Abstract
Background
We assessed the diagnostic efficacy of magnetic resonance imaging (MRI) in patients with acute myocardial infarction (AMI).
Methods
In this study, 116 patients with acute myocardial infarction (AMI) underwent direct PCI intervention, admitted to our hospital between January 2018 and January 2021 were selected. Based on the presence of intramyocardial hemorrhage (IMH), they were divided into the IMH group and the non-IMH group. There were 46 cases in the IMH group and 70 cases in the non-IMH group. All patients underwent cardiac magnetic resonance imaging (CMR) for detection. CMR was used to detect IMH and non-IMH infarction sites. Cardiac indicators of IMH and non-IMH were compared using CMR and echocardiography (ECHO). The diagnostic efficacy of MRI in patients with AMI who had myocardial hemorrhage was compared by generating receiver operating characteristic (ROC) curves.
Results
The incidence of infarction sites was significantly higher in the IMH group than in the non-IMH group (all P < 0.05); myocardial detection results revealed a significantly higher incidence of ventricular aneurysm and pericardial fluid inclusion in the IMH group than in the non-IMH group (all P < 0.05); CMR evaluation revealed that the infarction size/left ventricular (IS/LV) volume percentage, patients with microvascular obstruction (MVO), and MVO/LV volume percentage were significantly higher in the IMH group than in the non-IMH group (all P < 0.05); global circumferential strain (GCS), global radial strain (GRS), and global longitudinal strain (GLS) in the IMH group were significantly lower than those in the non-IMH group (all P < 0.05); was both groups underwent echocardiography after percutaneous coronary intervention (PCI). The results indicated a significant decrease in left ventricular ejection fraction (LVEF) and a significant increase in left ventricular end-diastolic dimension (LVEDd) and IS/LV volume percentage in the IMH group compared to the non-IMH group (all P < 0.05); the area under the ROC curve of MRI for patients with AMI who had intramyocardial hemorrhage was 0.869, with high specificity and sensitivity; the sensitivity was 87.00, and the specificity was 85.00.
Conclusion
MRI can detect myocardial hemorrhage in patients with AMI after PCI, which suggests significant clinical diagnostic value and is worthy of utilization in clinical practice.
Keywords: Acute myocardial infarction, Diagnostic value, Intramyocardial hemorrhage, Magnetic resonance imaging
Introduction
Percutaneous coronary intervention (PCI) can enhance the survival rates of patients with acute myocardial infarction (AMI) according to recent clinical trials [1]. The early stages of pathological studies and clinical trials demonstrated that, despite the fact that timely treatment tends to normalize blood flow and myocardial cell function in patients with acute myocardial infarction, the microvascular function and myocardial perfusion of these patients remained inadequate. In clinical practice, this phenomenon was identified as the ‘no-reflow’ phenomenon, indicating an irreversible injury. Therefore, intramyocardial hemorrhage has indirectly become one of the major causes of no-reflow [2]. It resulted in severe and irreversible myocardial injury when the duration of coronary artery occlusion reached 40 min, characterized by myocardial necrosis ranging from the subendocardium to the epicardium in a layer-by-layer progression resembling a wavefront. Consequently, the myocardial ischemia within the myocardial layers generated two symptoms: microvascular obstruction (MVO) and intramyocardial ischemia (IMH), which led to myocardial infarction in the central area of the infarct core [3]. Furthermore, the majority of patients with acute myocardial infarction who received reperfusion therapy developed symptoms of IMH and MVO, resulting in irreversible ischemic microcirculation injuries due to myocardial ischemia. The correlation between MVO and adverse ventricular remodeling has been confirmed for a very long time, despite the fact that numerous early clinical studies had different perspectives on the relationship between MVO and IMH. Significant studies have also demonstrated the coexistence of IMH and MVO symptoms, a key indicator for evaluating adverse left ventricular remodeling [4]. One week after receiving reperfusion therapy, patients underwent cardiac magnetic resonance imaging (CMRI) to detect myocardial hemorrhage, the gold standard for diagnosing myocardial ischemia at this stage. However, there are currently few relevant investigations on CMRI in patients with AMI and intramyocardial hemorrhage [4]. Consequently, we selected 116 patients with acute myocardial infarction for analysis, investigating the treatment of patients with AMI and intramyocardial hemorrhage based on the role of magnetic resonance imaging. The results of this investigation will be presented below.
