Left ventricular blood flow kinetic energy by 4D flow magnetic resonance imaging in patients with acute myocardial infarction after revascularization

Introduction

Percutaneous coronary intervention (PCI) can quickly restore epicardial coronary blood flow in patients with acute myocardial infarction (MI) to rescue the ischemic myocardium. However, revascularization also frequently leads to a phenomenon known as coronary no-reflow, which results in microvascular damage and further myocyte necrosis. The main pathophysiological mechanism of no-reflow is microvascular obstruction (MVO), which results in myocardial ischemia, distal embolization, and reperfusion-related injury. MVO is associated with increased morbidity and mortality. In addition, MVO is often accompanied by intra-myocardial hemorrhage (IMH). The combination of MVO and IMH was observed in 35–51% of patients with ST-segment elevation myocardial infarction (STEMI) after treatment with PCI, and the hemorrhage area was approximately 3% of the left ventricular (LV) mass (1-4). The impact of the MI location on the mortality risk for patients with MI remains controversial. Most scholars believe that patients with acute anterior wall MI suffer more pronounced adverse LV remodeling and major adverse clinical events and that an anterior infarct location is one of the independent predictors of early death from STEMI. Further, infarction size remains the strongest predictor for medium-term major adverse clinical events (5).

Cardiac magnetic resonance (CMR) technology provides a comprehensive analysis of MI, including the assessment of abnormal myocardial motion and function, myocardial scarring, MVO, and IMH. CMR parameters provide information that is valuable for predicting adverse LV remodeling and major adverse cardiac events (3). Changes in LV intracavity flow patterns are a major cause of LV remodeling and are correlated with the myocardial motion state. Emerging four-dimensional flow cardiovascular magnetic resonance (4D flow CMR) has been used to assess LV intracavity flow and can reveal the flow velocity in all three spatial directions as well as with time. LV intracavity kinetic energy (KE) is described by simplified parameters to quantify the blood flow inside the LV throughout the complete cardiac cycle. Measurement of LV KE by 4D flow CMR has made it possible to routinely evaluate the complex patterns of blood flow in the LV and their behavior in clinical practice (6).

For patients with acute STEMI who undergo PCI, the complex patterns of LV blood flow and their effects on LV remodeling resulting in poor prognosis remain unclear. According to the known factors related to the prognosis of MI, such as ejection fraction (EF), MVO, IMH, and infarct location, the present study aimed to characterize LV KE parameters that could simplify LV blood flow evaluation, and attempt to find meaningful parameters that may explain the key pathophysiology of these cases that are prone to a poor prognosis based on hemodynamic insights, especially energetics. These results may provide a basis for further research to develop improved treatment strategies for these patients. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1298/rc).

Methods

Study cohort

Between February 2023 and May 2024, we prospectively included 32 individuals with acute STEMI who underwent CMR with a 4D flow sequence. The inclusion criteria were patients with first time acute STEMI treated by PCI within 12 h of the onset of chest pain. Acute STEMI was defined according to the current international guidelines (7). This prospective study was conducted at a single center and approved by the Institutional Review Board of Beijing Chaoyang Hospital, Capital Medical University. Written informed consent was obtained from all patients and healthy controls. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was registered at the Chinese Clinical Trial Registry (ChiCTR2200064755). Acute STEMI patients were scheduled for CMR imaging within 7 days after PCI. All patients were grouped based on the presence of anterior wall MI, MVO, and IMH, as well as the reduction in LV EF.

Participants were matched by age and sex to 21 healthy controls who had no evidence of heart and lung diseases, to obtain a reference group for 4D flow. Among the 21 healthy control participants, 8 underwent CMR with contrast enhancement, and the other 13 underwent CMR without contrast enhancement.

The following exclusion criteria were applied to both acute STEMI patients and healthy controls: nonischemic cardiomyopathy, severe valvular heart disease, known history of MI, glomerular filtration rate <30 mL/min/1.73 m², hemodynamic instability (Killip class III/IV requiring continuous intravenous diuretic therapy), and contraindications for CMR examination.

