View clinical trials related to Left Ventricular Hypertrophy.
Filter by: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.
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.
Aortic stenosis is the most common heart valve disease requiring intervention in high income countries. It is characterised by progressive valvular thickening, and restriction as well is hypertrophy and fibrosis of the left ventricle in response to pressure overload. The pathological processes in the left ventricle that ultimately result in heart failure and death are incompletely understood. Further elucidation of these processes and how they correlate with novel blood biomarkers may help us design new treatments and optimise the timing of surgical intervention. In brief, recruited patients with severe aortic stenosis and scheduled to undergo valve replacement surgery will be invited for some simple tests (blood sampling, ECG, echocardiogram). A septal myocardial biopsy will be taken at the time of surgery and the disease valve retained. These will be examined histologically and pathological changes compared with results obtained from ECG, echocardiogram and blood tests.
The frequency of cardiac amyloidosis among patients presenting with a so-called left ventricular hypertrophy remains unknown. This problem is especially relevant in the Caribbean's, where an amyloidosis-prone mutation of transthyretin gene might be frequent.
Assess the efficacy of fimasartan on left ventricular hypertrophy in hypertensive patients
The fibroblast growth factor-23-bone-kidney axis is part of newly discovered biological systems linking bone to other organ functions through a complex endocrine network that is integrated with the parathormone/vitamin D axis and which plays an equally important role in health and disease . Most of the known physiological function of fibroblast growth factor 23 to regulate mineral metabolism can be accounted for by actions of this hormone on the kidney.In a recent experimental study, fibroblast growth factor-23 was shown to cause pathological hypertrophy in rat cardiomyocytes by "calcineurin-nuclear factor of activated T cells" and treatment with fibroblast growth factor -blockers reduced left ventricular hypertrophy in experimental models of chronic renal failure.The current hypothesis is that, in healthy individuals, iron deficiency stimulates increased production of fibroblast growth factor23. At the same time, iron is thought to be the cofactor of enzymes taking part in the degradation of intact fibroblast growth factor-23 and thought to have a role in the excretion of degraded FGF-23 parts .Studies speculated that Angiotensin Converting Enzyme inhibitors may exert their anti-proteinuria effects at least in part by reducing serum fibroblast growth factor-23 levels although it is difficult from the results of this study to understand which comes first and brings about the other; decrease in proteinuria or fibroblast growth factor-23. Available evidence points to the deleterious effects of increased fibroblast growth factor-23 level in proteinuria, but the precise molecular mechanism still remains to be explored. An intricate and close association exists among parathormone, phosphorus, active vitamin D with FGF23, but the independent role of the latter on proteinuria is the least explored. Elaborately conducted studies that control effects of confounding factors adequately are needed to demonstrate the independent pathogenic role of FGF23.
Obstructive sleep apnea syndrome (OSA) is the most frequent sleep disorder characterized by excessive decrease in muscle tone of the soft palate, the tongue and the posterior pharyngeal wall. It leads to airway collapse. In cases of decreased airway passage hypoventilation (hypopnea) occurs while periodic lack of airflow is called apnea. An obstructive sleep apnea syndrome is recognized as an independent cardiovascular risk factor. OSA is very common in patients with resistant hypertension. RAH is diagnosed when blood pressure remains elevated despite simultaneous use of 3 antihypertensive agents from different groups of drugs at optimal to maximum doses, including a diuretic. In patients with OSA frequent episodes of hypoxemia during sleep result in the repeated activation of the sympathetic nervous system. What is more, the episodes of respiratory disorders increases in levels of aldosterone serum concentration with following sodium and water retention and elevation of blood pressure finally. An increased aldosterone level also stimulates synthesis of collagen, promotes stiffening of the arterial wall, myocardial fibrosis with heart muscle remodeling and takes part in development of left ventricular hypertrophy (LVH) - common complication of hypertensive patients with OSA. Several studies, including the Sleep Heart Health Study have confirmed that severe OSA is associated with high prevalence of concentric hypertrophy through sympathetic activation and vasoconstriction. Eplerenone is a selective mineralocorticoid receptor inhibitor. It has no affinity for glucocorticoid, progesterone and androgen receptors and therefore has lower risk of side effects. Eplerenone lowers blood pressure and inhibits heart muscle fibrosis. The hypotensive effect is caused by reduction of fluid retention. Probably, in patients with OSA, a reduction of fluid accumulation especially at the level of the neck may contribute to lowering the resistance in the upper respiratory tract and in that way it may help to decrease the severity of OSA. As LVH remains a strong and independent predictor of total mortality and death from cardiovascular causes, in this study we want to assess whether the addition of Eplerenone to a standard antihypertensive therapy will favorably change left ventricular geometry. We also want to check if the addition the Eplerenone to a standard antihypertensive therapy could be an effective therapeutic option for patients with OSA and RAH.
Background: Calcimimetic therapy has been shown to reduce systemic FGF23 levels, which themselves are associated with left ventricular hypertrophy (LVH) in chronic kidney disease (CKD). Methods/design: This is a randomized multicenter trial in which the effect of etelcalcetide in comparison to alfacalcidol on LVH and cardiac fibrosis in hemodialysis patients with secondary hyperparathyroidism (sHPT) will be investigated. The investigators will perform a comparative trial testing etelcalcetide vs. alfacalcidol treatment on top of conventional HPT therapy for 12 months. A total of 62 hemodialysis patients with sHPT and LVH will be enrolled in the study. After a washout of all calcimimetic and vitamin D treatment, subjects will be randomized at 1:1 ratio to either etelcalcetide or alfacalcidol. The participants will undergo cardiac imaging consisting of cardiac resonance imaging (cMRI) and strain echocardiography before and at baseline and one year. Etelcalcetide or alfacalcidol will be administered intravenously three times per week following chronic hemodialysis treatment. The primary end point will be a change in left ventricular mass index (LVMI) measured in g/m2. As secondary end points the changes in left atrial diameter (LAD), cardiac fibrosis, wall motion abnormalities and left ventricular function, changes in serum FGF 23 and soluble Klotho levels as well as changes in proBNP as well as pre- and postdialysis troponin T (TnT) levels will be determined. Additionally a quantitative analysis of the treatment influence on the individual metabolites of the renin-angiotensin-aldosterone system (RAAS) will be performed using mass spectrometry ("RAAS fingerprint").
The purpose of this study is to develop imaging protocols when using cardiovascular magnetic resonance (CMR) to assess cardiac functions, morphology and tissue characterization. The National Heart Research Institute Singapore (NHRIS) houses two dedicated CMR scanners to support the numerous investigator initiated projects in patients with various cardiac pathologists. By optimizing novel CMR sequences used in these studies, scanning time can be shortened for patients with underlying cardiac diseases.