Data and methods
General data
In this study, we selected 116 patients with AMI who were admitted to our hospital between January 2018 and January 2021. They were divided into the IMH group and the non-IMH group based on the presence of IMH. There were 46 cases in the IMH group and 70 cases in the non-IMH group, including 26 males and 20 females in the IMH group, aged 52–68 years old, with an average age of (62.56 ± 4.85) years old, and 41 males and 29 females in the non-IMH group, aged 51–69 years old, with an average age of (61.33 ± 4.91) years old; all patients included in the study signed the informed consent form, and the contents of the informed consent form were read to both the patients and their families: The treatments and detections used in this study are all known safe methods in clinical practice; the collected general information and clinical data were used exclusively for study analysis and for no other purpose; and patients were instructed to promptly report any discomfort during treatment to their attending physician to determine the next treatment plan. The entire treatment and observation period lasted four weeks, and patients were instructed to inform their physician immediately of any changes in their condition. Patients were not permitted to use any other drugs or treatment methods for their condition without prior approval and were instructed to inform their physician if they did. The Medical Ethics Committee of our hospital reviewed and approved this study.
Inclusion criteria: (1) The eligible patients were selected according to the clinical diagnostic criteria of Western medicine; (2) All selected patients were diagnosed with AMI; (3) Patients over the age of 18; (4) Patients requiring direct PCI in the emergency department; (5) Patients who provided informed consent and voluntarily agreed to participate in the study.
Exclusion criteria: (1) Patients presenting with cardiogenic shock, ventricular tachycardia, or ventricular fibrillation prior to the procedure; (2) Presence of valvular heart disease or congenital heart disease; (3) Patients who underwent revascularization PCI within the previous six months; (4) Patients who have contraindications to CMR; (5) Patients with incomplete medical records and relevant imaging data; (6) Participants in other relevant studies within the previous three months; (7) Pregnant or lactating women; (8) Patients with severe mental disorders who are incapable of providing their informed consent;
Rejection criteria: (1) Patients experiencing sudden deterioration of disease during the study; (2) Patients whose other diseases affect the study results; (3) Patients encountering unforeseen circumstances that make it difficult for them to continue their participation during the study; (4) Patients who have a significant impact on other researchers during the study.
Study methods
All patients underwent CMR imaging using a Philips all-digital 3.0 Ingenia magnetic resonance system. Cine sequences were used to assess left ventricular function, delayed enhancement sequences for tissue characterization, and T2-weighted imaging sequences to evaluate IMH. Patients were positioned supine and instructed to hold their breath for 12 to 15 s before images were obtained. First, the routine multi-position SE sequence scan was performed with a slice thickness and interval of 7 mm and 2.5 mm, respectively, followed by a sequence scan that included both four-to-two-chamber and long-short axis views. The echo time and repetition time were adjusted to 1.47 ms and 2.9 ms, respectively, with an angle of 45°. Then, the data of the left ventricular short-axis view and four-chamber view of the patient were collected and processed to ensure three-dimensional imaging and the content of the left ventricular volume. Gadodiamide contrast agent (Hokuriku Pharmaceutical Co., Ltd.) was administered intravenously at a rate of 3.5 ml/s and a dose of 0.2 mmol/kg for delayed enhancement imaging. After 10 min of injection, enhanced images were obtained through rapid low-angle shot sequence scanning. Specific parameters were set as follows: T1 ranged between 255 and 355 ms, with an angle of 25°. Before contrast agent administration, holding one’s breath was required for T2 data collection, information, and spin echo images. Short-axis orientation was quantified, identifying high-signal edema areas within the myocardial infarction site, with low-signal core areas surrounded by high-signal as IMH.
Left ventricular function was assessed using cine sequences. Left ventricular volume was captured in the short-axis view using a steady-state free precession (bSSFP) sequence, covering the entire heart with a slice thickness of 7 mm to minimize differences between different image types. After cine sequence imaging, the contraction and relaxation of each chamber throughout the cardiac cycle were observed, and measurements were taken of left ventricular volume (including end-diastolic and end-systolic volumes) and left ventricular myocardial mass. Left ventricular ejection fraction (LVEF) and left ventricular myocardial mass (LVMM) were calculated to evaluate cardiac function. Left ventricular function was measured by semi-automatically marking the endocardial and epicardial borders in the short-axis view at end-diastole and end-systole. End-diastole and end-systole were defined as the maximum and minimum left ventricular cavities in the central short-axis view. Papillary muscles and epicardial fat were included as part of the ventricular cavity. According to the Simpson’s rule, the sum of the delineated slices provided left ventricular end-diastolic volume (LVEDV, ml) and left ventricular end-systolic volume (LVESV, ml). LVEF (%) = (LVEDV - LVESV) (ml) / LVEDV (ml).