From 6–12 months after PCI, 8 patients (7 males and 1 female) with multiple risk factors for poor prognosis were examined by CMR, and LV flow components and KE parameters were calculated.

CMR examination

All CMR examinations were performed with a 3T system (MAGNETOM Prisma, Siemens Healthineers, Forchheim, Germany) and an 18-channel phased-array surface receiver coil. LV volume and EF were measured from the LV short-axis stack cine sequence of the 2D steady-state free precession. T2-weighted dark-blood fat-sat images and T2* mapping images of all LV short-axis stacks were acquired before enhancement. Inversion recovery late gadolinium enhancement (LGE) images were obtained 10–15 minutes after intravenous injection of 0.4 mL/kg gadopentetate dimeglumine (Northland, Beijing, China) in all patients and several healthy controls. A sagittal volume of whole-heart electrocardiographically gated 4D flow magnetic resonance imaging (MRI) was acquired during 6–9 minutes of free-breathing with diaphragmatic navigation, after injection of the gadolinium-based contrast agent for all patients and several healthy controls, and these images were acquired after sequences without enhancement for the other healthy controls. Images were acquired using the following parameters: velocity-encoding value of 150 cm/s in all directions, acceleration factor of 3.0, mean acquired spatial resolution of 2.5 mm × 2.5 mm × 2.5 mm, flip angle of 15° for examinations with enhancement, flip angle of 7° for examinations without enhancement, repetition time/echo time of 5.05 ms/2.71 ms, bandwidth of 496 Hz/Px, two views per segment, and temporal resolution of 40.4 ms reconstructed into 25 phases per cardiac cycle.

Image analysis

Postprocessing of all conventional images was conducted using offline commercial software (Cvi42 version 5.14.3; Circle Cardiovascular Imaging, Calgary, Canada). To assess cardiac function according to body surface area, including LV EF, LV end-diastolic volume (EDV), LV end-diastolic/end-systolic volume index (EDVI/ESVI), LV stroke volume index (SVI), and cardiac output index (CI), measurements were taken by tracing the endo- and epicardial borders on the stacks of short-axis cine images at end diastole and end systole. The presence, localization, and distribution patterns of LGE and edema were assessed visually on short- and long-axis images and defined as present only if detectable in two orthogonal planes. If LGE was present in the anterior wall visually and involved the interventricular septum, the case was assigned to the anterior group. If LGE was present in the inferior or lateral wall visually, the case was assigned to the inferior/posterior group. The infarct size in the LGE sequence was quantified in a semi-automated manner using a threshold of at least 5 standard deviations (SDs) exceeding the mean for normal myocardium and expressed as a percentage of LV volume. MVO was defined as a subendocardial dark area within the hyper-enhanced myocardium; it was assessed on LGE images and quantified by semi-automated contouring the hypointense zone within the enhanced areas using the “no reflow contour” application, which were shown as a percentage of LV volume. MVO was included in the measurements of LGE. IMH was quantified as hypointense signal on T2* maps within the infarcted myocardium showing signal intensity <2 SDs of the mean signal intensity in the remote myocardium. The myocardial edema size in T2-weighted dark-blood fat-sat sequences was quantified in a semi-automated manner using a threshold of at least 2 SDs exceeding the mean for normal myocardium and expressed as a percentage of LV volume. Feature-tracking, including LV global peak circumferential strain (GPCS) and LV global peak longitudinal strain (GPLS), which were shown to have better clinical and prognostic value in a previous study (5), was estimated from the short axis, two- and four-chamber cine series in strain application.

