Abstract
Background Hemorrhage in association with microvascular obstruction (MVO) is a new independent predictor of adverse remodeling following acute myocardial infarction (AMI), occurring in ~35% of patients presenting with STEMI [1,2]. However, it remains unsettled whether hemorrhage is simply a marker of severity or directly contributes to the ongoing remodeling process. The aim of our study was to to probe the downstream consequences of hemorrhage in chronic remodeling following AMI by employing a novel minimally-invasive model of myocardial hemorrhage in an experimental setting.
Highlights
Hemorrhage in association with microvascular obstruction (MVO) is a new independent predictor of adverse remodeling following acute myocardial infarction (AMI), occurring in ~35% of patients presenting with STEMI [1,2]
Animals (N=12) were divided into three groups based on the type ischemia-reperfusion injury inflicted in the left anterior descending artery (LAD) - Group 1 (N=3) 45 min occlusion with saline; Group 2 (N=5): 8 min ischemia with col; and Group 3 (N=4): 45 min occlusion with collagenase
At day 1, low T2* values in the infarct region confirmed the presence of myocardial hemorrhage in the collagenase
Summary
Hemorrhage in association with microvascular obstruction (MVO) is a new independent predictor of adverse remodeling following acute myocardial infarction (AMI), occurring in ~35% of patients presenting with STEMI [1,2]. It remains unsettled whether hemorrhage is a marker of severity or directly contributes to the ongoing remodeling process. The aim of our study was to to probe the downstream consequences of hemorrhage in chronic remodeling following AMI by employing a novel minimally-invasive model of myocardial hemorrhage in an experimental setting
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