View clinical trials related to Hypertrophy, Left Ventricular.
Filter by: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
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").
To assess the efficacy of Left Ventricular Hypertrophy (LVH) reduction and 24-hour blood pressure control of Valsartan 80mg or Nebivolol/Valsartan 5/80mg once daily as replacement therapy for currently treated or untreated hypertensive patients with LVH not at BP goal.
Chronic kidney disease (CKD) is present in 1 in 7 of the population and confers a high risk of cardiovascular disease. The pathophysiology of cardiovascular disease in CKD is poorly understood because CKD is always accompanied by confounding factors including the underlying disease process (e.g. diabetes mellitus, systemic vasculitis) and the consequences of CKD including hypertension, anaemia and inflammation. Nephrectomy in kidney donors causes a 30% reduction in renal function providing an ideal study population to measure prospectively the effects of reduced kidney function on the cardiovascular system. The CRIB-Donor study (ClinicalTrials.gov Identifier:NCT01028703) demonstrated adverse effects on cardiovascular structure and function at 12 months compared to controls including an increase in left ventricular mass. This proposal will measure the changes in cardiovascular structure and function, cardiovascular age and biochemical changes at 5 years providing information on the long term effects of reduced renal function.
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.
The purpose of this study is to evaluate the effectiveness of a technology-based behavioral Healthy Lifestyle intervention on adiposity (body mass index z-score), blood pressure (mean clinic systolic BP), and heart size (LVM) in comparison to standard care.