KE measurements

We performed 4D flow data postprocessing using the Cvi42 4D flow module. This data analysis was conducted using offline commercial software (Cvi42 version 5.14.3; Circle Cardiovascular Imaging) by two radiologists (M.X.L. and L.L., with 8 years of experience in CMR). After automatic correction for eddy current effects on the whole volume by third order surface interpolation, each 4D flow image was imported into the Cvi42 4D flow module. After rectification of a series of images, including displacement and anti-signal aliasing correction, the post-processed layer was confirmed to cover the entire left ventricle. The plane range for the mitral valve and aortic valve was delineated according to the three-chamber LV cine images. The software automatically tracks the blood flow particles passing through the plane of the mitral valve and aortic valve in one cardiac cycle, and the particles are released during isovolumic contraction and tracked forward and backward. As isovolumetric contraction particles were emitted, they were traced both forward and backward until isovolumetric relaxation, and the results were then checked and corrected against aortic and mitral valve contours. According to the flow rate of particles through the valve opening, the blood flow was divided into the following four components: direct flow, delayed injection flow, retained flow, and residual volume. The KE parameters for each component in the left ventricle were calculated as follows. The number of particles for each component was multiplied by the individual particle volume to calculate the total blood flow for each component (Figure 1). For each volumetric element (voxel), KE was computed as KE =1/2 ρ_blood•V_voxel•v², where ρ_blood represents blood density (1.06 g/cm³), V_voxel represents voxel volume, and v represents the velocity of the corresponding voxel (8,9). All KE parameters were normalized to EDV (KEi_EDV) and presented in µJ/mL. KEi_EDV parameters were extracted from the time-resolved KEi_EDV curve. The LV KE parameters used in this study are described in Table 1.

Figure 1 Measurement of KE parameters on 4D flow CMR. (A) The first step involves automatically detecting and adjusting the positions of the mitral and aortic valves in the three-chamber left ventricle cine images. (B) The second step involves automatically defining the positions of the valve orifice. Next, we adjust the region of interest range based on the direction and position of the blood flow, to ensure complete coverage of the aortic and mitral valve blood flow. (C,D) The final steps were defining the starting point of the isovolumetric relaxation phase and generating the LV blood flow image and flow curves, including each blood flow component and corresponding KE value. The red curve in (C) shows the aortic valve flow curve in a cardiac cycle, and the green curve shows the mitral valve flow curve in a cardiac cycle. In (D), green = direct flow; blue = delayed ejection flow; yellow = retained inflow; red = residual volume. AV, aortic valve; CMR, cardiac magnetic resonance; KE, kinetic energy; LV, left ventricular; MV, mitral valve.

Statistical analysis

Statistical analysis was performed using IBM SPSS Statistics 25.0. All tests were two-sided, and P values less than 0.05 defined statistical significance. Quantitative parameters are presented as mean ± SD or median and interquartile range, where appropriate. Demographic data were compared with independent-samples t-test or nonparametric test. Count data were compared between groups using Fisher’s exact test and the χ² test. Imaging data were analyzed by analysis of variance (ANOVA) and pairwise comparisons between groups according to the normality of data distribution and homogeneity of variance. Correlations between KE parameters and parameters of LV function and strain as well as the amount of LGE, MVO size, and myocardial edema size were evaluated by Pearson or Spearman correlation analysis. Intra- and inter-observer reliability tests were applied to calculate inter-class correlation coefficients.

Results

Characteristics of study participants

A total of 32 acute STEMI patients (mean age, 54.7±13.1 years; 29 males and 3 females) and 21 healthy controls (mean age, 49.2±11.2 years; 18 males and 3 females) were initially included because clinical information was complete and 4D flow images were clearly available. Controls and patients were matched for age, gender, body surface area, etc. (Table 2).

The patients were divided into subgroups based on the presence of anterior MI (anterior group, n=17) vs. the inferior/posterior MI (inferior/posterior group, n=15); MI with MVO (MVO group, n=18) vs. MI without MVO (non-MVO group, n=14); and MI with IMH (IMH group, n=15) vs. MI without IMH (non-IMH group, n=17). Subgroups were also created for patients with EF ≥50% and those with EF <50% (EF ≥50% group and EF <50% group, n=16 for both subgroups).