Delayed enhancement imaging (late gadolinium enhancement, LGE) was performed to characterize tissue. During delayed enhancement imaging, normal myocardium does not enhance and appears hypointense because the contrast agent is cleared from the extracellular space. However, necrotic myocardium appears hyperintense due to disrupted cell membrane structure and prolonged contrast agent retention. Specifically, gadoteric acid was rapidly injected via a high-pressure injector into the antecubital vein at a dose of 0.2 ml/kg and a flow rate of 2 ml/s. Ten to fifteen minutes later, under electrocardiographic gating, images were acquired at end-expiration using an ECG-triggered inversion-recovery sequence. The flip time was adjusted to suppress normal myocardial signals to zero, providing clearer images of lesions. Two-chamber, four-chamber, and six to eight short-axis views of the left ventricle were acquired.
Infarct size (IS) was determined from delayed enhancement images. On LGE images, IS was defined as the high-signal (> 2 standard deviations) area in the left ventricular myocardium supplied by the infarct-related artery. Myocardial necrosis was qualitatively defined as subendocardial (enhanced segment range < 50% of total wall thickness) or transmural (enhanced segment range > 50%). Quantitatively, the Simpson’s rule was used: infarct mass (IM) (g) = ∑ (enhanced area) × myocardial layer thickness × myocardial density (1.05 g/ml). The percentage of infarct size (IS%) = infarct mass (g) / left ventricular mass (g) × 100%. Microvascular obstruction (MVO) was defined on LGE images as a low-signal area within a high-enhanced infarct zone. The extent of MVO was calculated using the Simpson’s method, with MVO defined as the percentage of low-enhanced mass relative to total left ventricular mass: MVO degree = (low-enhanced mass / left ventricular mass) × 100%.
T2-weighted imaging (T2WI) was performed using an ECG-triggered fast spin-echo sequence (turbo spin-echo, TSE). By leveraging differences in tissue water content, images were acquired at the same short-axis positions used for cine images and were primarily used to assess myocardial edema and intramyocardial hemorrhage.
Radiologists with 10 years of experience and graduate students conducted the analysis of the cardiac magnetic resonance imaging (CMR) images. Image measurements were conducted using customized software, MR WorkSpace 2.6.3.5. Furthermore, manual delineation of the left ventricular long-short axis view, and diastolic/systolic endocardium, and epicardium was required for CMR strain analysis. Peak cardiac strain at each stage was calculated and analyzed, including global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS). Strain parameters were measured using the long-short axis view of the heart.
The relevant myocardial staining and scoring methods for contrast agents are as follows: Grade 0: absence of myocardial imaging and absence of contrast density; Grade 1: Imaging reveals partial or a minor amount of myocardial imaging or contrast agent density; Grade 2: Imaging revealed moderate partial myocardial imaging or contrast density but significantly lower expression compared to myocardial imaging or contrast density on ipsilateral or contralateral non-infarct-related contrast, indicating myocardial partial perfusion; Grade 3: It manifests as normal myocardial imaging or contrast density, but with nearly identical expression compared to myocardial imaging or contrast density on ipsilateral or contralateral non-infarct-related contrast, indicating complete reperfusion of myocardial expression. Myocardial imaging refers to the signal intensity of myocardial tissue displayed on delayed enhancement scans, which reflects the viability of myocardial cells; Contrast density quantifies the degree of contrast agent deposition within the myocardium, directly related to low perfusion in areas of necrosis or fibrosis. Both are indirectly reflected by signal intensity in CMR and are considered equivalent indicators in this scoring system.
Observation indicators
Observe the detection of IMH and non-IMH infarction sites by CMR.
Compare the results between IMH and non-IMH myocardial conditions by CMR.
Compare the results between IMH and non-IMH cardiac indicators by CMR.
Compare the results between IMH and non-IMH cardiac indicators by echocardiography.
Compare the diagnostic performance of MRI in patients with AMI and intramyocardial hemorrhage by ROC curve. IMH detected by CMR was validated against a clinical composite reference standard (including peak troponin levels within 72 h post-PCI, dynamic ECG changes, and regional wall motion abnormalities on echocardiography). True positive (TP) was defined as CMR-positive IMH with clinical confirmation; false positive (FP) as CMR-positive without clinical evidence; true negative (TN) as CMR-negative without clinical IMH; false negative (FN) as CMR-negative with clinical IMH. Sensitivity and specificity were calculated as: Sensitivity = TP / (TP + FN) × 100%. Specificity = TN / (TN + FP) × 100%. ROC curves were generated using SPSS 26.0, with AUC quantifying diagnostic performance.
Statistical methods
In this research, all data were organized, and corresponding databases were established for analysis. All databases were entered into SPSS 26.0 for data processing, which included a normality test on the measurement data (expressed as mean ± standard deviation), a multi-group test conforming to normality (expressed as F), inter-group comparisons performed by t-tests, rates expressed as percentages (%), and we used the chi-squared test. ROC curves were used to compare the diagnostic performance of MRI in patients with AMI and intramyocardial hemorrhage. The difference between the datasets was statistically significant. (P < 0.05)
Results
Detection of IMH and non-IMH infarction sites using CMR
Infarction sites of the anterior wall, ventricular septum, and apex differed significantly between the two groups. The incidence of infarction sites was significantly higher in the IMH group compared to the non-IMH group (all P < 0.05). There were no statistically significant differences in the incidence of infarction at other sites between the two groups (all P > 0.05), as shown in Table 1.
