Clinical and cardiac magnetic resonance imaging features for differentiation between acute myocardial infarction with and without obstructive coronary arteries
Original Article

Clinical and cardiac magnetic resonance imaging features for differentiation between acute myocardial infarction with and without obstructive coronary arteries

Li-Ting Shen1, Zhi-Gang Yang1, Ying-Kun Guo2, Wen-Lei Qian1, Wei-Feng Yan1, Yi-Ning Jiang1, Ke Shi1, Yuan Li1

1Department of Radiology, West China Hospital, Sichuan University, Chengdu, China; 2Department of Radiology, West China Second Hospital, Sichuan University, Chengdu, China

Contributions: (I) Conception and design: LT Shen, ZG Yang, K Shi; (II) Administrative support: YK Guo, ZG Yang; (III) Provision of study materials or patients: LT Shen, WL Qian, WF Yan; (IV) Collection and assembly of data: LT Shen, YN Jiang; (V) Data analysis and interpretation: LT Shen, Y Li; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Ke Shi, MD; Yuan Li, MD. Department of Radiology, West China Hospital, Sichuan University, No. 37 Guoxue Lane, Chengdu 610041, China. Email: kshi0110@qq.com; dr.liyuan@163.com.

Background: Misdiagnosis often occurs in patients with myocardial infarction (MI) with nonobstructive coronary arteries (MINOCA) and MI with obstructive coronary arteries (MIOCA). This study explored the clinical and imaging characteristics of patients with MINOCA and MIOCA.

Methods: Patients with acute MI (AMI) who underwent cardiac magnetic resonance (CMR) imaging and coronary angiography (CAG) were evaluated. According to coronary stenosis degree (>50%), patients with AMI (n=147) were divided into the MINOCA and MIOCA groups. The cardiac function and CMR characteristics of the two subgroups were emphasized in analysis.

Results: The MINOCA group had a lower proportion of patients with hypertension (29.4% vs. 55.2%), hyperlipoproteinemia (9.8% vs. 16.7%), diabetes (19.6% vs. 37.5%), wall motion abnormalities (39.3% vs. 75%), complex (both epicardial and subendocardial infarction) infarct type (19.6% vs. 29.2%), and multiple infarct territories (58.8% vs. 77.1%) than did the MIOCA group. Compared with the MIOCA group, the MINOCA group had a smaller left ventricular (LV) infarct size and a lower infarct size rate. The MINOCA group had a higher LV ejection fraction (LVEF) and global peak strain (GPS) in the three directions compared with the MIOCA group. The GPS in three directions were inversely associated with increased N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, a greater LV infarct extent, and decreased LVEF in patients with AMI. NT-proBNP level was shown to be an independent determinant of the global longitudinal peak strain (GLPS) in patients with MINOCA and GPS in three directions in patients with MIOCA. Infarct size was an independent determinant of GPS in three directions in the MINOCA and MIOCA groups.

Conclusions: MINOCA had a specific etiology, and patients with MINOCA had better myocardial function than those with MIOCA. Strain, infarct size on CMR imaging, and NT-proBNP level are reliable for monitoring cardiac dysfunction in patients with MINOCA. GLPS and global circumferential peak strain are useful early biomarkers of subclinical impairment in MINOCA.

Keywords: Acute myocardial infarction (AMI); myocardial infarction with nonobstructive coronary arteries (MINOCA); magnetic resonance imaging (MRI); late enhancement; feature tracking


Submitted Jun 18, 2025. Accepted for publication Oct 24, 2025. Published online Dec 31, 2025.

doi: 10.21037/qims-2025-1331


Introduction

Acute myocardial infarction (AMI) contributes significantly to mortality and morbidity worldwide. However, patient prognosis has improved over decades (1,2). Myocardial infarction (MI) with nonobstructive coronary arteries (MINOCA) is associated with an increased risk for major adverse cardiovascular events (3). With an increasing aging population and the widespread use of coronary angiography (CAG), clinical studies have reported a prevalence of MINOCA of 5–6% of AMI cases, with a range between 5% and 15% depending on the population examined (4). Previous research has reported the cardiac structure and function injury of patients with MI with obstructive coronary arteries (MIOCA) and MINOCA, respectively (5-7). However, the clinical and imaging characteristics of MIOCA and MINOCA are still controversial due to a lack of systematic and comprehensive research.

