View clinical trials related to Left Ventricular Hypertrophy.
Filter by: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").
Left ventricular hypertrophy (LVH) is common in people with type 2 diabetes (70%) and is the strongest independent risk factor for cardiovascular events and all-cause mortality that there is. It is worse than triple vessel coronary disease. LVH often occurs in patients with "normal" blood pressures (BP). Apart from BP, the other three main factors causing LVH are insulin resistance, obesity and cardiac preload. Dapagliflozin reduces ALL four factors known to promote LVH i.e. Dapagliflozin reduces weight, glycaemia, preload and blood pressure and is therefore the ideal agent to reduce LVH since it uniquely attacks all four known mediators of LVH. This trial will investigate the ability of dapagliflozin to regress LVH in 64 participants with normotensive diabetes. This will be done by seeing if dapagliflozin reduces left ventricular mass as measured by cardiac magnetic resonance imaging (MRI). This trial may identify a novel way to reduce the strong independent risk factor of LVH which often persists despite optimum medical therapy in patients with diabetes. If dapagliflozin does reduce LVH, this would be a key sign of which subgroup of patients with diabetes (those with LVH) should be especially targeted with dapagliflozin. 64 participants with type 2 diabetes and LVH will be recruited through the Scottish Diabetes Research Network (SDRN), Scottish Primary Care Research Network (SPCRN) and other routes, in this single centre study. Participants will be randomised to receive either 10mg dapagliflozin or placebo daily for 12 months. Cardiac MRI will be performed at baseline and at 12 months, this will be assessed for the primary outcome of change in left ventricular mass. Secondary outcomes will examine change in 24 hour blood pressure and weight.
Background: In 2010, approximately 39000 Canadians had end-stage renal disease (ESRD), and the prevalence rate of dialysis has increased by 189% over the past 2 decades. The annual mortality rate remains high at ~15%, and cardiovascular events are the leading cause of death. Intensification of conventional dialysis schedules has been the major focus in recent years. Currently, most Canadian dialysis patients receive conventional in-center hemodialysis (CHD), which is administered as a 3-4 hour session 3/week. Recent research has focused on home nocturnal hemodialysis (8 hours of hemodialysis at home for 5-6 nights/week), which may have substantial cardiovascular benefits, including regression of left ventricular (LV) hypertrophy, improved LV ejection fraction and enhanced blood pressure control. Nevertheless, this dialysis modality is only feasible in a highly selected minority of ESRD patients who can self-manage their dialysis treatment at home. In-center nocturnal hemodialysis (INHD), administered as 7-8 hours of hemodialysis in hospital for 3nights/week, represents a promising and practical alternative for many dialysis patients. In a Canadian Institutes for Health Research (CIHR) supported cohort study, the investigators have recruited 67 patients and have completed 1-year follow-up. There is a compelling need for longer-term follow-up, since all the published randomized controlled trials are of short duration (6-12 months), while renal replacement therapy is a life-long treatment. Furthermore, the observed large variability of cardiac remodeling in individual ESRD patients remains poorly understood. Therefore, the current study is an extended follow-up phase (5 years from enrollment) on the completed 1-year follow-up period and the purpose of this study is to objectively evaluate the long-term effects of more intensified hemodialysis treatment which the INHD modality offers. Need for Long-term and Generalizable Data: In contrast to the seminal Alberta trial which showed a significant LV mass reduction with home nocturnal hemodialysis, the recently reported Frequent Hemodialysis Network Nocturnal Trial demonstrated only a trend toward reduction in LV mass. It is likely that the highly selected participants, inadequate trial power and duration (12 months) account for the observed results. Currently, it is unknown whether INHD, which is less intensive but more feasible for most ESRD patients, is associated with similar cardiovascular benefits in the long term. Objective: 1. To determine the long-term effects of INHD on (i) LV mass; (ii) global and regional LV systolic and diastolic function; (iii) myocardial tissue characteristics; (iv) left atrial structure and function; (v) selected cardiovascular biomarkers in ESRD patients. 2. To examine the determinants and mechanisms of cardiac remodeling in ESRD Hypothesis: Conversion to INHD is associated with sustained improvements in cardiovascular structure and function, as compared to conventional hemodialysis (CHD) in patients with end-stage renal disease (ESRD). Study Design and Population: This will be a 2-centre, prospective, longitudinal cohort study of 67 adult ESRD patients (INHD subjects and CHD controls) enrolled in the original study. All eligible participants who provide consent will undergo cardiac Magnetic Resonance Imaging (MRI) examination and bloodwork at 5 years since enrollment in the study. Other follow-up procedures include the following -electrocardiogram, transthoracic echocardiogram, ambulatory blood pressure monitoring, lateral x-ray of the aorta, and completion of questionnaires. Outcome: The primary endpoint is the change in LV mass over 5 years, as measured by cardiac MRI. Secondary endpoints include LV size, global and regional diastolic and systolic function, left atrial size and function, changes in myocardial tissue characteristics, blood pressure, serum troponin, norepinephrine, Brain Natriuretic Peptide (BNP), high sensitivity C-Reactive Protein (hsCRP), interleukin-6, matrix metalloproteinases, fibroblast growth factor-23, fetuin-A, transforming growth factor-beta, connective tissue growth factor, clinical events, and quality of life. Significance: The provision of an enhanced dialysis regimen has emerged as the most promising avenue through which to modify the dismal cardiovascular outcomes in patients receiving chronic hemodialysis. INHD represents a means of administering such therapy to a broad spectrum of dialysis patients for whom home therapies would not be feasible. This study will be the first to precisely define the long-term cardiac effects of intensified dialysis and to elucidate the mechanisms of cardiac remodeling in ESRD, using cardiac MRI and other novel biomarkers. These important observational findings may have a major impact on the optimal management and outcome of ESRD patients in the real world.
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.
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.
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.