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Improved Regional Myocardial Blood Flow, Left Ventricular Unloading, and Infarct Salvage Using an Axial-Flow, Transvalvular Left Ventricular Assist Device

Richard W. Smalling, David B. Cassidy, Robert Barrett,Bruce Lachterman, Patty Felli, James Amirian
The concept of salvage of ischemic myocardial tissue by reperfusion therapy has been suggested by animal1 and human2 studies. Some investigators have reported that the level of collateral flow to the bed at risk determines ultimate infarct size3 others have suggested that the amount of collateral flow and degree of functional recovery are not correlated.4 An additional possible benefit of reperfusion therapy is the concept that late reperfusion may not salvage left ventricular (LV) tissue or function but may limit infarct expansion.5 Additionally, reperfusion may induce further myocardial damage; however, there is no clear consensus regarding the extent or possible modification of this problem.6 Recent interest has focused on the actions of free radicals and use of free radical scavengers at the time of reperfusion. Unfortunately, at the present time, these studies have yielded conflicting results possibly because of differences in models and agents used.7,8

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