Comparison of baseline CMR results between the STEMI patient and control groups

Some patients in the STEMI group had hypertension, and therefore, we included a similar proportion of control individuals who showed elevated blood pressure during scanning. Heart rate was comparable between the STEMI patients and control groups (72±10 vs. 70±12 bpm, P=0.603). Most baseline functional CMR parameters differed significantly between the STEMI patients and control groups. The LV global peak circumferential strain (LVGPCS) and LV global peak longitudinal strain (LVGPLS) were lower in the STEMI group than in the control group [−13.91%±2.97% vs. −18.66%±2.22% (P<0.001) and −10.28%±3.89% vs. −13.78%±2.90% (P<0.001), respectively]. In all STEMI patients, the direct flow component was lower than that in the healthy control group (29.4%±10.6% vs. 35.9%±7.0%, P=0.028). The values reflecting diastolic function such as peak E-wave KEi_EDV, peak A-wave KEi_EDV, and KEi_EDV E/A ratio differed from those in the healthy control group. Comparisons of the baseline clinical and CMR characteristics between the two groups are presented in Table 2.

Comparison of LV flow components between STEMI patient subgroups and healthy controls

Among the STEMI patient subgroups, the delayed ejection flow component was higher in the anterior group vs. the inferior/posterior group (F=3.847, P=0.028), in the MVO group vs. the non-MVO group (F=6.035, P=0.004), in the IMH group vs. the non-IMH group (F=4.164, P=0.021), and in the EF <50% group vs. the EF ≥50% group (F=5.488, P=0.007).

In the anterior group (F=4.014, P=0.024), MVO group (F=4.481, P=0.016), and EF <50% group (F=3.209, P=0.049), the direct flow component was lower than that in the healthy control group. Also, the direct flow component in the IMH group was significantly lower than that in the non-IMH group and the control group (25.9%±9.7% vs. 32.5%±10.7% vs. 35.9%±7.0%; F=5.285, P=0.008). The differences in flow components between the MVO and non-MVO groups are presented in Table 3.

The differences in the four flow components between the healthy control, non-MVO, and MVO groups are illustrated in the example cases presented in Figures 2-4. The box and whisker plots of the direct flow component and delayed ejection flow component are shown in Figure 5.

Figure 2 LV flow components and KE curve for a 60-year-old male control individual. (A) Pseudo-colored maps of systolic and diastolic LV flow in the CMR cine sequence. (B) Proportions of the flow components. (C) LV KEi_EDV curve in a cardiac cycle with three peaks representing the systolic, diastolic E wave, and diastolic A wave KEi_EDV. The direct flow/delayed ejection flow ratio of peak systolic KEi_EDV (P_d/P_de) was 1.37. CMR, cardiac magnetic resonance; KE, kinetic energy; KEi_EDV, KE parameters normalized to left ventricular end diastolic volume; LV, left ventricular.

Figure 3 LV flow components and KE curve for a 57-year-old male patient, with an LV ejection fraction of 46.8%. (A,B) Subendocardial late gadolinium enhancement and myocardial edema in the mid-ventricular anterior and septal wall. (C) Pseudo-colored maps of the systolic and diastolic LV flow in the CMR cine sequence. (D) Proportions of the LV flow components. (E) LV KEi_EDV curve in a cardiac cycle with three peaks representing the systolic, diastolic E wave, and diastolic A wave KEi_EDV. The proportion of direct flow components was still higher than that of delayed ejection flow, and the direct flow/delayed ejection flow ratio of peak systolic KEi_EDV (P_d/P_de) was 1.72. CMR, cardiac magnetic resonance; KE, kinetic energy; KEi_EDV, KE parameters normalized to left ventricular end diastolic volume; LV, left ventricular.

Figure 4 LV flow components and KE curve for a 47-year-old male patient, with an LV ejection fraction of 30.9%. (A,B) Transmural late gadolinium enhancement and myocardial edema in the mid-ventricular anterior and septal wall with microvascular obstruction and intra-myocardial hemorrhage. (C) Pseudo-colored maps of the systolic and diastolic LV flow in the CMR cine sequence. (D) Proportions of the LV flow components. (E) LV KEi_EDV curve in a cardiac cycle with three peaks representing the systolic, diastolic E wave, and diastolic A wave KEi_EDV. The proportion of delayed ejection flow components was higher than that of direct flow components, and the direct flow/delayed ejection flow ratio of peak systolic KEi_EDV (P_d/P_de) was 0.32. The proportion of residual volume increased as well. CMR, cardiac magnetic resonance; KE, kinetic energy; KEi_EDV, KE parameters normalized to left ventricular end diastolic volume; LV, left ventricular.

