View clinical trials related to Hypertrophy, Left Ventricular.
Filter by:Left ventricular hypertrophy (LVH) is the most common result of the heart trying to pump blood against the high afterload, as in hypertension and aortic stenosis.Although hypertension is the most common cause of LVH, LVH can also be found in athletes and cardiomyopathies or in storage disorders such as amyloidosis. In addition, genetic diseases also play an important role in the pathogenesis of LVH. Fabry disease is another disease that should be considered in patients with left ventricular hypertrophy.Left ventricular hypertrophy is a common and potentially modifiable cardiovascular risk factor that is frequently overlooked in clinical practice.The benefit of combining ECG and echocardiography in the diagnosis of LVH has been demonstrated.Early diagnosis and treatment-related regression of LVH, reduces adverse cardiovascular events and improves survival.Therefore, the investigators planned to perform a retrospective, observational LVH-TR study in order to determine the etiologic causes of LVH, the symptoms presented by the patients, and the effects of patients' demographic characteristics on LVH.
The working hypothesis is that cardiac macrophages specific for the compensated cardiac hypertrophic phase limit the progression toward the decompensated state of heart failure by promoting an inflammatory environment favouring cardiomyocyte survival and preservation of the pump function. The investigators will perform studies in human plasma and monos, cardiac tissues and macrophages to validate this hypothesis.
The main purpose of this study is to determine the prevalence of ATTR Cardiomyopathy among patients admitted due to Left Ventricular Hypertrophy (LVH) >15mm of unknown etiology by using a 99mTc-tracer scintigraphy based protocol
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.
Cardiovascular disease (CVD) is the major risk factor for death in end stage renal diseases (ESRD). Approximately 80% of ESRD patients have some degrees of left ventricular abnormalities at initiation of dialysis. Carotid intima media thickness (CIMT) has been widely accepted as an useful marker to assess CVD in ESRD children. In addition, cardiac mechanics parameters are used to evaluate cardiac function more precisely. However, measuring CIMT and cardiac mechanics parameters are expensive and difficult to perform as a routine method. Mean platelet volume (MPV) is a hematological index which shows the size of platelets. Uremic state causes inflammatory condition that affects MPV. Previous studies on people with normal renal function have shown that this parameter can also have association with CVD. However the data in children with ESRD is scarce. The aim of this study is to find a simple hematologic marker to use regularly in ESRD children finding patients at risk of CVD. Therefore, we will investigate the relationship between mean platelet volume and CIMT and cardiac mechanic parameters in children with ESRD.
Premature cardiovascular disease (CVD) is the leading cause of death in patients with kidney disease (CKD). Excessive cardiac mortality is thought to be secondary to non-atherosclerotic processes, with left ventricular (LV) hypertrophy (LVH) and remodelling being the predominant phenotypical features. Along with other risk factors, subclinical ischaemia and haemodynamic perturbations associated with haemodialysis (HD) are thought to contribute to the ultimate development of LV systolic and diastolic dysfunction. The development of these adverse features reflects a specific cardiomyopathy due to CKD and subsequently, to uraemia. Patients receiving hemodialysis (HD) have a higher incidence rate of heart failure (predominantly with preserved ejection fraction), with phenotypically eccentric hypertrophic remodelling, systolic and diastolic dysfunction as well as high rate of interstitial myocardial fibrosis. Detection and ultimately reversal of the development of this CKD-related cardiomyopathy are important goals for improving the CVD, morbidity and mortality of CKD patients.The objectives of this study are, firstly, to investigate the complex myocardial phenotype in patients with various stages of CKD, secondly, to relate the CMR-measures to outcome, and thirdly, to be able to estimate the effects of chronic uremia/hypervolemia. Deciphering the predominant driver of remodelling on an individual level may help to personalise anti-remodelling strategies. Native T1 and T2 mapping imaging provide non-invasive imaging tools to detect myocardial fibrosis and oedema, respectively. Prognostic associations of these measures may clarify the relative prevalence of adverse phenotype and their relative contribution to adverse events and poor outcome. The role of chronic water retention and uraemia may be associated with interstitial myocardial oedema promoting further the remodelling process.
To compare changes in Left Ventricular Mass (LVM) depending on each blood pressure regulation between the intensive care group and the usual care group for patients with hypertension accompanied by aortic valve disease and evaluate an influence of blood pressure regulation on improvement of left ventricular hypertrophy and its safety
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.
To review the accuracy of electrocardiography in screening for left ventricular hypertrophy in patients with hypertension.
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.