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Speckle Tracking Imaging and Realtime 3 Dimensional Echocardiograhy to Study LV Function and Remodeling After Acute Myocardial Infarction (AMI)

National Taiwan University Hospital · 2007
ClinicalTrials.gov · Datasets · License: Public Domain · 2007
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acute-myocardial-infarctioncongestive-heart-failure
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.
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