Figure 5 Box and whisker plots for the direct flow component, delayed ejection flow component, and ratio of peak systolic KEi_EDV between the direct flow and delayed ejection flow (P_d/P_de), demonstrating changes of different degrees between the acute STEMI subgroups and healthy controls. In the anterior group, MVO group, IMH group and EF <50% group, the direct flow component was lower than that in the healthy control group. Moreover, the above value in the IMH group was significantly lower than that in the non-IMH group. The delayed ejection flow component was higher in the anterior group, the MVO group, the IMH group and the EF <50% group vs. other subgroups, and was significantly higher than that in the healthy controls as well. The P_d/P_de was significantly lower in the MVO and IMH group. Data are presented as mean ± standard deviation. * and o, outlier in the IBM SPSS Statistics 25.0. EF, ejection fraction; IMH, intra-myocardial hemorrhage; KE, kinetic energy; KEi_EDV, KE parameters normalized to left ventricular end diastolic volume; MVO, microvascular obstruction; STEMI, ST-segment elevation myocardial infarction.

Comparison of KE parameters between STEMI patient subgroups and healthy controls

The average systolic KEi_EDV was significantly lower in the MVO group than in the non-MVO group and the healthy control group (10.04±3.16 vs. 13.54±5.10 vs. 14.13±6.77 µJ/mL; P=0.041). Additionally, the ratio of peak systolic KEi_EDV between the direct flow and delayed ejection flow (P_d/P_de) was significantly lower in MVO group than in the non-MVO group and the healthy control group (1.17±0.55 vs. 2.31±1.60 vs. 1.98±1.15; P=0.006; Table 3). The average systolic KEi_EDV in the IMH group appeared lower than that in the non-IMH group and the healthy control group, but the differences were not statistically significant. However, the P_d/P_de in the IMH group was significantly lower than that in the non-IMH group and the healthy control group (1.16±0.58 vs. 2.12±1.51 vs. 1.98±1.15; P=0.006).

The peak systolic KEi_EDV in the EF <50% group was significantly lower than that in the EF ≥50% group and the healthy control group (20.15±6.02 vs. 28.45±10.11 vs. 29.16±13.47 µJ/mL; P=0.006). Also, the average systolic KEi_EDV in the EF <50% group was significantly lower than that in the EF ≥50% group and in the healthy control group (9.50±2.27 vs. 13.65±5.10 vs. 14.13±6.77 µJ/mL, F=7.405, P=0.003). The values reflecting systolic function were not significantly different between the anterior group and the inferior/posterior group.

Additionally, the values of some parameters reflecting diastolic function differed among STEMI subgroups. The peak A-wave KEi_EDV was significantly higher in the inferior/posterior group than in the healthy control group (24.15±15.91 vs. 14.33±5.73 µJ/mL, P=0.025), while the KEi_EDV E/A ratio in the anterior group was lower than that in the healthy control group (0.99±0.67 vs. 1.99±1.67, P=0.041). The KEi_EDV E/A was significantly lower in the non-MVO group (0.73±0.36) and non-IMH group (0.83±0.39) than in the healthy control group (1.99±1.67) (P<0.05). Meanwhile, peak E-wave KEi_EDV and peak A-wave KEi_EDV differed significantly between the non-MVO group and the healthy control group (Table 3). The peak E-wave KEi_EDV was significantly lower in the EF <50% group than in the healthy control group (14.96±7.36 vs. 23.35±12.41, P<0.05). The time difference between the peak-E wave of the direct flow and delayed ejection flow during early diastolic filling (Te) also was lower in the EF <50% group (14.00±26.47 ms) than in the healthy control group (26.66±23.59 ms) but higher in the EF ≥50% group (32.53±10.13 ms) than in the healthy control group. The difference in Te between the EF <50% group and the EF ≥50% group was statistically significant (F=3.488, P=0.044). The KE curve differences and trends of a cardiac cycle in healthy control, non-MVO, and MVO patients are shown respectively in Figures 2-4. The box and whisker plots of P_d/P_de are shown in Figure 5.