Table 1.
Comparison of detection between IMH and non-IMH infarction sites using CMR
| Infarction site | Non-IMH group (n = 70) | IMH group (n = 46) | χ2 | P |
|---|---|---|---|---|
| Anterior wall | 15(21.43) | 24(52.17) | 11.758 | 0.001 |
| Anteroseptal wall | 0(0.00) | 1(2.17) | 1.535 | 0.215 |
| Inferior wall | 39(55.71) | 21(45.65) | 1.126 | 0.289 |
| Posterior wall | 6(8.57) | 1(2.17) | 2.004 | 0.157 |
| Lateral wall | 12(17.14) | 9(19.57) | 0.110 | 0.740 |
| Interventricular septum | 34(48.57) | 35(76.09) | 8.720 | 0.003 |
| Apex | 22(31.43) | 24(52.17) | 4.992 | 0.025 |
Comparison of results between IMH and non-IMH myocardial conditions using CMR
Myocardial conditions in both groups were detected, and the incidence of ventricular aneurysms and pericardial fluid was significantly higher in the IMH group compared to the non-IMH group (all P < 0.05). As shown in Table 2, there were no significant differences in other myocardial conditions between the two groups (all P > 0.05).
Table 2.
Comparison of the detection results between IMH and non-IMH myocardium using CMR
| Parameters | Non-IMH group (n = 70) | IMH group (n = 46) | χ2/t | P |
|---|---|---|---|---|
| Myocardial thickening n (%) | 6(8.57) | 3(6.52) | 0.163 | 0.686 |
| Cardiothoracic ratio (%) | 0.54 ± 0.03 | 0.54 ± 0.03 | 1.756 | 0.082 |
| Pericardial effusion n (%) | 6(8.57) | 14(30.43) | 9.299 | 0.002 |
| Ventricular aneurysm n (%) | 3(4.29) | 12(26.01) | 11.718 | 0.001 |
| Mitral regurgitation n (%) | 36(51.43) | 17(36.96) | 2.343 | 0.126 |
| Tricuspid regurgitation n (%) | 22(31.43) | 11(23.91) | 0.770 | 0.380 |
| Thrombus n (%) | 0(0.00) | 1(2.17) | 1.535 | 0.215 |
Comparison of results between IMH and non-IMH cardiac indicators using CMR
The results of CMR evaluation revealed that the percentage of IS/LV volume, the number of patients with MVO, and the percentage of MVO/LV volume in the IMH group were significantly higher than in the non-IMH group (all P < 0.05). Table 3 demonstrates that the GCS, GRS, and GLS values of patients in the IMH group were significantly lower than those in the non-IMH group, and the differences were statistically significant (all P < 0.05).
Table 3.
Comparison of cardiac indicators between IMH and non-IMH using CMR
| Parameters | Non-IMH group (n = 70) | IMH group (n = 46) | χ2/t | P |
|---|---|---|---|---|
| MVO n(%) | 35(50.00) | 34(73.91) | 6.586 | 0.010 |
| MVO/LV volume percentage (%) | 1.25 ± 0.15 | 3.35 ± 0.59 | -28.740 | < 0.001 |
| Post-procedure days of MRI (days) | 7.79 ± 1.56 | 4.33 ± 1.89 | 10.736 | < 0.001 |
| GRS(%) | 21.05 ± 3.18 | 17.09 ± 7.66 | 3.856 | < 0.001 |
| GCS(%) | -15.39 ± 1.18 | -10.35 ± 1.87 | -17.809 | < 0.001 |
| GLS(%) | -11.05 ± 1.52 | -7.51 ± 2.37 | -9.809 | < 0.001 |
Comparison of results between IMH and non-IMH cardiac indicators using echocardiography (ECHO)
Patients in both groups underwent echocardiography following PCI. The results revealed that compared with the non-IMH group, LVEF in the IMH group was significantly decreased, LVEDd and IS/LV volume percentages were significantly increased, and the differences were statistically significant (all P < 0.05). Consistent with prior studies, CMR and ECHO showed high agreement in assessing LVEF and LVEDd (Table 4). Importantly, the IMH group exhibited significantly impaired cardiac function across both modalities, further underscoring the clinical relevance of IMH detection.
Table 4.
