Characterization of Edematous Mycocardial Tissue in Post-Infarct Mice by T2-weighted MRI.

摘要

Following coronary occlusion, a need exists to differentiate infarct (MI) from salvaged area (SA) that together defines the area at risk (AAR). T2-weighted cardiac MRI (T2w CMR) detects myocardial edema that delineates the AAR, while late gadolinium-enhanced (LGE) CMR delineates the MI. Past T2w CMR studies have been performed in larger animals, but not in mice. We developed a T2w CMR method for mice to quantify post-MI MR. For this, we measured inhomogeneities in mice at 7 Tesla to develop a T2w CMR sequence resistant to artifacts, and applied it in vivo in mice to quantify MR and SA.;Inhomogeneity maps in mice hearts quantified Deltao at +/-1000 Hz and DeltaB1 at +/-19%. The sequence design used T2 prep with an adiabatic pulse Malcolm Levitt train, and gradient echo readout. In vivo imaging included three post-MI mice groups with different occlusion times. Group one (60 minute occlusion) was imaged for four days, and had an AAR = 45.7 +/- 2.6 (mean +/- SEM) % LV mass that was significantly larger than MI = 33.2 +/- 1.5% LV mass (p 0.001). Group two (20--30 minute occlusion) was imaged from hour-3 through day-33. Day-2 AAR = 34.0 +/- 2.8% LV mass and also significantly larger than MI = 18.7 +/- 2.4% LV mass (p 0.0001). The AAR contrast to noise ratio was 48.5 +/- 3.8 over normal myocardium. Both AAR and MI from short occlusion were significantly smaller than from long occlusion (p 0.012 and p 0.00003 respectively). Short occlusion had significantly higher 46.4 +/- 4.8% of AAR salvaged (SA) than long occlusion with 27.1 +/- 1.6 salvaged (p 0.0005). Group three (20 minute occlusion) was imaged on day-2, then sacrificed for histological AAR confirmation. There was linear agreement (R² = 0.86), and small -1.6% bias between T2w and histological AAR. Interobserver analysis of T2w AAR by independent analysts showed linear agreement (R² = 0.91) and low -0.15% bias between analysts.;T2w CMR in mice may investigate short and long-term individual genetic pathways and pharmaceutical strategies for increasing the SA after MI.