Cardiac magnetic resonance (CMR) imaging is a useful tool to provide insights into potential causes in patients with MINOCA and provide confirmation of the diagnosis of AMI (8,9). Quantification of AMI size by contrast-enhanced CMR has been validated to predict cardiovascular events, and is considered the “gold standard” for infarct assessment (10-12). CMR-feature tracking has emerged as a new technique that can measure intramyocardial motion in three dimensions (longitudinal, radial, circumferential), with very low inter- and intra-observer variability (13,14). Misdiagnosis in patients with MINOCA due to occult imaging characteristics can lead to disease deterioration (15). Therefore, the present study aimed to explore the clinical and imaging characteristics of patients with MINOCA and MIOCA using CMR to provide valuable identification information for clinical decision-making and treatment of diseases. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1331/rc).


Methods

Study population

This study retrospectively enrolled 147 patients diagnosed with AMI who underwent CMR and CAG examinations at West China Hospital. The inclusion criteria were as follows: (I) patients aged ≥18 years; (II) those fulfilling the AMI criteria according to the 4th Universal Definition of Infarction (16); and (III) and those who underwent CAG during admission and CMR within 1 week. The exclusion criteria were as follows: (I) patients having a previous history of MI; (II) those who received percutaneous coronary intervention or underwent coronary artery bypass grafting; (III) those who had a previous history of heart diseases and congestive heart failure; (IV) those who had a glomerular filtration rate below 30 mL/min/1.73 m2; and (V) those who had a poor CMR image quality. Further, according to the diagnostic criteria of MINOCA published by the European Society of Cardiology (AMI without angiographically obstructive coronary artery disease or a stenosis rate of ≤50%) (8), the patients were divided into a MINOCA group (n=51) and a MIOCA group (n=96). Finally, 59 healthy controls (51 men, mean age: 59.18±9.74 years) were included in this study. Figure 1 shows a detailed flowchart illustrating the above process.

Figure 1 Flowchart of this study. AMI, acute myocardial infarction; CABG, coronary artery bypass grafting; CAG, coronary angiography; CMR, cardiac magnetic resonance; MI, myocardial infarction; MINOCA, myocardial infarction with nonobstructive coronary arteries; MIOCA, myocardial infarction with obstructive coronary arteries; PCI, percutaneous coronary intervention.

Definition of clinical disease indicators

Hypertension was defined as office systolic blood pressure values ≥140 mmHg and/or diastolic blood pressure values ≥90 mmHg without antihypertensive medication or current antihypertensive treatment. Diabetes mellitus was interpreted as a clear history of diabetes or diabetes treatment. A hyperlipoproteinemia diagnosis was made with reference to the corresponding Chinese guidelines on the prevention and treatment of dyslipidemia in adults (2016 revised edition) (15).

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Biomedical Research Ethics Committee of the West China Hospital, Sichuan University (No. 2019-756) and the requirement for individual consent for this retrospective analysis was waived.

CMR scanning protocol

All participants underwent CMR examination using a 3.0-T whole-body scanner (MAGNETOM Skyra/Tim Trio; Siemens Healthcare, Erlangen, Germany) in the supine position. Standard electrocardiogram (ECG)-triggering equipment was used, and the patients performed end-inspiratory breath-holding. An axial stack of steady-state free precession (SSFP) imaging, which is included in the routine cardiac magnetic resonance imaging (MRI) protocol, was debugged with the following parameters: temporal resolution =224.16 ms, echo time (TE) =1.23 ms, slice thickness =6.0 mm, flip angle (FA) =60°, acquisition matrix =126×256 pixels, and field of view (FOV) =340×255 mm2. For cine imaging, a balanced SSFP sequence was performed with the following parameters: repetition time (TR) =3.4 or 2.8 ms, TE =1.22 ms, slice thickness =8.0 mm, FA =40°/50°, matrix size =166×256 or 139×208, and FOV =284×340 mm2 or 303×360 mm2. Subsequently, gadobenate dimeglumine (MultiHance 0.5 mmol/mL; Bracco, Milan, Italy) at a dose of 0.2 mL/kg body weight was administered intravenously at a flow rate of 2.5–3.0 mL/s. Then, 20 mL of saline flush was injected immediately at a rate of 3.0 mL/s. The remaining first-pass perfusion images in three standard short-axis slices (basal, midventricular, and apical) and in one slice of the four-chamber view were acquired using an inversion recovery prepared echo-planar imaging sequence (TR =149.8 or 163.2 ms, TE =0.99 or 1.06 ms, slice thickness =8 mm, FA =10°, matrix size =144×192 or 132×176, and FOV =270×360 or 240×320 mm2). Finally, late gadolinium enhancement (LGE) images were acquired in the corresponding slice position as in cine imaging 10–15 minutes after contrast agent injection. The images were determined via a phase-sensitive inversion recovery sequence (TR =700/500 ms, TE =1.18/1.07 ms, slice thickness =8.0 mm, FA =40°, matrix size =184×256, and FOV =350×295 mm2).