Comparison of cardiac indicators between IMH and non-IMH using cardiac ultrasonic cardiography
| Parameters | Non-IMH group (n = 70) | IMH group (n = 46) | t | P |
|---|---|---|---|---|
| LVEF(%) | 58.59 ± 9.67 | 42.19 ± 7.64 | 9.682 | < 0.001 |
| Cardiac output (L/min) | 3.35 ± 0.58 | 3.49 ± 0.52 | -1.324 | 0.188 |
| Left ventricular wall thickness (cm) | 0.85 ± 0.09 | 0.82 ± 0.11 | 1.607 | 0.111 |
| LVEDV(mL) | 85.77 ± 18.26 | 99.23 ± 20.81 | -3.673 | < 0.001 |
| IS/LV volume percentage (%) | 16.82 ± 10.59 | 28.37 ± 10.42 | -5.813 | < 0.001 |
Diagnostic performance of magnetic resonance imaging in patients with acute myocardial infarction and intramyocardial hemorrhage
As shown in Table 5; Fig. 1, the area under the ROC curve of MRI for evaluating patients with AMI and intramyocardial hemorrhage was 0.869, 95% confidence interval (CI): [0.812, 0.963]; with high specificity and sensitivity, the sensitivity was 87.00 (95%CI: [0.833, 0.959]) and the specificity was 85.00 (95%CI: [0.805, 0.947]).
Table 5.
Diagnostic performance of MRI in patients with intramyocardial hemorrhage and acute myocardial infarction
| Indicators | Accuracy | Sensitivity (95% CI) | Specificity (95% CI) | AUC (95% CI) |
Jordan index |
|---|---|---|---|---|---|
| Combined detection | 92.50 | 87.00 (0.833 ~ 0.959) | 85.00 (0.805 ~ 0.947) | 0.869 (0.812 ~ 0.963) | 0.720 |
Fig. 1.
ROC curve of the diagnostic performance of MRI in patients with acute myocardial infarction and intramyocardial hemorrhage
Discussion
IMH and MVO symptoms are primarily present in patients with AMI undergoing reperfusion therapy as a consequence of ischemic microcirculation injury due to persistent coronary artery occlusion. However, the presence of IMH and MVO symptoms has a limited impact on vascular endothelial integrity, leading to erythrocyte extravasation in blood vessels and impeding the healing of myocardial hemorrhage. Recognized clinically, these two symptoms represent the dual effects of structure and function induced by myocardial ischemia-reperfusion injury [5]. In addition, IMH causes more severe injuries to patients than MVO. Therefore, myocardial ischemia-reperfusion injury poses a substantial hidden risk to the prognosis of patients with AMI undergoing direct PCI [6].
The IMH group had a significantly higher incidence of infarction sites than the non-IMH group (all P < 0.05); the incidence of ventricular aneurysm and pericardial fluid was also significantly higher in the IMH group than in the non-IMH group (all P < 0.05). Analyzing the primary cause, the range of myocardial necrosis extends from the subendocardium to the epicardium in a layer-by-layer progression resembling a wavefront during the onset of acute myocardial infarction. In the process of myocardial infarction, the most severe hemorrhage occurred in the center of the infarction core, whereas the hemorrhage in the periphery of infarction core was significantly alleviated [7]. Thus, there was an extremely significant difference in that no intramyocardial hemorrhage was observed in the marginal infarction area, where microvessels remained healthy, and red blood cell coagulation and numerous neutrophils were observed, indicating reperfusion therapy can reverse myocardial tissue injury in the marginal infarction area. However, coronary artery occlusion results in a certain degree of vascular endothelial hypoxia, resulting in functional microvessel injury, and in severe cases, vascular occlusion and necrosis may occur. The primary mechanism for inducing intramyocardial hemorrhage is the loss of vascular endothelial integrity due to microvascular injury [8, 9]. Clinical trials have demonstrated that myocardial ischemia typically causes swelling of myocardial and vascular endothelial cells without resulting in intramyocardial hemorrhage. However, when reperfusion therapy is administered, red blood cells from microvessels will overflow into the myocardium, impeding the healing of myocardial hemorrhage and eventually precipitating intramyocardial hemorrhage. Consequently, once intramyocardial hemorrhage is detected in a patient, it is indicative of concomitant severe microvascular injury. To ensure the prognosis for the patient, timely and corresponding treatment should be given in such circumstances [10, 11].
