Volume 12 Supplement 1
Evolution of edema, hemorrhage and microvascular obstruction after acute myocardial infarction
© Ghugre et al; licensee BioMed Central Ltd. 2010
Published: 21 January 2010
In acute myocardial infarction (AMI), the no-reflow phenomenon is caused by ischemia-induced microvascular injury/obstruction and has been correlated with adverse remodeling. The severity of the initial ischemic insult may also lead to intramyocardial hemorrhage. Alongside, intracellular and interstitial edema is a consistent feature of AMI and has been associated with the salvageable area-at-risk. The (in-vivo) evolution of these processes throughout infarct healing is not well-characterized but is important in grading severity and evaluating treatment strategies, potentially improving clinical outcome.
To characterize the time course of edema (T2), hemorrhage (T2*) and microvascular obstruction (MVO) in porcine myocardium following AMI and observe the relative resolution of these pathophysiological mechanisms.
7 pigs underwent MRI before LAD infarction (control) with subgroups studied at 2,7,14, and 30-42 days post-infarction. Histology was performed upon sacrifice at either Day 14 (n = 3) or Day 30-42 (n = 4). Imaging was performed on a 3 T MRI scanner (MR 750, GE Healthcare). A previously validated T2-prepared spiral sequence was utilized for T2 quantification and T2* was determined using a multi-echo gradient-echo acquisition. An early (~3 min) contrast-enhanced (CE) IR-GRE sequence was used for infarct/MVO delineation. Diastolic-wall-thickness (DWT) was measured from CINE-SSFP imaging.
Post-infarct remodeling is a complex process and comparison with remote myocardium is equally important. In this respect quantitative T2 and T2* mapping techniques are potentially more specific than intensity measures in single images. Edema and hemorrhage have counter-acting effects on T2, hence care should be taken while evaluating day 2. Our study demonstrates that multi-factorial MR-based parameters, acquired in a longitudinal fashion, can be employed to assess the evolution of myocardial infarction.
This article is published under license to BioMed Central Ltd.