CMR image analysis

All CMR images were evaluated by two radiologists with >5 years of experience who were blinded to the clinical data. Left ventricular (LV) wall motion and hypertrophy were measured according to the American Heart Association classification (17). The presence of microvascular obstruction was visually confirmed on first-pass perfusion images. The LGE images were visually reviewed for the presence, anatomical distribution, and extent of subendocardial or/and transmural contrast enhancement.

All CMR images were transferred to the offline system using the commercial software (cvi42, Circle Cardiovascular Imaging Inc., Calgary, Alberta, Canada). Endocardial and epicardial traces of the LV myocardium were manually delineated in the serial short-axis slices during the end-diastolic and end-systolic phases on the short-3D module. The papillary muscles and epicardial fat were excluded from the LV mass (LVM). Subsequently, cardiac function and geometry parameters including LVM at end diastole, LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), LV stroke volume (LVSV), and LV ejection fraction (LVEF) were automatically calculated. According to the Mosteller formula, the LVM, LVEDV, LVESV, and LVSV indexed for body surface area were computed and expressed as MI, end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and stroke volume index (SVI). The LV remodeling index was defined as the LVM-to-LV end-diastolic volume (EDV) ratio.

For myocardial strain analysis of the LV, long-axis two-chamber, four-chamber, and short-axis slices were simultaneously imported into the tissue tracking module. The LV global peak strain (PS) parameters [including global radial peak strain (GRPS), global circumferential peak strain (GCPS), and global longitudinal peak strain (GLPS)]; peak systolic strain rate (PSSR) in the radial (PSSR-R), circumferential (PSSR-C), and longitudinal (PSSR-L) directions; and peak diastolic strain rate (PDSR) in the radial (PDSR-R), circumferential (PDSR-C), and longitudinal (PDSR-L) directions were acquired automatically (Figure 2). For LGE imaging analysis, LV segment-based analysis was implemented using the 16-segment model of the American Heart Association. The hyper-enhanced myocardial area was defined as the infarct area on the LGE short-axis images when the signal intensity was five standard deviations above the mean intensity of the normal myocardium (Figure 2D,2H) (16). Two radiologists, each of whom had >5 years of CMR experience, evaluated the images separately. If the results were inconsistent, a discussion was made to achieve a consensus agreement.

Figure 2 Measurement of LV global strain and enhanced area in LGE. Cardiac magnetic resonance tissue tracking in long-axis two-chamber and four-chamber cine images at end-diastole (A,B) and three-dimensional diagram (C). (E-G) LV global PS curve in radial, circumferential and longitudinal direction. (D,H) LGE images for quantification of infarct size; the signal intensity of yellow region was five standard deviations above the mean intensity of the normal myocardium (blue circle). GCPS, global circumferential peak strain; GLPS, global longitudinal peak strain; GRPS, global radial peak strain; LGE, late gadolinium enhancement; LV, left ventricle; PS, peak strain; RAL, directional indication, right, anterior, left.

Variability analysis

For intraobserver variability, the LV deformation and LGE parameters in 50 random cases including 40 patients with AMI and 10 normal controls were measured twice within 1 month by the same radiologist. The interobserver variability of the same participants was obtained and compared with the independent measurements of another observer who was blinded to the findings of the first radiologist.

