Purpose: To evaluate the relationship between myocardial infarction ( MI myocardial infarction ) severity at magnetic resonance (MR) imaging and regional and global postinfarction left ventricular ( LV left ventricular ) remodeling.
Materials and methods: This HIPAA-compliant study was institutional review board approved. In 186 patients, reperfused ST segment elevation MI myocardial infarction (mean age ± standard deviation, 59 years ± 11) was prospectively studied the first week and 4 months after infarction. Microvascular obstruction ( MVO microvascular obstruction ) and intramyocardial hemorrhage ( IMH intramyocardial hemorrhage ) helped define three infarct severity groups: S0, no MVO microvascular obstruction or IMH intramyocardial hemorrhage (n = 68); S1, MVO microvascular obstruction , no IMH intramyocardial hemorrhage (n = 84); and S2, MVO microvascular obstruction and IMH intramyocardial hemorrhage (n = 34).
Results: were compared in 40 control patients (mean age, 58 years ± 10). One-way analysis of variance or Kruskal-Wallis test with post hoc Bonferroni correction was used. Follow-up analysis was performed with paired Student t test or Mann-Whitney U test. Results Infarct severity was positively related (P < .001) to peak of troponin I, inflammatory biomarkers, area at risk, and infarct volume and inversely related to myocardial salvage ratio, systolic wall thickening ( SWT systolic wall thickening ) in the infarct, and adjacent myocardium and LV left ventricular ejection fraction ( EF ejection fraction ). At follow-up, LV left ventricular EF ejection fraction significantly improved in S0 and S1 (S0: 53% ± 8 to 56% ± 8, P < .001; S1: 48% ± 8 to 52% ± 10, P = .006), while S2 adversely remodeled with increase in LV left ventricular end-diastolic (175 mL ± 35 to 201 mL ± 40) and end-systolic (100 mL ± 24 to 115 mL ± 29) volumes (P < .001). SWT systolic wall thickening recovery in the infarct (S0: 32% ± 21 to 42% ± 24, P < .001; S1: 19% ± 13 to 29% ± 19, P < .001; S2: 11% ± 9 to 15% ± 15, P = .22) and adjacent (S0: 41% ± 19 to 52% ± 21, P < .001; S1: 32% ± 11 to 38% ± 16, P = .002; S2: 24% ± 13 to 29% ± 14, P = .092) and remote (S0: 54% ± 18 to 62% ± 20, P = .002; S1: 53% ± 18 to 57% ± 20, P = .092; S2: 50% ± 35 to 53% ± 22, P = .75) myocardium was related to infarct severity. LV left ventricular wall thinning with LV left ventricular mass decrease occurred at follow-up (S0: 110 g ± 27 to 100 g ± 27, P < .001; S1: 115 g ± 24 to 109 g ± 26, P = .019; S2: 134 g ± 35 to 117 g ± 27, P = .043).
Conclusion: MVO microvascular obstruction and IMH intramyocardial hemorrhage significantly affect postinfarct myocardial and LV left ventricular remodeling; hemorrhagic infarcts behave worse than nonhemorrhagic infarcts, with lack of functional recovery and adverse LV left ventricular remodeling extending to remote myocardium.