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Hypertrophy, Left Ventricular clinical trials

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NCT ID: NCT05726695 Active, not recruiting - Heart Failure Clinical Trials

The Use of Blood Biochemical Markers for Diagnostics of Heart Muscle Diseases

Start date: June 1, 2018
Phase:
Study type: Observational

The aim of the study is to determine the analytical characteristics of the microRNA enzymatic immunoassay (miREIA) method and to determine various relations among miRNA biomarkers and heart failure (HF) with reduced ejection fraction(HFrEF). The investigators assume that there are correlations between levels of selected miRNA and HFrEF. These correlations provide information to formulate pathophysiological conclusions, which will significantly contribute to early diagnostics and also the treatment of this disease.

NCT ID: NCT04862273 Active, not recruiting - Clinical trials for Heart Failure With Preserved Ejection Fraction

Native T1 CMR Imaging for Diagnosis of Cardiac Amyloidosis

CMR for CA
Start date: April 1, 2021
Phase:
Study type: Observational

The study aims to test the diagnostic accuracy of native T1 mapping for the diagnosis of cardiac amyloidosis prospectively. The hypothesis is that native T1 mapping with a cut-off value of 1341ms (3 tesla CMR) in older patients with symptomatic heart failure, increased LV wall thickness and elevated cardiac biomarkers is non-inferior to the reference method to diagnose cardiac amyloidosis (CA). As secondary measure, a web-based ATTR probability estimator for the diagnosis of CA will be evaluated.

NCT ID: NCT03094143 Active, not recruiting - Clinical trials for Aortic Valve Stenosis

Early Valve Replacement Guided by Biomarkers of LV Decompensation in Asymptomatic Patients With Severe AS

EVoLVeD
Start date: July 21, 2017
Phase: N/A
Study type: Interventional

Aortic stenosis is the most common valvular disease in the Western world. It is caused by progressive narrowing of the aortic valve leading to increased strain on the heart muscle which has to work increasingly hard to pump blood through the narrowed valve. Over time the heart muscle thickens to generate more force, but eventually the heart fails leading to death if the valve is not replaced with an operation. No medical treatments exist to stop or reverse the heart valve narrowing. Current clinical guidelines suggest that an operation should be performed only when symptoms develop or the heart muscle is visibly weak on cardiac ultrasound scanning. However, symptoms can be difficult to interpret and in many patients the heart muscle has become irreversibly damaged and the heart fails to recover following surgery. Using MRI scans of the heart, the investigators have identified heart scarring which seems to develop as the heart muscle thickens. Several studies now show that people who have developed this scarring are more likely to suffer poor outcomes including death. The investigators have also identified clinical risks that predict the presence of scarring. The investigators propose a study where patients with severe aortic stenosis but no indications for valve replacement as per current guidelines are assessed for those clinical risks. If a participant's risk of having scarring is higher they will undergo a cardiac MRI scan. If scarring is present participants will be randomised to routine clinical care, or referral for valve replacement surgery. Participants with no evidence of scarring will be randomised routine care with study follow or not. The investigators of this study hypothesize that early surgery will lead to fewer complications and reduced risk of death compared to standard care.

NCT ID: NCT02599480 Active, not recruiting - Clinical trials for Hypertrophy, Left Ventricular

Assessment of Efficacy of Mirabegron, a New beta3-adrenergic Receptor in the Prevention of Heart Failure

Beta3_LVH
Start date: April 2016
Phase: Phase 2
Study type: Interventional

This study will assess the efficacy of mirabegron, a new beta3-adrenergic receptor in the prevention of heart failure. This is a two armed, prospective, randomized, placebo-controlled, multi-centric european phase IIb trial with placebo and mirabegron distributed in a 1:1 fashion. The patients enrolled will have cardiac structural remodeling with or without symptoms of heart failure (maximum NYHA II). Patients will be monitored for change in left ventricular mass (assessed by cardiac MRI) and/or changes in diastolic function (assessed by echocardiography) after 12 months of treatment.

NCT ID: NCT00871611 Active, not recruiting - Fabry Disease Clinical Trials

Viennese Prevalence Study of Anderson-Fabry Disease

VIEPAF
Start date: January 2009
Phase: N/A
Study type: Observational

The prevalence of Anderson - Fabry disease in patients with left ventricular hypertrophy is unclear. The investigators will examine urine - α - Galactosidase activity and globotriaosylceramide isoforms in these patients.

NCT ID: NCT00418041 Active, not recruiting - Heart Failure Clinical Trials

Chronic Heart Failure Analysis and Registry in the Tohoku District 2 (CHART-2 Study)

Start date: October 2006
Phase: N/A
Study type: Observational

Chronic Heart Failure Analysis and Registry in the Tohoku District 2 (CHART-2 Study) is a large, prospective, hospital-based cohort study to investigate the following: - Characteristics of patients with chronic heart failure and prognostic risks of these patients. - Characteristics of patients with high risk for heart failure and critical factors which predict the development of symptomatic heart failure in these patients. - The incidence and prognostic impact of metabolic syndrome in patients with chronic heart failure. - The association between metabolic syndrome and the development of symptomatic heart failure.

NCT ID: NCT00294775 Active, not recruiting - Atrial Fibrillation Clinical Trials

Effect of Angiotensin II Receptor Blockers (ARB) on Left Ventricular Reverse Remodelling After Aortic Valve Replacement in Severe Valvular Aortic Stenosis

Start date: February 2006
Phase: Phase 3
Study type: Interventional

The consequence of aortic valve stenosis (AVS) is increased pressure load on the left ventricle which causes left ventricular (LV) hypertrophy, and myocardial stretch will cause activation of cardiac peptides and activation of the renin angiotensin aldosterone system (RAAS). The consequence of LV hypertrophy is increased chamber-stiffness and delayed active LV relaxation which initially will cause diastolic and later systolic dysfunction. In heart failure (HF) and ischemic heart disease the degree of diastolic dysfunction has been demonstrated to correlate with functional class, neurohormonal activation and prognosis which also recently have been suggested for AVS. With longstanding elevated filling pressures the left atrium (LA) will dilate. Only limited data are available on the degree and importance of LA dilatation in AVS. When apparent, symptoms of HF in AVS are associated with high mortality rates. If LV systolic dysfunction also is present prognosis will deteriorate further. In these cases aorta valve replacement (AVR) is recommended. AVR will normalize pressure overload and thereby decreases LV hypertrophy. Previously it was believed that in time LV hypertrophy regressed towards normal and even normalized. Recent studies however have demonstrated that LV hypertrophy regression mainly happens during the first year after AVR, and little subsequent changes are seen during the remaining 10 years. Furthermore, patients that experience most regression of hypertrophy have more favourable outcome and better functional class than patients with less regression of hypertrophy. Thus absence of reverse remodelling is associated with poor outcome after AVR. Importantly the regression of LV hypertrophy is closely paralleled by decreasing RAAS hyperactivity. RAAS hyperactivity may be attenuated pharmacologically with angiotensin II receptor blockers (ARB) which in systemic hypertension with LV hypertrophy has been associated with reverse remodelling. The hypothesis is that in patients undergoing AVR for symptomatic AVS, 12 months post operative blockade of the angiotensin II receptor will accelerate LV and LA reverse remodelling, reduce filling pressures and suppress neurohormonal activation compared with conventional therapy. This will lead to improved exercise tolerance and due to improved left atrial function reducing the risk of atrial arrythmias.