Statistical analysis

The Shapiro-Wilk test was used to complete normality test of the data and the Levene’s test for the homogeneity test of continuous variables. Continuous data with a normal distribution were expressed as mean ± standard deviation. Variables with a non-normal distribution were expressed as median (interquartile range, IQR). Categorical variables were expressed as frequencies. One-way analysis of variance (ANOVA) was used to evaluate differences among the MINOCA, MIOCA, and control groups. Similar methods were applied to compare the parameters among all the AMI patients in the different LVEF groups and the control group. Univariate linear regression analyses were performed to explore the correlations of global strains of the LV with multiple clinical risk factors and other CMR parameters. To identify the determinants of impaired LV strains, variables with an absence of collinearity and with P values of <0.1 in the univariate analyses were included in the stepwise multivariate linear regression models. A P value of <0.05 was considered statistically significant. Inter- and intraobserver agreements were assessed using the intraclass correlation coefficient. A two-tailed P value of <0.05 was considered statistically significant. Statistical analyses were performed with the software SPSS 21.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism version 7.0a (GraphPad Software, San Diego, CA, USA).


Results

Characteristics of all participants

Table 1 shows the baseline characteristics of the research cohort. Of the 147 patients with AMI, 51 were included in the MINOCA group [48 (81.4%) men, mean age: 58.86±14.01 years] and 96 in the MIOCA group [81 (84.4%) men, mean age: 60.71±12.34 years]. Compared with the controls and patients with MINOCA, patients with MIOCA were older. Regarding cardiovascular risk factors, the MINOCA group had a lower proportion of patients with hypertension, hyperlipoproteinemia, and diabetes (29.4% vs. 55.2%, 9.8% vs. 16.7%, 19.6% vs. 37.5%) than the MIOCA group. Compared with controls and patients with MINOCA, patients with MIOCA had lower levels of high-density lipoprotein (HDL), and had higher levels of fasting blood glucose, glycated hemoglobin (HbA1c), troponin T, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) (all P<0.05). In patients with MINOCA, the median (IQR) Gensini score was 3 (0–10), and the numbers (%) of patients with one-, two-, and three or more-vessel disease were 15 (29.41%), 7 (13.73%), and 7 (13.73%), respectively. In the MIOCA group, 53 patients received the percutaneous coronary intervention after admission, and the median (IQR) Gensini score was 93 (48.8–145.8), and the numbers (%) of patients with one-, two-, and three or more-vessel disease were 11 (11.46%), 16 (16.67%), and 69 (71.87%), severally. The thrombolysis in myocardial infarction (TIMI) flow grade before percutaneous coronary intervention in patients with MINOCA was significantly better than that of patients with MIOCA (all P<0.001).

Table 1

Baseline characteristics of the study population

Characteristics Normal (n=59) MINOCA (n=51) MIOCA (n=96) P value
Age, years 59.18±9.74 58.86±14.01 60.71±12.34*§ 0.002
Gender, male 51 (86.4) 48 (81.4) 81 (84.4) 0.345
Cardiovascular risk factors
   BMI, kg/m2 23.53±3.48 24.93±4.05 27.75±18.89 0.228
   BSA, m2 1.66±0.18 1.72±0.25 1.83±0.81 0.183
   SBP, mmHg 122.68±14.11 125.08±18.2 125.35±21.44 0.671
   DBP, mmHg 81.22±10.01 81.24±15.52 78.92±15.68 0.511
   HR, bpm 74.42±8.92 72.73±17 74.66±13.62 0.455
   Hypertension 15 (29.4) 53 (55.21)§ 0.003
   Hyperlipoproteinemia 5 (9.8) 16 (16.67)§ 0.028
   Diabetes 10 (19.6) 36 (37.5)§ 0.026
   Previous/current smoking 18 (35.29) 38 (39.58) 0.61
Laboratory values
   FPG, mmol/L 5.44±1.52 7.26±3.68 7.43±3.3*§ <0.001
   HbA1c, % 5.58±0.48 6.46±1.09* 7.07±2*§ 0.005
   TG, mmol/L 1.6±0.93 1.49±0.85* 1.89±1.08* 0.039
   TC, mmol/L 4.41±1.03 3.99±0.97 3.66±1.65 0.103
   HDL, mmol/L 1.15±0.28 1.18±0.26 1.02±0.27*§ <0.001
   LDL, mmol/L 2.44±0.85 2.25±0.77 2.03±1.53 0.122
   eGFR, mL/min/1.73 m2 91.26±20.96 80.2±22.54 79.66±21.52 0.893
   Troponin T, ng/L 21.7 (12.8, 373) 26.7 (11.38, 155.78)§ 0.039
   NT-proBNP, pg/mL 536 (124, 1,867) 689 (268, 2,083)§ 0.006
Diseased vessels
   1/2/≥3 15/7/7 11/16/69
TIMI flow grade before PCI
   3 49 18§ <0.001
   ≤2 2 78§ <0.001
Gensini score 3 (0,10) 93 (48.8, 145.8)§ <0.001
Stent implanted after admission 0 53
Medication
   Aspirin 43 (84.31) 84 (87.5) 0.112
   Clopidogrel/prasugrel/ticagrelor 36 (70.59) 86 (89.58)* 0.039
   Statin 48 (94.12) 87 (90.63) 0.798
   Betablocker 33 (64.71) 72 (75) 0.123
   ACE-inhibitor/AT-1 antagonist 29 (58.86) 45 (46.88) 0.095
   Calcium-channel blocker 24 (47.06) 31 (32.29)* 0.012
   Diuretics 11 (21.57) 38 (39.58) 0.341
   Others 8 (15.69) 21 (21.88) 0.098

