000			01714nam a2200265 4500
001			ESSALUD
005			20260902151149.0
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040			_aBMG
041			_aeng
100			_aMargulies, Kenneth B. _eAutor _954429
245			_aPatching up damaged hearts
300			_apáginas: 2054-2055
520			_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.
650			_aCARDIOLOGÍA GENERAL _953638
650			_aCARDIOMIOPATÍA _937409
650			_aMIOCARDITIS _938353
650			_aCIRUGÍA CARDIOVASCULAR _953947
650			_aINSUFICIENCIA CARDIACA _911699
650			_aTRASPLANTE _97847
650			_aPERICARDITIS _939732
773	0		_022717 _922665 _dMassachusetts NEJM Group _oNEJM013 _tThe New England Journal of Medicine _wESSALUD _x0028-4793
942			_cARTICULOS _e2026-08-28 _zsqb
999			_c22892 _d22892