01584nam a2200241   4500001000800000005001700008007000300025008004100028040000800069041000800077100003400085245003100119300002500150520091300175650002601088650002101114650001601135650002901151650002701180650001501207650001701222773010301239ESSALUD20260902151149.0ta      t        pe ||||| |||| 00| 0 spa d  aBMG  aeng  aMargulies, Kenneth B. eAutor  aPatching up damaged hearts  apáginas: 2054-2055  aHeart failure resulting from previous myocardial infarction or ischemic cardiomyopathy remains a leading cause of death and complications worldwide. The central pathophysiological processes in ischemic cardiomyopathy are the loss of myocardial tissue from necrosis after a coronary-artery occlusion, followed by replacement fibrosis that confers a disposition to heart failure and arrhythmias. Because the adult heart cannot regenerate lost myocardium, current therapies for ischemic cardiomyopathy are focused on countering maladaptive systemic neurohormonal responses that promote vasoconstriction, salt and water retention, unfavorable myocardial remodeling, and progressive heart failure. Despite these therapies, many patients have progression to advanced heart failure, for which donor shortages limit transplantation while modern, durable mechanical-support devices remain both complicated and costly.  aCARDIOLOGÍA GENERAL  aCARDIOMIOPATÍA  aMIOCARDITIS  aCIRUGÍA CARDIOVASCULAR  aINSUFICIENCIA CARDIACA  aTRASPLANTE  aPERICARDITIS0 022717dMassachusetts NEJM GroupoNEJM013tThe New England Journal of Medicine wESSALUDx0028-4793