Data are presented as mean ± standard deviation, n, n (%) or median (interquartile range). *, P<0.05 vs. controls; §, P<0.05 vs. MINOCA group. ACE, angiotensin-converting enzyme; AT-1, angiotensin type-1 receptor; BMI, body mass index; BSA, body surface area; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; FPG, fasting plasma glucose; HbA1c, glycated hemoglobin; HDL, high-density lipoprotein; HR, heart rate; LDL, low-density lipoprotein; MINOCA, myocardial infarction with nonobstructive coronary arteries; MIOCA, myocardial infarction with obstructive coronary arteries; NT-proBNP, N-terminal pro-brain natriuretic peptide; PCI, percutaneous coronary intervention; SBP, systolic blood pressure; TC, total cholesterol; TG, triglycerides.

Findings on CMR conventional sequences in patients with MINOCA and MIOCA

Regarding the cine, first-pass perfusion, and LGE sequence, patients with MINOCA had lower incidence rates of wall motion abnormalities, complex (both epicardial and subendocardial infarction) infarct type, and multiple infarct territories (39.3% vs. 75%, 29.2% vs. 19.6%, and 58.8% vs. 77.1%, respectively) than did patients with MIOCA. There was no difference in the single presence of LGE or single infarct territory in the two AMI subgroups. The microvascular obstruction rate-derived first-pass perfusion imaging was similar between the two subgroups of patients with AMI (P=0.851). Compared with the MIOCA group, the MINOCA group had a lower infarct size and LV infarct size (all P<0.001) (Table 2).

Table 2

Findings on cardiac MR

Findings MINOCA (n=51) MIOCA (n=96) P value
Cine mode
   Septal or apical segment hypertrophy 11 (21.6) 30 (31.3) 0.213
   Wall motion abnormalities 24 (39.3) 72 (75.0)* <0.001
First-pass perfusion imaging
   Microvascular obstruction 30 (50.8) 58 (60.4) 0.851
Presence of LGE
   Subendocardial 34 (55.7) 59 (61.5) 0.477
   Transmural 7 (13.7) 9 (9.4) 0.420
   Both 10 (19.6) 28 (29.2)* 0.028
Infarct territory
   Interventricular septum 7 (13.7) 5 (5.2) 0.073
   Inferior 4 (7.8) 8 (8.3) 0.918
   Lateral 2 (3.9) 2 (2.1) 0.514
   Anterior 5 (9.8) 7 (7.3) 0.596
   ≥2 affected territory 30 (58.8) 74 (77.1)* 0.021
Infarct size, g 15.51±13.34 31.3±20.54* <0.001
Infarct size of LV, % 15.54±12.04 27.98±15.05* <0.001

Data are presented as mean ± standard deviation or n (%). *, P<0.05 vs. MINOCA group. LGE, late gadolinium enhancement; LV, left ventricle; MINOCA, myocardial infarction with nonobstructive coronary arteries; MIOCA, myocardial infarction with obstructive coronary arteries; MR, magnetic resonance.

Comparison of LV function and deformation among the three groups

Table 3 depicts the CMR imaging results for LV function and deformation. The MINOCA group had a higher LVEDVI, LVESVI, and myocardial mass index (MMI) and a lower LVSVI, LVEF, and remodeling index than the control group (all P<0.001). The MIOCA group had a higher LVESVI and a lower LVSVI and LVEF than the MINOCA and control groups (all P<0.001). There was no difference in terms of the LVEDVI, MMI, and remodeling index between the MIOCA and MINOCA groups.

