Why the study?
The exact mechanism underlying myocardial maladaptive changes post-STEMI remains unclear, prompting investigation into the impact of tissue-flow interactions on adverse cardiac remodeling.
Do CMR 4D-flow parameters and feature tracking strain at 3 months predict adverse LV remodeling at 12 months in patients with first STEMI?
Do CMR 4D-flow parameters and feature tracking strain at 3 months predict adverse LV remodeling at 12 months in patients with first STEMI?
CMR 4D-flow derived direct flow and infarct size at 3 months post-STEMI independently predict adverse LV remodeling at 12 months, outperforming conventional LV function parameters.
Early tissue-flow interaction may flag post-STEMI remodeling risk; leaves open whether 4D-flow CMR improves risk stratification beyond standard imaging.
Background The exact mechanism underlying myocardial maladaptive changes post ST-elevation myocardial infarction (STEMI) remains unclear. Objectives To assess the impact of the tissue-flow interaction on the development of adverse cardiac remodeling 12 months (M) after acute STEMI. Materials and methods 49 first-STEMI patients (M:F=26:13; mean age=58±10) prospectively underwent 3 T CMR acutely, at 3 M and 12 M post-STEMI. The CMR protocol included left ventricular (LV) cine-images for LV end-diastolic (LVEDV) and end-systolic (LVESV) volumes, stroke volume (SV) and ejection fraction (LVEF); 4D-flow; LGE imaging. The 3 M outcome measures included: 4D-flow derived LV flow kinetic energy indexed to EDV (KE iEDV ) and functional flow components [LV- KE iEDV , minimal- KE iEDV , diastolic- KE iEDV , and residual volume (RV), retained inflow (RI), delayed ejection (DE), direct flow (DF)]; global radial, circumferential and longitudinal strain (GRS, GCS, GLS) by feature tracking (FT); infarct size (IS). Adverse LV remodeling (LV remod ) was defined by a ≥ 20% increase in LVEDVi at 12 M from baseline, in opposition to the non-remodeling group (LV non-remod ). Association between SV, FT-strain, KE and 4D flow parameters were assessed, as well as predictors of adverse remodeling at 12 M post-STEMI. Results There were 23 LV remod patients. At 3 M post-STEMI, LV remod patients had significantly reduced LVEF, increased IS, abnormal FT-strain, systolic KE iEDV , DF and RV compared to LV non-remod patients. Ther was no significant difference in SV between the 2 groups. FT-strain parameters significantly correlated with DF (GRS: r=0.62; GCS: r=-0.67; GLS: r=-0.58, all p<0.001); RV (GRS: r=-0.56; GCS: r=0.51; GLS: r=0.53, all p<0.001); Peak-A-wave KE iEDV (GRS: r=0.38, p=0.008; GCS: r=-0.30, p=0.038; GLS: r=-0.29, p=0.04); Systolic KE iEDV (GRS: r=0.31, p=0.033, GLS: r=-0.35, p=0.012). DF outperformed conventional LV function parameters (SV and LVEF) in the LV remod prediction. DF and IS were the only independent predictors of 12 M adverse remodeling after adjustment for LVEF, SV, FT-strain and KE iEDV parameters. Conclusions Our study suggests a potential early interaction between FT-strain and 4D-flow parameters post-STEMI leading to the development of adverse remodeling. Within the limitations of our sample size, DF and IS were independent predictors of LV remodelling after adjustment for LVEF, SV, FT-strain and KE parameters. These findings suggest that these parameters may contribute to further risk stratification at 3 M for the development of adverse remodeling at 12 M post-STEMI, above conventional LV function parameters. Larger studies are needed to confirm these results.
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Kamani et al. (2025) studied this question.
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