Reperfusion therapy is a highly effective treatment for patients with AMI. However, it comes with the inevitable risk of inducing functional injury due to the treatment method. If reperfusion injury causes myocardial hemorrhage and microvascular embolism, to a certain extent, this indicates the presence of tissue edema, a significant increase in white blood cells and platelets, incomplete and continuous inflammation of endothelial cells, and in severe cases, even metabolic disorder, all of which have a significant correlation with this treatment method [12, 13]. After CMR evaluation, the results of this study revealed that the IS/LV volume percentage, the number of patients with MVO, and the MVO/LV volume percentage average were significantly higher in the IMH group than in the non-IMH group (all P < 0.05). The IMH group had significantly lower GCS, GRS, and GLS than the non-IMH group (all P < 0.05). After PCI, echocardiography was conducted on both groups, and the results revealed that the IMH group had a significant decrease in LVEF compared to the non-IMH group, along with a significant increase in LVEDd and IS/LV volume percentages (all P < 0.05). The presence of the aforementioned symptoms indicated that cardiac magnetic resonance scanning could be used to detect microvascular embolism and intramyocardial hemorrhage. In addition, as numerous studies have shown, a reduction in LVEF and an increase in LVEDd are widely recognized as predictive factors for an increased risk of cardiac events and mortality. The presence of MVO is also considered an independent predictor of poor myocardial recovery and adverse prognosis [14–16]. Our findings were consistent with the aforementioned studies. CMRI and MRI, which include multiple sequences (T1, T2, and T2*), can display high-intensity signals for myocardial hemorrhage and hemorrhagic injury tissue, and the results are consistent with those of histopathological studies, thus rendering them suitable for the characteristic diagnosis of myocardial tissue [17]. The results of this study also indicated that the area under the ROC curve for MRI in the evaluation of patients with AMI and intramyocardial hemorrhage was 0.869, demonstrating high specificity and sensitivity. It also indicated that CMRI can be used extensively in clinical practice to detect myocardial function and whether microvascular injury occurs. In the diagnosis of intramyocardial hemorrhage, where acute myocardial cells and microvascular endothelial cells are in a swollen state, the T2 sequence can only clearly describe the high-signal core area [18]. During this time, combining gadolinium enhancement (LGE) with the T2 sequence enhances the sensitivity to detect MVO and IMH symptoms [19], further achieving high intensity, and the utilization of the T2* improves detection efficiency by using a high-pass filter (HPF) for processing. The low signal in the magnetic field can be filtered out, and the hemosiderin content in the blood can also be increased [20, 21]. At the current stage of clinical research, the high-pass filter can measure intramyocardial hemorrhage at the milliliter level, provide data support for evaluating the hemorrhage volume during reperfusion therapy, and analyze the efficacy of anticoagulant drugs and thrombolytic drugs [22, 23]. Although this research yielded certain results, there are still some limitations. In this study, we were unable to demonstrate the efficacy of MRI as we did not compare it to other diagnostic methods. In order to confirm the significance of MRI in the treatment of patients with AMI and intramyocardial hemorrhage, future studies should consider increasing the sample size to compare MRI and other examination methods. At the same time, as an observational study, this research had not yet established a clear link between the high incidence of IMH in specific anatomical locations and any clinical factors. It is possible that this association may be related to the microvascular density, hemodynamic characteristics or the susceptibility of the myocardial tissue in those regions. However, these hypotheses require further validation in future studies with larger sample sizes and more detailed clinical data.
In conjunction with our previous investigations on AMI after PCI, MRI can be used to detect myocardial hemorrhage, which provides significant clinical examination and diagnostic value and justifies its wider application in clinical practice.
Conclusion
While several studies have demonstrated the capability of CMR to detect IMH, our study adds significant novelty by comprehensively evaluating the diagnostic efficacy of CMR in detecting IMH in patients with AMI following PCI. We highlight that CMR serves as a robust tool with high sensitivity and specificity for identifying IMH, as evidenced by the ROC curve analysis yielding an AUC of 0.869. This study underscores the clinical potential of CMR to assess myocardial hemorrhage and its impact on cardiac function and adverse outcomes, offering valuable diagnostic insights that can guide clinical management and prognosis evaluation in AMI patients. Our findings reinforce the importance of incorporating CMR into clinical practice for the detection of IMH and evaluation of myocardial injury following PCI,.
Acknowledgements
We would like to acknowledge the hard and dedicated work of all the staff that implemented the intervention and evaluation components of the study.
Author contributions
Xiao-Long Mi and Dong Sun conceived the idea and conceptualised the study. Yan-Hui Zhang, Peng-Fei Ding and Zheng Xu collected the data. Xiao-Long Mi, Dong Sun, Li-Li Zhang, Yan-Hui Zhang, Peng-Fei Ding and Zheng Xu analysed the data. Xiao-Long Mi and Li-Li Zhang drafted the manuscript, then Xiao-Long Mi and Dong Sun reviewed the manuscript. All authors read and approved the final draft.
Funding
2023 New Coronavirus Infection emergency research project(No.2023xg09-1), Health Commission of Shanxi Province Scientific research subject (2024009), ShanxiTraditional Chinese Medicine Administration Scientifc Research Project(2024ZYY2C036).
Data availability
The data used to support the findings of this study are available from the corresponding author upon request.
