Patching up damaged hearts

Por: Margulies, Kenneth B [Autor]Tipo de material: TextoTextoIdioma: Inglés Descripción: páginas: 2054-2055Tema(s): CARDIOLOGÍA GENERAL | CARDIOMIOPATÍA | MIOCARDITIS | CIRUGÍA CARDIOVASCULAR | INSUFICIENCIA CARDIACA | TRASPLANTE | PERICARDITIS En: The New England Journal of MedicineResumen: Heart 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.
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Colección General NEJM (Navegar estantería) Vol.394, No.20 (2026) Disponible NEJM013

Heart 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.