Left ventricular flow kinetics and myocardial deformation following acute infarction: Additional predictive value of cardiac magnetic resonance four-dimensional flow for left ventricular remodeling post-ST-elevation myocardial infarction

Abstract

Background: The exact mechanism underlying myocardial maladaptive changes post ST-elevation myocardial infarction (STEMI) remains unclear. We sought 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: Forty-nine first-STEMI patients (M:F = 26:13; mean age = 58 ± 10) prospectively underwent 3T cardiovascular magnetic resonance (CMR) acutely, at 3 months (3M) and 12M post-STEMI. The CMR protocol included left ventricular (LV) cine-images for LV end-diastolic (LVEDV) and end-systolic volumes, stroke volume (SV), and ejection fraction (LVEF); four-dimensional (4D)-flow and late gadolinium enhancement imaging. The 3M 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, delayed ejection, 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 12M from baseline, in opposition to the non-remodeling group (LV_non-remod). Association between SV, FT-strain, KE, and 4D flow parameters was assessed, as well as predictors of adverse remodeling at 12M post-STEMI.

Results: There were 23 LV_remod patients. At 3M 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. There was no significant difference in SV between the two 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 12M 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 remodeling after adjustment for LVEF, SV, FT-strain, and KE parameters. These findings suggest that these parameters may contribute to further risk stratification at 3M for the development of adverse remodeling at 12M post-STEMI, above conventional LV function parameters. Larger studies are needed to confirm these results.

Keywords: 4D flow parameters; CMR post MI; Global FT strain parameters; Interaction of FT strain and 4D flow parameters; Prediction of LV adverse remodeling at 12 months post STEMI.

(A) Two-cavity and short-axis view of an illustrative patient showing transmural LGE in the mid and apical inferior segment in the acute setting. (B) Illustration of the myocardial mechanistics and LV intracavitary flow at 3 months post STEMI. Direct flow at 3 months post STEMI was significantly correlated with global feature tracking parameters. (C) Two-cavity and short-axis view of an illustrative patient showing LV remodelling at 12 months post STEMI. LGE late gadolinium enhancement, LV left ventricular, STEMI ST elevation myocardial infarction;

Fig. 1

Overview of the study timeline and assessments. V₀ represents STEMI onset. CMR with feature tracking (FT) and 4D flow kinetic assessment was performed at V₁ (3–5 days post-STEMI), V₂ (3 months post-STEMI), and V₃ (12 months post-STEMI). Remodeling groups were defined based on changes between the acute (V₁) and 12 months (V₃) CMR. 4D four-dimensional, STEMI ST-elevation myocardial infarction, CMR cardiovascular magnetic resonance

Fig. 2

Assessment of FT strain parameters. (A) Illustration of the manual contouring of the endocardial and epicardial borders in the end-diastolic frame for all short- and long-axis slices. Right ventricular insertion points were also manually defined within the LV. (B) 3D deformation model obtained from short- and long-axis images. (C) Illustration of LV mesh overlay in short- and long-axis images for quality control of tracking and segmentation. Illustration of the global results for: GCS (D), GRS (E), GLS (F) as well as the segmental GLS results (G) FT feature tracking, LV left ventricular, GCS global circumferential strain, GRS global radial strain, GLS global longitudinal strain

Fig. 3

(A, B) Illustration of the 4D flow post processing. (A) Illustration of the manual contouring of the endocardial and epicardial borders. The segmentation was performed for all short-axis cine images. (B) Registration process between short-axis cine images and 4D flow data to correct for any patient movement between acquisitions. (C, D) Illustration of the 4D flow components: (C) direct flow (green line): blood flowing into the LV during diastole and exiting the LV during systole in the examined cardiac cycle. Retained volume (yellow line): blood flowing into the LV during diastole and not exiting the LV during systole in the examined cardiac cycle. Delayed ejection (flow (blue line): blood starting and remaining within the LV during diastole, and exiting during systole. Residual volume (red line): blood remaining within the LV for a minimum of two cardiac cycles. (D) LV blood flow KE curves during the cardiac cycle. Red curve represents LV endocardium. Blue curve represents basal LV myocardial segments. Green curve represents mid LV myocardial segments. White curve represents apical LV myocardial curves. Minimal KE_iEDV average KE of the LV flow at any time point during the whole cardiac cycle, Average KE_iEDV average KE of the LV flow at any time point during the whole cardiac cycle, Systolic KE_iEDV average KE of the LV flow during the systole, Diastolic KE_iEDV average KE of the LV flow during the diastole, Peak E-wave KE_iEDV peak KE of the LV flow during early diastolic filling, Peak A-wave KE_iEDV peak KE of the LV flow during late diastolic filling, 4D four-dimensional, LV left ventricular

Fig. 4

Correlations between direct flow and myocardial deformation at 3 months. (A) GRS vs direct flow (%); (B) GCS vs direct flow (%); (C) GLS vs direct flow (%). (D) Subgroup analysis of 4D flow-derived direct flow between LV_remod and LV_non-remod patients. Patients prone to develop adverse cardiac remodeling at 12 months post STEMI (blue circle) had significantly lower percentage of direct flow at 3 months post STEMI in comparison to those without adverse cardiac remodeling at 12 months post STEMI (red circle). GCS global circumferential strain, GLS global longitudinal strain, GRS global radial strain, LV_remod adverse left ventricular remodeling at 12 months post STEMI, LV_non-remod no adverse left ventricular remodeling at 12 months post STEMI, STEMI ST-elevation myocardial infarction, 4D four-dimensional

Fig. 5

Correlation between residual volume and myocardial deformation at 3 months. (A) GRS vs residual flow, (B) GCS vs residual flow, (C) GLS vs residual flow. (D) Subgroup analysis of 4D flow-derived residual flow between LV_remod and LV_non-remod patients. Patients prone to develop adverse cardiac remodeling at 12 months post STEMI (blue circle) had significantly higher percentage of residual volume at 3 months post STEMI in comparison to those without adverse cardiac remodeling at 12 months post STEMI (blue circle). GCS global circumferential strain, GLS global longitudinal strain, GRS global radial strain, LV_remod adverse left ventricular remodeling at 12 months post STEMI, LV_non-remod no adverse left ventricular remodeling at 12 months post STEMI, STEMI ST-elevation myocardial infarction, 4D four-dimensional