left ventricular hypertrophy (LVH). Patients with HCM can be born with an enlarged left ventricle or they may develop the condition in childhood or adolescence, usually during the time when the body is rapidly growing. However, not all patients with the abnormal genes linked to HCM have the characteristic LVH. Currently, it is impossible to tell if a patient with the genes for HCM will develop LVH. A recently developed ultrasound tool called an integrated backscatter analysis (IBS), may allow researchers to determine those children who may later develop HCM and LVH. In order to test this, researchers plan to use IBS to study normal children with relatives diagnosed with HCM. This study will compare the results of IBS done on normal children with relatives diagnosed with HCM , normal children, and children with evidence enlarged heart muscle (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).
This is a single arm Phase 2 trial to evaluate the efficacy and safety of RP-A501, a recombinant adeno-associated virus serotype 9 (AAV9) containing the human lysosome-associated membrane protein 2 isoform B (LAMP2B) transgene, in male patients with Danon Disease.
Pediatric primary hypertension is increasingly common, occurring in 5-10% of normal-weight children and up to 25% of children with obesity. It is a risk factor for adult cardiovascular and renal disease. But even during childhood, hypertension is associated with significant morbidity, including cognitive impairment and organ damage. In the heart and kidneys, this organ damage is characterized by thickened heart muscle (left ventricular hypertrophy) and spillage of protein in the urine (albuminuria). Obese children are also at risk for fatty liver disease. However, the cause of pediatric primary hypertension, the role of obesity, and the mechanisms behind heart and kidney injury are poorly understood. Due to these limitations, there are no first-line medications, and treatment is often inadequate. An altered renin-angiotensin system may cause primary hypertension and related organ damage. Evidence suggests uric acid, FGF23, klotho, and obesity play a role in renin-angiotensin system-mediated injury. An improved comprehension of the pathophysiology of pediatric primary hypertension could enhance clinical care by targeting treatment to the cause of disease and informing novel measurement of organ damage.
The purpose of this study was to investigate the effects of initiation of sacubitril/valsartan vs enalapril treatment on objective measures of both waking activity and sleep in subjects with heart failure with reduced ejection fraction.
This is a pilot feasibility study to determine the effects of an activated vitamin D compound (paricalcitol) on heart structure (size) and function (ability to relax) in patients with normal kidney function and a form of heart failure known as HFPEF (heart failure and preserved ejection fraction). This study will also examine heart failure-related hospitalizations and changes in cardiac-stretch and biological markers that are believed to change along with heart size. Patients in this pilot study will be treated for a period of 48 weeks with paricalcitol at a dose previously approved by FDA (1 mcg per day) and followed-up for 4 weeks after treatment is completed.