PNNL

Abstract

Sudden blockage of coronary artery contributes to approximately one million people in the US experiencing heart attacks (myocardial infarction, MI) each year. Although re-opening the arteries (revascularization therapies) have been instrumental in saving MI patients from immediate death, nearly half of the patients with revascularized MI develop heart failure and die within a 5-year period. Although acute MI size has been hypothesized as the primary driver of heart failure months to years later, why some patients accelerate toward fatal heart failure while others do not remains an open question. We hypothesized that when revascularization leads to intramyocardial hemorrhage (evident in nearly half of the revascularized MI patients), a set of time-dependent cascading events initiated by the red-blood-cell-derived iron, drives fat deposition (lipomatous metaplasia) in the MI territory, which leads to adverse remodeling of the heart defined by loss of cardiac function.