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  • Open Access

Myocardial remodeling in reperfused myocardial infarction with multiparametric CMR: does diffuse fibrosis occur in remote noninfarcted myocardium?

  • 2,
  • 1,
  • 1,
  • 1, 4,
  • 1, 3 and
  • 1, 4
Journal of Cardiovascular Magnetic Resonance201315 (Suppl 1) :P137

https://doi.org/10.1186/1532-429X-15-S1-P137

  • Published:

Keywords

  • Infarct Size
  • Left Ventricular Volume
  • Left Ventricular Remodel
  • Delay Enhancement
  • Infarct Region

Background

Although mortality from myocardial infarction (MI) has decreased due to improved reperfusion strategies, adverse left ventricular (LV) remodeling after MI is associated with poor long-term prognosis and is thus an important therapeutic target. We developed a Yucatan mini-pig model of reperfused MI using percutaneous techniques for coronary occlusion/reperfusion, and sought to characterize remodeling in both the infarct and remote territories using multiparametric CMR techniques.

Methods

To create the infarct, a 9.0 x 2.5 mm angioplasty balloon was inflated in the LAD distal to the 2nd diagonal branch for 90 minutes followed by reperfusion. CMR imaging was performed at baseline, 2 days (d) and 30d post-MI. The protocol included SSFP cine, T2 mapping with a T2-prep, T1 mapping using a modified MOLLI technique both pre- and 10 minutes after injection of 0.2 mmol/kg of Gd-DTPA, and delayed enhancement (DE) imaging. LV volumes and function were quantified from the cine images, and infarct size was determined from DE images. The T2s and T1s pre- and post-contrast were measured at baseline and in the infarct and remote territories at 2d and 30d post-MI. Additionally partition coefficient (λ) maps were generated.

Results

Eight animals with an infarct size greater than 10% of the LV were analyzed. Figure 1 shows an example case. Multiparametric CMR data is summarized in Table 1. There was an increase in LV volumes and a reduction in EF at one month. The average infarct size at 2d was 22±7%, which decreased to 13±4% by 30d. T2 did not change in the noninfarcted myocardium at any timepoint. In the infarct region, T2 was increased and remained elevated at 30d. Pre-contrast noninfarcted myocardium T1 was increased at 2d, but returned to baseline values by 30d. Similar to T2, the infarct zone pre-contrast T1 was increased and remained elevated at 30d. The λ of noninfarcted myocardium did not change significantly from baseline to 30d post-MI. The infarct region λ increased by more than two-fold at 2d, and remained elevated at one month.
Figure 1
Figure 1

Multiparametric CMR images from one pig at baseline, day 2, and day 30 showing an anteroseptal infarct (arrow). At day 2 there is thickening of the infarct region with prominent edema and nearly transmural DE. At day 30 the infarct region is thinned with evidence of remodeling. (DE = Delayed enhancement; λ = Partition Coefficient)

Table 1

Summary of multiparametric CMR data at each timepoint.

 

Time point post-MI

 

Baseline

Day 2

Day 30

End-diastolic volume (ml)

54.7 ± 13.1

61.0 ± 11.0

70.4 ± 9.6*

End-systolic volume (ml)

22.7 ± 8.4

29.4 ± 8.3

38.6 ± 10.2*

Ejection fraction (%)

59.3 ± 7.4

52.0 ± 9.3

45.6 ± 10.4*

Infarct size (%)

-

21.7 ± 7.3

13.1 ± 4.6†

T2, noninfarcted (ms)

492 ± 44

484 ± 58

501 ± 109

T2, infarct (ms)

-

653 ± 57‡

670 ± 106‡

T1 pre, noninfarcted (ms)

895 ± 52

939 ± 23*

916 ± 26

T1 pre, infarct (ms)

-

1000 ± 54‡

1089 ± 30‡

T1 post, noninfarcted (ms)

486 ± 53

530 ± 61

491 ± 42.0

T1 post, infarct (ms)

-

327 ± 58‡

330 ± 46‡

λ, non-infarcted

0.37 ± 0.02

0.37 ± 0.03

0.39 ± 0.03

λ, infarct

-

0.967 ± 0.25‡

0.881 ± 0.13‡

Data presented as mean ± SD. (λ = Partition Coefficient) * p-value < 0.05 vs. Baseline. † p-value < 0.05 vs. Day 2. ‡ p-value < 0.05 vs. non-infarcted myocardium at Baseline, Day 2 and Day 30.

Conclusions

Adverse infarct remodeling is readily characterized by multiparametric CMR imaging. In this model T2 and pre-contrast T1 remained elevated in the infarct zone 30d post-MI. Notably, there was no significant acute or late change in λ of the remote noninfarcted myocardium. Thus, there is no evidence of remote fibrosis during LV remodeling. There is, however, a large magnitude change in infarct λ which may be an important parameter for monitoring LV remodeling.

Funding

AHA 10SDG2650038, NIH K23 HL112910-01, 5T32EB003841, UVA/Astra-Zeneca Research Alliance

Authors’ Affiliations

(1)
Medicine, University of Virginia, Charlottesville, VA, USA
(2)
Biomedical Engineering, University of Virginia, Charlottesville, VA, USA
(3)
Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA
(4)
Radiology, University of Virginia, Charlottesville, VA, USA

Copyright

© Pan et al; licensee BioMed Central Ltd. 2013

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

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