View clinical trials related to Ventricular Remodeling.
Filter by:This study aims to determine whether thyroid hormone levels are predictive of cardiac remodeling following myocardial infarction and the prognosis in patients with STEMI receiving primary percutaneous coronary intervention.
In Singapore, hypertension is very common in the adult population. Hypertensive heart disease is a leading cause of heart failure and cardiovascular death. Current management relies primarily on achieving blood pressure targets. However, the optimal blood pressure goals are controversial and there are inherent difficulties in measuring blood pressure using external devices applied to peripheral arteries. As a result of (usually longstanding) hypertension, the heart thickens (i.e. hypertrophies) to maintain function. Ultimately, HF may occur due to long standing energy deficits, muscle injury/death and diffuse interstitial fibrosis (heart muscle scarring). In an ongoing study (REMODEL, ClinicalTrial.gov Identifier NCT02670031), we have been able to undertake preliminary analyses with respect to factors associated with the development of fibrosis. In this randomize controlled trial, we will be examining a novel therapy that has the potential to induce regression cardiac hypertrophy and fibrosis.
role of different risk scores in acute coronary syndrome to predict left ventricular remodeling
Approximately 60 patients with ST-segment elevation myocardial infarction successfully treated with primary percutaneous coronary intervention will be enrolled and randomized to receive the sodium tanshinone IIA sulfonate in addition to standard therapy or the same volume/day of normal saline. The primary endpoint is the variation in LV end-diastolic volume index (LVEDVi) assessed with cardiac magnetic resonance imaging (MRI) at baseline and 6 months.
The proposed research aims to compare Left ventricular remodeling outcomes among patients with AMI and elevated NT-pro-B-type natriuretic peptide receiving telemedicine-guided post-MI treatment vs. non-telemedicine guided treatment.
The purpose of the study is to evaluate the novel role of ticagrelor to improve long-term LV remodeling following ST-segment elevation myocardial infarction.
This project focuses on the physiopathology of left ventricular remodeling associated with type II diabetes in patients with aortic valve stenosis referred for surgical aortic valve replacement. The main objective is to compare the reverse left ventricular remodeling between patients with type II diabetes and case-control patients without diabetes at one(1) year after surgical aortic valve replacement. The secondary objectives are : 1. assess the influence of type II diabetes on left ventricular remodeling in patients presenting with aortic valve stenosis, 2. assess the predictive value of myocardial fibrosis and other LV characteristics present prior to aortic valve surgery on the LV reverse remodeling and their influence on cardiovascular events at one (1) year after surgery, 3. assess the influence of type II diabetes on cardiovascular morbidity and mortality post aortic valve surgery. The investigators main hypothesis is that patients with type II diabetes and aortic valve stenosis requiring aortic valve replacement have poorer LV function and less favorable post surgery clinical outcomes than patients without type II diabetes.
Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. The recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI. As a leading cause of heart failure, postinfarction LV remodeling represents an important target for therapeutic interventions. Within the ventricular mass, size, shape, connections and orientation in a three-dimensional space of every single constituent determine its functional behavior. The complex architecture of the ventricular mass creates multiple inhomogeneities of electrical and mechanical loads at the cellular and the microscopic tissue level, that cause cardiac function to be 'stochastic in nature'. The myocardial infarction will altered the ventricular shape and functional inhomogeneities carrying the morphodynamic advantages such as impaired suction for diastole after diminishing recoil relaxation with decreased twisting strain in systole. The alteration in contractile mechanics interacts with the intraventricular fluid dynamic filed that influence the regional myocardial shearing stress. Altered LV transmural wall strains have been proposed to cause infarct extension and may have an important role in propagating LV remodeling.