Declarations
Ethics approval and consent to participate
I confirm that I have read the Editorial Policy pages. This study was conducted with approval from the Ethics Committee of Shanxi Bethune Hospital. This study was conducted in accordance with the declaration of Helsinki. Written informed consent was obtained from all participants.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Xiao-Long Mi and Li-Li Zhang contributed equally to this study.
References
- 1.Lloyd SG, Farris GR. MRI apparent diffusion coefficient in reperfused acute myocardial infarction: new use of an old technique. Radiology. 2020;295(3):550–1. 10.1148/radiol.2020200495. Epub 2020 Mar 24. PMID: 32208963. [DOI] [PubMed] [Google Scholar]
- 2.Moulin K, Viallon M, Romero W, Chazot A, Mewton N, Isaaz K, Croisille P. MRI of reperfused acute myocardial infarction edema: ADC quantification versus T1 and T2 mapping. Radiology. 2020;295(3):542–9. 10.1148/radiol.2020192186. Epub 2020 Mar 24. PMID: 32208095. [DOI] [PubMed] [Google Scholar]
- 3.Kassab K, Matar R, Alyousef T, Malhotra S. Acute myocardial infarction in a young woman: role of cardiac magnetic resonance imaging in Establishing the diagnosis. Cureus. 2020;12(4):e7526. 10.7759/cureus.7526. PMID: 32377474; PMCID: PMC7198087. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Arai H, Kawakubo M, Abe K, Hatashima H, Sanui K, Nishimura H, Kadokami T. Quantification of intramyocardial hemorrhage volume using magnetic resonance imaging with three-dimensional T1-weighted sequence in patients with ischemia-reperfusion injury: a semi-automated image processing technique. Int J Cardiovasc Imaging. 2020;36(1):111–9. 10.1007/s10554-019-01697-4. Epub 2019 Sep 14. PMID: 31522312. [DOI] [PubMed] [Google Scholar]
- 5.Goldfarb JW, Craft J, Cao JJ. Water-fat separation and parameter mapping in cardiac MRI via deep learning with a convolutional neural network. J Magn Reson Imaging. 2019;50(2):655–65. 10.1002/jmri.26658. Epub 2019 Jan 30. PMID: 30701621. [DOI] [PubMed] [Google Scholar]
- 6.Dong LI, Ren W, Radiology D. O.Application of cardiac magnetic resonance imaging in acute ST-segment elevation myocardial infarction:recent advances. Acad J Second Military Med Univ 2019,4(21):525–9.
- 7.Igual Munoz B, Elena Sanchez ESLC, Lacuesta JLDG, Jose Luis Diez Gil MFV, Maria Ferre Valverdu FTM, Francisco Ten Morro VMP, Vicente Miro Palau ME, Maryem Ezzitouny, JLPB Jose Leandro Perez Bosca., R P S Rafael Paya Serrano.P824 Impact of cardiovascular risk factors and treatment strategies on the presence of intramyocardial hemorrhage visualized by magnetic resonance in patients with reperfused infarction. European Heart Journal-Cardiovascular Imaging. 2020;21(Supplement 1):jez319.475.
- 8.Debeaumarche H, Alaa El Din A, Thouant P, Maza M, Ricolfi F, Zeller M, Bichat F, Baudoin N, Béjot Y. Cottin. Progression in cerebral microbleeds number after acute myocardial infarction:harmful role of triple antithrombotic therapy[J]. Archives Cardiovasc Dis Supplements. 2020;12(1):5–6. [Google Scholar]
- 9.Yew SN, Carrick D, Corcoran D, Ahmed N, Carberry J, Teng Yue May V, McEntegart M, Petrie MC, Eteiba H, Lindsay M, Hood S, Watkins S, Davie A, Mahrous A, Mordi I, Ford I, Oldroyd KG, Berry C. Coronary thermodilution waveforms after acute reperfused ST-Segment-Elevation myocardial infarction: relation to microvascular obstruction and prognosis. J Am Heart Assoc. 2018;7(15):e008957. 10.1161/JAHA.118.008957. PMID: 30371237; PMCID: PMC6201480. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Chang SM, Palanisamy S, Wu TH, Chen CY, Cheng KH, Lee CY, Yuan SF, Wang YM. Utilization of silicon nanowire field-effect transistors for the detection of a cardiac biomarker, cardiac troponin I and their applications involving animal models. Sci Rep. 2020;10(1):22027. 10.1038/s41598-020-78829-7. PMID: 33328513; PMCID: PMC7745037. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Karthikeyan B, Sonkawade SD, Pokharel S, Preda M, Schweser F, Zivadinov R, Kim M, Sharma UC. Tagged cine magnetic resonance imaging to quantify regional mechanical changes after acute myocardial infarction. Magn Reson Imaging. 