Correlations between KE parameters and standard cardiac parameters

Many KE parameters were moderately or strongly associated with LV functional parameters, notably the delayed ejection flow component, P_d/P_de, and Te (P<0.05). Additionally, many KE parameters were moderately or strongly associated with infarct size, MVO size, and myocardial edema size, especially the delayed ejection flow component and P_d/P_de (P<0.05). Several KE parameters also were moderately associated with LV GPCS and GPLS, including the delayed ejection flow component, P_d/P_de, and Te. The results for correlations between KE and standard CMR parameters are presented in Table 4.

Intra-/inter-observer reliability of KE parameters

The intra-class correlation coefficients (ICCs) were excellent for all flow components and the global KE value on intra-observer tests (average ICC=0.995, P<0.001) and on inter-observer tests (average ICC=0.994, P<0.001). The mean intra- and inter-observer differences in these measurements were small with good limits of agreement.

Follow-up of STEMI patients

During the subsequent 6–12 months of follow-up, clinical CMR examination was recommended for 8 patients in the STEMI group with multiple risk factors for poor prognosis. Two patients had risk factors such as hypertension and diabetes (without associated cardiomyopathy). Although the EF values for these patients showed improvement, the EF values remained below normal levels (EF <55%).

In the MVO group, only one patient had some residual MVO. Apical ventricular aneurysm was observed in two patients, and one of them had hemosiderin deposition in the LV myocardium (Figure 6). None of the patients experienced significant improvement in KE parameters compared with the baseline levels.

Figure 6 LV flow components and KE curve on follow-up of the same patient whose data are presented in Figure 4, showing an increase in the LV ejection fraction to 44.4%. (A,B) Well-defined transmural late gadolinium enhancement and myocardial hemosiderin deposition in the mid-ventricular anterior and septal wall. (C) Pseudo-colored maps of the systolic and diastolic LV flow in the CMR cine sequence. (D) Proportions of the LV flow components. (E) LV KEi_EDV curve in a cardiac cycle with three peaks representing the systolic, diastolic E wave, and diastolic A wave KEi_EDV. The proportion of delayed ejection flow components was higher than that of direct flow components, and the direct flow/delayed ejection flow ratio of peak systolic KEi_EDV (P_d/P_de) was 0.65. CMR, cardiac magnetic resonance; KE, kinetic energy; KEi_EDV, KE parameters normalized to left ventricular end diastolic volume; LV, left ventricular.

Discussion

This study aimed to characterize the LV KE of acute STEMI patients after PCI and to further explore the predictive value of KE parameters for poor prognosis. The results showed that the delayed ejection flow component was increased and the direct flow component was reduced relative to control conditions in the groups with anterior, MVO, IMH, and an EF <50%. The direct flow component in STEMI patients with IMH also was significantly lower than in control individuals. Some systolic KE parameters were reduced in patients with MVO and an EF <50%. Our results also emphasize the need to focus on myocardial diastolic function in STEMI patients, and diastolic function was decreased more obviously in the non-MVO group. Several KEi_EDV parameters in the STEMI group were strongly and moderately correlated with parameters reflecting LV function and structure, especially the delayed ejection flow component, direct flow component, P_d/P_de, and Te.

