01718nam a2200265   4500001000800000005001700008007000300025008004100028040000800069041000800077100004100085245003100126300002500157520091300182650003301095650002801128650002301156650003601179650003401215650002101249650002401270773011001294942003101404999001701435ESSALUD20260902151149.0ta      t        pe ||||| |||| 00| 0 spa d  aBMG  aeng  aMargulies, Kenneth B. eAutor954429  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 GENERAL953638  aCARDIOMIOPATÍA937409  aMIOCARDITIS938353  aCIRUGÍA CARDIOVASCULAR953947  aINSUFICIENCIA CARDIACA911699  aTRASPLANTE97847  aPERICARDITIS9397320 022717922665dMassachusetts NEJM GroupoNEJM013tThe New England Journal of Medicine wESSALUDx0028-4793  cARTICULOSe2026-08-28zsqb  c22892d22892