2020;66:208–18. 10.1016/j.mri.2019.09.010. Epub 2019 Oct 24. PMID: 31668928; PMCID: PMC7031039. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Beijnink CWH, van der Hoeven NW, Konijnenberg LSF, Kim RJ, Bekkers SCAM, Kloner RA, Everaars H, El Messaoudi S, van Rossum AC, van Royen N, Nijveldt R. Cardiac MRI to visualize myocardial damage after ST-Segment elevation myocardial infarction: A review of its histologic validation. Radiology. 2021;301(1):4–18. 10.1148/radiol.2021204265. Epub 2021 Aug 24. PMID: 34427461. [DOI] [PubMed] [Google Scholar]
- 13.Heidenreich JF, Gassenmaier T, Ankenbrand MJ, Bley TA, Wech T. Self-configuring nnU-net pipeline enables fully automatic infarct segmentation in late enhancement MRI after myocardial infarction. Eur J Radiol. 2021;141:109817. 10.1016/j.ejrad.2021.109817. Epub 2021 Jun 9. PMID: 34144308. [DOI] [PubMed] [Google Scholar]
- 14.Netti L, Ioannou A, Martinez-Naharro A, Razvi Y, Porcari A, Venneri L, Maestrini V, Knight D, Virsinskaite R, Rauf MU, Kotecha T, Patel RK, Wechelakar A, Lachmann H, Kellman P, Manisty C, Moon J, Hawkins PN, Gillmore JD, Fontana M. Microvascular obstruction in cardiac amyloidosis. Eur J Heart Fail. 2024 Oct 18. 10.1002/ejhf.3481. Epub ahead of print. PMID: 39422337. [DOI] [PubMed]
- 15.Guo Z, Liu X, Cheng X, Liu C, Li P, He Y, Rao R, Li C, Chen Y, Zhang Y, Luo X, Wang J. Combination of left ventricular End-Diastolic diameter and QRS duration strongly predicts good response to and prognosis of cardiac resynchronization therapy. Cardiol Res Pract. 2020;2020:1257578. 10.1155/2020/1257578. PMID: 32411441; PMCID: PMC7201746. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Sato R, Sanfilippo F, Hasegawa D, Prasitlumkum N, Duggal A, Dugar S. Prevalence and prognosis of hyperdynamic left ventricular systolic function in septic patients: a systematic review and meta-analysis. Ann Intensive Care. 2024;14(1):22. 10.1186/s13613-024-01255-9. PMID: 38308701; PMCID: PMC10838258. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Capaccione KM, Leb JS, D’souza B, Utukuri P, Salvatore MM. Acute myocardial infarction secondary to COVID-19 infection: A case report and review of the literature. Clin Imaging. 2021;72:178–82. 10.1016/j.clinimag.2020.11.030. Epub 2020 Nov 14. PMID: 33296828; PMCID: PMC7666611. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Song PS, Lee SH, Jeon KH, Hahn JY, Hur SH, Rha SW, Yoon CH, Jeong MH, Jeong JO, Seong IW, Song YB, Gwon HC. KAMIR-NIH investigators. blood pressure at 6 months after acute myocardial infarction and outcomes at 2 years: the perils associated with excessively low blood pressures. Can J Cardiol. 2020;36(10):1641–8. Epub 2020 Feb 8. PMID: 32413339. [DOI] [PubMed] [Google Scholar]
- 19.Wu YL, Cardiac MRI, Assessment of Mouse Myocardial Infarction and Regeneration. Methods Mol Biol. 2021;2158:81–106. 10.1007/978-1-0716-0668-1_8. PMID: 32857368. [DOI] [PubMed]
- 20.Ma JC. Framework for automatic evaluation of myocardial infarction from Delayed-Enhancement cardiac MRI. 2020,19(22):315–9.
- 21.Zhang YC. Convolutional neural network for automatic myocardial infarction segmentation from Delayed-Enhancement cardiac MRI.2020,36(1):262–8.
- 22.Liang K, Williams M, Bucciarelli-Ducci C. Cardiac magnetic resonance imaging unmasks presumed embolic myocardial infarction due to patent foramen ovale case report. Eur Heart J Case Rep. 2022;6(2):ytac029. 10.1093/ehjcr/ytac029. PMID: 35146325; PMCID: PMC8824762. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Grewal D, Mohammad A, Swamy P, Abudayyeh I, Mamas MA, Parwani P. Diffuse coronary artery vasospasm in a patient with subarachnoid hemorrhage: A case report. World J Cardiol. 2020;12(9):468–74. 10.4330/wjc.v12.i9.468. PMID: 33014294; PMCID: PMC7509992. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data used to support the findings of this study are available from the corresponding author upon request.