View clinical trials related to Hypertrophy, Left Ventricular.
Filter by:Aim of the study is to evaluate the effects of Armolipid Plus on insulin sensitivity in patients with MetS and increased LV mass. 168 patients will be enrolled in this randomized, double-blind, parallel-group, placebo-controlled trial and treated for 24 weeks.
The presence of Left ventricular hypertrophy (LVH) confers high cardiovascular risk in hypertensive patients. LVH remains highly prevalent even when blood pressure (BP) is controlled. There is increasing evidence that a major non-haemodynamic contributor to LVH is oxidative stress. Allopurinol is known to markedly reduce oxidative stress. This pragmatic randomised double blind placebo controlled trial will examine whether allopurinol (300 mg bd) regresses LV mass as assessed by cardiac magnetic resonance (CMR) in 66 patients with treated hypertension but who have persisting LVH. Endothelial and vascular function will also be assessed via flow mediated dilatation (FMD) and pulse wave analysis respectively (PWA) and plasma biomarkers of oxidative stress will be measured. The treatment (allopurinol or placebo) will last 12 months.
Thickening of the heart muscle (left ventricle) known medically as Left Ventricular Hypertrophy (LVH) is very common in patients with heart disease. This increases risk of cerebrovascular/cardiovascular event. LVH is asymptomatic and managed by the use of medication to control blood pressure, however LVH may be seen in normotensive patients where factors such as obesity and insulin resistance are present. Insulin resistance is a condition where although the body produces insulin it is unable to utilize it effectively. Metformin, a drug used to treat diabetes, can reduce insulin resistance and cause weight loss, it may therefore improve LVH. This study will investigate the ability of metformin to reduce LVH in patients with heart disease, this may be a novel way forward in the risk reduction of cerebrovascular/cardiovascular events. Participants will be identified throughout NHS Tayside, those eligible will be randomly allocated to either metformin or a dummy medication (placebo) and will receive one year of treatment. At the beginning of the study, the thickness of the heart muscle will be measured by ultrasound scan and cardiac Magnetic Resonance Imaging (cMRI). We will also perform non-invasive tests to measure blood vessel function. These tests will be repeated after one year. At the end of the study, we will investigate the difference between placebo treatment and metformin treatment. This study is funded by the British Heart Foundation.
New-onset diabetes (NODAT) after solid organ transplantation is an important clinical challenge associated to increased risk of cardiovascular (CV) events. In end-stage renal disease (ESRD) patients, the impact of arterial stiffness on all-cause and CV mortality has been clearly documented. Arterial stiffness has a pivotal role in the genesis of high blood pressure (SBP), increased left ventricular hypertrophy (LVH), and consequently CV mortality. Both LVH and arterial stiffness are independent determinants of CV disease in patients with ESRD. The aim of this study is to evaluate the relationship between post-transplant new-onset diabetes and arterial stiffness and left ventricular mass index (LVMI) in kidney transplant recipients.
Kidney patients on dialysis commonly die because of heart disease. One of the biggest problems in their hearts is that the muscle wall of the heart thickens. This makes it less efficient. We found in patients with mild kidney disease that a drug normally used to treat gout (allopurinol) had the remarkable side effect of being able to reduce this thickening of their heart wall. In this new study we aim to find out if this benefit of allopurinol also occurs in severe kidney patients i.e. those on regular dialysis. We also are trying to figure out the best dose of allopurinol to use. To do this we are planning a study where we will recruit patients with kidney disease who are on dialysis. The 1st phase of the trial will be to determine the best dose of allopurinol to use and the second phase will be to do a clinical trial where patients will be randomly allocated to either this optimum dose of allopurinol or a dummy medication (placebo) and will receive one year of treatment. They will have a special scan of the heart using an MRI machine to measure the extent of thickening of their heart muscle before they start on treatment and will have a further MRI scan when their one year treatment finishes. Phase 1- the dose finding study, will involve 10 patients who will have between 3 and 7 visits to the hospital scheduled around 4 to 17 dialysis sessions. The later study will involve up to 76 patients who will be asked to attend the hospital up to 8 times over a 13 month period.
The aims of the presented study are as follows: 1. To evaluate the endothelial function and arterial stiffness in a large cohort of prevalent CKD patients by means of non-invasive applantion tonometry. 2. To evaluate the association between the serum levels of the representatives of the various classes of uremic toxins and markers of endothelial function and arterial stiffness. 3. To evaluate the association between markers of inflammation and oxidative stress and markers of endothelial function and arterial stiffness. 4. To evaluate the association between echocardiographic parameters and markers of arterial stiffness
Left ventricular non-compaction (LVNC) is a rare cardiomyopathy characterized by numerous excessively prominent left ventricular (LV) trabeculation and deep intertrabecular recesses communicating with the ventricular cavity and severely altering myocardial structure. Although most authors assume a developmental arrest in embryogenesis as the underlying pathology, the mechanisms of LVNC are not fully understood yet. Several gene mutations have been identified to be linked with LVNC and an autosomal dominant inheritance pattern is frequent To date the most commonly used imaging tool for diagnosing LVNC is echocardiography applying the criteria established by Jenni and coauthors However, qualitative parameters to differentiate normal compaction of the myocardium in healthy subjects from LVNC or from other cardiomyopathies like dilative cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) may fail due to highly variable LV trabeculation. Therefore, absolute quantification should be performed. Cardiac magnetic resonance (CMR) has been reported as a promising imaging modality to characterize patients with LVNC as it provides both a high spatial resolution and a good contrast between trabeculation and blood pool Jacquier et al. recently described a value of trabeculated LV myocardial mass above 20% of the global mass of the LV to be highly sensitive and specific for LVNC However, in their approach, a substantial degree of the LV cavity was included into calculated trabecular LV mass and led to systemic overestimation of the latter. Furthermore, the role and prognostic value of myocardial scarring as assessed by delayed enhancement (DE) CMR was not evaluated. The aim of the retrospective study was to establish revised and extended CMR criteria to distinguish LVNC from DCM, HCM and a group of healthy controls and to improve the assessment of trabeculated mass by excluding intertrabecular blood pool.
Unfavorably high sodium intakes remain prevalent around the world. A negative sodium gradient in hemodialysis treatment results in absolute sodium removal via diffusive transport of sodium from the blood to the dialysate, and it may be a potentially useful tool to improve sodium loading due to excess dietary sodium intake. The purpose of this study is to determine whether a in small negative sodium gradient could improve blood pressure level, arterial stiffness and left ventricular hypertrophy in hypertensive hemodialysis patients, who had been achieving and maintaining their dry weight assessed by bioimpedance spectroscopy.
The study hypothesis is stress-related regional tissue dynamics is related to left ventricular outflow tract blood flow.
The study hypothesis: Valsartan as an angiotensin II receptor blocker treatment has beneficial effects on both midwall mechanics and myocardial functions in hypertensive patients with Left ventricular hypertrophy.