Skip to main content

Evolution of edema, hemorrhage and microvascular obstruction after acute myocardial infarction

Introduction

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.

Purpose

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.

Methods

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.

Results

Figure 1 demonstrates T2, T2* maps and early CE images for an anterio-septal infarct in a short-axis slice for a representative animal at three time points. T2-maps represent edematous changes (bright regions), T2*-maps indicate hemorrhage (dark regions) while CE images delineate MVO (signal voids within infarct). Figure 2 shows the cumulative time course of T2, T2* and DWT within the infarct. T2 was indistinguishable from control at day 2 (p = 0.38) while the T2 elevation beyond week 1 was statistically significant (p < 0.05). T2* was reduced up to week 1 as a result of hemorrhage and its normalization at week 4 coincided with resolution of MVO. DWT was significantly increased at day 2 (7.5 vs 5.3 mm, p = 0.06) suggesting increased tissue water content while it fell below control values at week 6 (4.3 mm, p = 0.003) indicating scar formation.

Figure 1
figure1

At day 2 in this animal, T2 elevation usually associated with edema was not apparent in the infarct zone (39.2 ms vs 39.1 ms contrl); however DWT was increased by 34% suggesting edematous swelling. Lower T2* (arrows) indicated presence of hemorrhage (18.5 ms vs 34.2 ms whle the CE image showed a large MVO. At Week 1, T2 was elevated in most of the infarct (51.1 ms) with reduced T2* (20.5 ms) indicating diffuse hemorrhagic by-products. CE imge showed only a slight MVO. By week 4, hemorrhage/MVO were resolved.

Figure 2
figure2

Plots demostrate longitudinal fluctuations in T2, T2* and DWT in infarct zone compared to remote myocardium averaged over all animals

Conclusion

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.

Author information

Affiliations

Authors

Corresponding author

Correspondence to Nilesh R Ghugre.

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and Permissions

About this article

Cite this article

Ghugre, N.R., Ramanan, V., Pop, M. et al. Evolution of edema, hemorrhage and microvascular obstruction after acute myocardial infarction. J Cardiovasc Magn Reson 12, P150 (2010). https://doi.org/10.1186/1532-429X-12-S1-P150

Download citation

Keywords

  • Acute Myocardial Infarction
  • Acute Myocardial Infarction
  • Microvascular Obstruction
  • Tissue Water Content
  • Infarct Healing