Abstract
The pathophysiological changes in the remote myocardium after acute myocardial infarction (MI) remains less understood. To assess the inflammation in the remote myocardium post-MI and its association with left ventricular (LV) remodeling using T2 mapping. Prospective. Twelve pigs at 3-day post-MI, 6 pigs at 3-month post-MI, 6 healthy pigs; 54 patients at 3-day and 3-month post-MI, 31 healthy volunteers; FIELD STRENGTH/SEQUENCE: A 3T MRI/ steady-state free-precession sequence for T2 mapping (animals: 0, 30, and 55 msec; human: 0, 25, and 55 msec), phase-sensitive inversion recovery gradient echo for late gadolinium enhancement (LGE), balanced steady free-precession sequence for cine. Infarcted myocardium was defined on LGE, remote T2 was measured on T2 maps. LV remodeling was evaluated as LV end-diastolic volume change index between two scans using cine. CD68 staining was conducted to detect monocyte/macrophage. Student-t test and one-way ANOVA were used to compare remote T2 with normal controls. The association of remote T2 with LV remodeling was assessed using linear regression. P values of <0.05 were used to denote statistical significance. Compared with healthy pigs, remote T2 significantly increased from 3 days to 3months post-MI (31.43 ± 0.67 vs. 33.53 ± 1.15 vs. 36.43 ± 1.07 msec). CD68 staining demonstrated the inflammation in remote myocardium post-MI but not in healthy pigs. Significant remote myocardial alterations in T2 were also observed in human group (40.51 ± 1.79 vs. 41.94 ± 1.14 vs. 42.52 ± 1.71 msec). In patients, the 3-month remote T2 (β=0.432) and remote T2 variation between two scans (β=0.554) were both independently associated with LV remodeling. T2 mapping could characterize the abnormalities in the remote myocardium post-MI, which was potentially caused by the inflammatory response. Moreover, variations in remote T2 were associated with LV remodeling. 1 TECHNICAL EFFICACY: Stage 3.
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