The LV flow patterns often indicate the efficiency of blood transport, with a higher proportion of direct flow implying more efficient blood transport (10). In the present study, the direct flow component was reduced by varying degrees in patients with acute STEMI, while the delayed ejection flow component was increased, especially in specific subgroups. However, no significant differences in the retained inflow and residual volume components were observed between the subgroups of these patients and the healthy control group. The observed reduction in the direct flow is similar to that seen in chronic MI (10) and dilated cardiomyopathy (11), while the changes in the other flow components differ. In patients with acute STEMI, especially those with an anterior wall lesion, the proportion of the delayed ejection flow component increased in our study. However, while the proportions of retained inflow and residual volume components were previously shown to increase (12,13), these changes were not seen in our study. The main reason may be differences in the characteristics of MI in the acute MI group; for example, more patients had preserved EF. The use of different calculation software may be another reason (13). Moreover, the observed changes in LV flow patterns differ from those due to right ventricular enlargement caused by pulmonary hypertension (14).

The KE parameters in the STEMI group and the healthy control group of the present study were similar to those reported in the literature, but only some diastolic parameters in subgroups showed statistical differences from those in the healthy control group, which varies somewhat from the literature. This may be related to the inclusion of more patients with preserved EF in our study and to the use of a different calculation method for total KE values in systole and diastole compared with previous studies (8,13,15). This suggests that the parameters and procedures applied for assessing intraventricular blood flow characteristics should be more standardized, as standard methods would be more conducive to repeatability across centers in order to assure consistent high-quality 4D flow CMR output and computation in both clinical and research settings (16,17). The results of the present study suggest that after PCI, STEMI patients require careful monitoring of diastolic function, especially those without MVO. As is well known, acute MI leads to a loss of contractile fibers, thereby reducing systolic function. Parallel to its effect on systolic function, MI can also affect diastolic function, but this relationship is less well understood. Both the active relaxation and passive filling phases of diastole require energy and are impaired by myocardial ischemia and infarction. Another cause of impaired diastolic function following acute MI is electromechanical dyssynchrony, in which the myocardial segments do not contract simultaneously. This causes some segments to actively contract after global systole ends and even during early filling. The Te values observed in this study may reflect this situation, suggesting early diastolic dysfunction and compensatory changes, but further research with a larger sample size is needed. Additionally, Interstitial edema or fibrosis caused by acute MI can impair LV compliance. The interaction between myocardial edema or fibrotic segments and overall diastolic function is unclear (18). Currently, the clinical assessment of LV diastolic function is primarily performed using non-invasive echocardiography. The restrictive transmitral filling pattern is a powerful predictor of survival after acute MI, independent of LV size and systolic function markers, and is associated with clinical factors (19,20). Evaluation of diastolic KE parameters on 4D flow CMR can provide a new perspective and method for assessing LV diastolic function. Its use is expected to identify early and sensitive indicators of poor prognosis after acute MI. However, many factors affect diastolic function, and comorbidities such as hypertension, diabetes, hypertrophic cardiomyopathy, and older age are risk factors for LV remodeling (18,21,22). Compared with echocardiography, CMR scanning takes more time, and the image quality and measurement results are affected by many factors, such as the patient’s breath-holding and heart rhythm. In addition, reference values for diastolic function parameters on CMR are lacking, and post-processing software is limited. Some methods for evaluating diastolic function and distinguishing different types of heart failure, such as left atrial volume and function assessment, strain, and hemodynamic analysis, are still in the exploratory stage, and the exact thresholds as well as the patterns by which these parameters change in diastolic dysfunction require further extensive research. Furthermore, post-processing software is expensive and cannot be widely popularized (23,24). The CMR imaging indicators and thresholds such as diastolic KEi_EDV parameters should be refined, clarified, and summarized for early assessment of cardiac diastolic function, which will be a direction of subsequent research.

In this study, we divided STEMI patients into groups based on the presence MVO and IMH after PCI and found many significant differences in KE parameters among the subgroups and between the subgroups and the control group. The direct flow component was significantly reduced in the subgroups with MVO and IMH, and the delayed ejection flow component was significantly increased, especially in patients with IMH. This blood flow status severely affected blood flow transport and work efficiency. MVO had a greater impact on systolic function, with significant reductions specifically in the average systolic KEi_EDV and P_d/P_de. However, several systolic function parameters also seemed to be reduced in the IMH subgroup, but the differences were not statistically significant. Decreased systolic work efficiency may be one reason for the poor prognosis of these patients after PCI (4), and P_d/P_de seems to be more specific. In our STEMI group, 18 patients had MVO combined with IMH, the most severe form of reperfusion injury (25), and only 3 patients did not have IMH. Therefore, further studies with larger sample sizes are needed to evaluate the impact of IMH on intraventricular blood flow in the left ventricle.

