This proposal will test the hypothesis that temporary left ventricular assistance (LVAD) can accelerate recovery of left ventricular function by reducing left ventricular (LV) wall stresses, strains and myocardial creep and by accelerating recovery of the functional borderzone after acute myocardial infarction (AMI). These changes may accelerate LV remodeling, reduce final Ventricular volumes and preserve more contractile function after AMI in addition to preventing continuing myocardial ischemia and necrosis during evolution of infarcts in patients with multivessel disease. The project will utilize sonomicrometry to accurately measure LV dimensions throughout the cardiac cycle. The method developed to image LV geometry in 2 dimensions will be developed further to 3-dimensional mapping of LV geometry. This will allow estimations of regional LV wall stresses in pathologic infarcted ventricles based on direct measurements. The pathophysiology of reversible ischemia and LV distention (related to myocardial creep) will be investigated. The evolution of an apical myocardial infarct to apical LV aneurysm will be described in terms of LV mechanics and 02 consumption. These studies will be compared to evolution of circumflex coronary artery infarcts to scar and to the effects of LVAD on LV mechanics and 02 consumption at various time periods during evolution of both types of infarcts. The studies will focus on quantitation of - regional stresses, strains and creep in adjacent and remote myocardium after infarction and will assess changes in ventricular volumes and contractility with and without LVAD. The study will also determine the effects of changes in regional stresses and strains produced by LVAD or aneurysm plication (a model to acutely alter LV volume and regional stresses) on ventricular volumes, contractility and remodelling. Previous work compared several temporary extracorporeal circulatory assist systems that could be implemented without thoracotomy and determined that LVAD produces the most dramatic decreases in LV volumes and wall stresses in pathologic hearts. Therefore, the project seeks to understand the mechanisms involved in the recovery of LV function after AMI and to favorably influence this recovery by the use of LVAD without thoracotomy during the postinfarction period.
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