Myocardial remodeling in reperfused myocardial infarction with multiparametric CMR: does diffuse fibrosis occur in remote noninfarcted myocardium?
Journal of Cardiovascular Magnetic Resonance volume 15, Article number: P137 (2013)
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.
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.
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.
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.
AHA 10SDG2650038, NIH K23 HL112910-01, 5T32EB003841, UVA/Astra-Zeneca Research Alliance
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Pan, J.A., Pollak, P.M., Lopez, D. et al. Myocardial remodeling in reperfused myocardial infarction with multiparametric CMR: does diffuse fibrosis occur in remote noninfarcted myocardium?. J Cardiovasc Magn Reson 15 (Suppl 1), P137 (2013). https://doi.org/10.1186/1532-429X-15-S1-P137