During 6–12 months of follow-up, clinical CMR reexamination was recommended for 8 patients in our STEMI group with multiple risk factors for poor prognosis. We found that the baseline P_d/P_de values for 7 of these patients was lower than the average baseline value in the study, and the direct flow component was lower than the delayed ejection flow component in 5 patients. We also observed no significant improvement in P_d/P_de, the direct flow component, or the delayed ejection flow component on the follow-up CMR examinations. The P_d/P_de was even lower in two patients with new-onset ventricular aneurysms. In such cases, the ejection efficiency was previously found to be significantly reduced, and the LV EF value stayed below 50% during follow-up (26). Thus, P_d/P_de measurement may indicate the abnormal blood flow state in patients with ventricular aneurysms. However, the global and focal hemodynamic characteristics of ventricular aneurysm formation remain unclear (15), and our findings may provide some implications for future studies. In the present study, the P_d/P_de, the direct flow component, and the delayed ejection flow component were well correlated with parameters reflecting LV function and structure. Therefore, we suggest that the P_d/P_de, the direct flow component, and the delayed ejection flow component may be new imaging biomarkers reflecting an increased risk of poor prognosis. However, further research with a larger sample size and longer follow-up is needed to determine the predictive thresholds for these parameters.

There are several limitations in this study. First, the results were obtained from a small cohort of STEMI patients, limiting our ability to adjust for multiple variables. Additionally, several of the patients had hypertension. Thus, the healthy control group included a similar proportion of healthy volunteers who exhibited hypertension during the CMR examination. Second, in this pilot study, follow-up was conducted for only a few patients in our cohort, because the clinician only referred patients with multiple risk factors for poor prognosis for CMR reevaluation. However, our research findings may promote the exploration of early warning markers of poor prognosis. We will continue to follow these patients in the future research to obtain more data on intraventricular flow in the chronic phase of STEMI, and to verify the value of these parameters in assessing prognosis and LV remodeling. Third, in our clinical examination protocol, the 4D flow sequence was our main sequence. Thus, myocardial delayed enhancement was identified in LGE sequences, but an early gadolinium enhancement (EGE) sequence was not obtained. The existence of IMH was evaluated, but the size of IMH was not calculated yet. Fourthly, based on the consensus statement (15), the data for 4D flow sequences were obtained from several healthy controls without enhancement, but these data with or without enhancement were not compared yet to detect any differences. Finally, our study mainly assessed the overall situation of LV KE parameters, specifically evaluating the differences in KE parameters between the direct flow component and delayed ejection flow component, rather than evaluating the differences in KE parameters at different levels and in different segments as in other studies. Thus, larger multicenter studies involving more acute MI patients are still necessary to validate these preliminary results and to determine the cut-off values for KE parameters that provide early warning of poor prognosis.

Conclusions

In conclusion, LV flow components and KE parameters can be derived from 4D flow CMR, an emerging and sensitive imaging method for quantitatively assessing LV hemodynamics and work efficiency. Specifically, the P_d/P_de, the direct flow component, and the delayed ejection flow component may explain the key pathophysiology changes responsible for the poor prognosis of STEMI patients from a hemodynamic perspective, especially energetics. Decreased systolic work efficiency may be one reason for the poor prognosis of these patients after PCI with MVO and IMH, and P_d/P_de seems to be more specific. Our results also indicate the need for careful monitoring of diastolic function in STEMI patients.

Acknowledgments

We would like to thank all the participants and staff involved in the CMR scanning, image collection, and data post-processing performed for this study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1298/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1298/dss

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1298/coif). J.A. is an employee of Siemens Healthineers. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of Beijing Chaoyang Hospital, Capital Medical University. Written informed consent was obtained from all patients and healthy controls.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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