Abstract
Objectives: LV remodeling plays a critical role in the outcome of ST-elevation myocardial infarction (STEMI) patients. The aim of this study was to assess with CMR the impact of MI severity on structural/functional abnormalities throughout the ventricle. Material and methods: We studied a cohort of 186 reperfused STEMI patients (59±11yr,85%men) at 1week and 4months post-MI using comprehensive CMR including cine, T2-weighted, and late gadolinium enhancement (LGE) imaging allowing assessment of ventricular function, area at risk, myocardial necrosis/fibrosis, microvascular obstruction (MVO) and myocardial hemorrhage. Three groups of infarct severity were defined: severity (S) 0 (no MVO, no myocardial hemorrhage, n=68), S1 (MVO, no myocardial hemorrhage, n=84) and S2 (MVO and myocardial hemorrhage, n=34). Information on end diastolic wall thickness (EDWTh) and systolic wall thickening (SWT) in the infarct, adjacent and remote region was obtained using merging of LGE and cine imaging. A group of 40 age-matched patients without evidence of CAD and without LGE at CMR (58±10yr,85%men) served as controls. Between controls and MI patients no significant differences were present in arterial hypertension. Results: At baseline, increasing infarct severity was associated with significantly higher cardiac enzymes, larger areas-at-risk, infarct sizes and lower myocardial salvage ratios; and was related with increased EDVs and LV mass and decreased EFs. Infarct patients presented, compared to controls, increased EDWTh and decreased SWT (both p<0.001), and the magnitude of abnormalities increased toward the infarcted myocardium. With increasing infarct severity, depression in SWT was more pronounced in the infarcted and adjacent myocardium. At FU, LVEF significantly improved in S0 and S1 (p<0.001), while S2 adversely remodeled with significant increase in LVEDV and ESV (p<0.001). At myocardial level, a decrease in EDWTh was observed, increasing with increasing infarct severity. Significant improvement in SWT was noticed in S0 and SI in the infarcted and adjacent myocardium (all p<0.01). Changes between baseline and FU in LV ESV were inversely related to changes in SWT (r= -0.293, p=0.0001). Conclusion: Infarct severity has a significant influence on early post-infarction remodeling, infarct healing and post-infarction myocardial and ventricular remodeling. Hemorrhagic infarcts behave different than non-hemorrhagic infarcts with more pronounced wall thinning, lack of functional recovery and adverse LV remodeling.
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