Table 3

Comparison of LV volumetric and strain parameters among groups

Parameters Normal (n=59) MINOCA (n=51) MIOCA (n=96) P value
LV volumetric parameters
   EDVI, mL/m2 78.69±17.44 112.6±40.09* 117.13±46.98* <0.001
   ESVI, mL/m2 29.8±8.55 63.87±38.54* 72.21±47.82*§ <0.001
   SVI, mL/m2 49±11.87 48.72±21.43 38.72±13.42*§ <0.001
   EF, % 61.6±6.5 58±12.1* 44.7±16.6*§ <0.001
   MMI, g/m2 41.06±10 62.53±20.67* 62.21±23* <0.001
   Remodeling index, g/mL 0.61±0.12 0.59±0.22* 0.58±0.17* 0.043
LV strain parameters
   GRPS, % 35.63±9.84 22.62±11.29* 16.48±9.22*§ <0.001
   GCPS, % −19.87±2.78 −14.32±5.7* −10.95±5.13*§ <0.001
   GLPS, % −13.83±3.31 −9.03±4.42* −7.25±5*§ <0.001
   PSSR-R, 1/s 2.14±0.72 1.4±0.62 1.16±0.93*§ <0.001
   PSSR-C, 1/s −1.03±0.39 −0.81±0.31* −0.61±0.27*§ <0.001
   PSSR-L, 1/s −0.76±0.48 −0.58 (−0.77, −0.38)* −0.47 (−0.66, −0.29)*§ 0.002
   PDSR-R, 1/s −2.64±0.94 −1.36±0.78 −1.11±0.87*§ <0.001
   PDSR-C, 1/s 1.24±0.28 0.81±0.33* 0.65±0.29*§ <0.001
   PDSR-L, 1/s 0.89±0.28 0.61±0.27* 0.53±0.31*§ <0.001

Data are presented as mean ± standard deviation or median (interquartile range). *, P<0.05 vs. controls; §, P<0.05 vs. MINOCA group. C, circumferential; EDVI, end-diastolic volume index; EF, ejection fraction; ESVI, end-systolic volume index; GCPS, global circumferential peak strain; GLPS, global longitudinal peak strain; GRPS, global radial peak strain; L, longitudinal; LV, left ventricular; MINOCA, myocardial infarction with nonobstructive coronary arteries; MIOCA, myocardial infarction with obstructive coronary arteries; MMI, myocardial mass index; PDSR, peak diastolic strain rate; PSSR, peak systolic strain rate; R, radial; SVI, stroke volume index.

Regarding LV deformation, the MIOCA group had a lower global radial, circumferential, and longitudinal PS, PSSR, and PDSR (all P<0.005) than the MINOCA and control groups. The MINOCA group had a lower global radial PS, circumferential PS, PSSR, and PDSR, and longitudinal PS, PSSR, and PDSR (all P<0.001) than the control group. There was no statistically significant difference in terms of the PSSR and PDSR in both radial directions between the MINOCA and control groups.

Comparison of LV global strains among patients with AMI who presented with different LVEF and controls

According to LVEF, patients with MI were divided into two subgroups: patients with LVEF of ≥40% (n=72) and those with LVEF of <40% (n=75). Figure 3 shows the CMR-derived global PS parameters about the left ventricle of the observed groups. All of the global strains of the LV declined progressively from the control group, through the MI (LVEF ≥40%) group, to the MI (LVEF <40%) group (all P<0.017). Meanwhile, the PSSR-L did not significantly differ between the LVEF ≥40% and control groups (P>0.017).

Figure 3 Comparison of LV global strains among all MI patients with LVEF ≥40% and LVEF <40% and normal controls. *, P<0.017 vs. control group; #, P<0.017 vs. MI (LVEF ≥40%) group. C, circumferential; GPS, global peak strain; L, longitudinal; LVEF, left ventricular ejection fraction; MI, myocardial infarct; PDSR, peak diastolic strain rate; PSSR, peak systolic strain rate; R, radial.

Determinants of impaired LV function in all patients with AMI

In patients with AMI, the incremental NT-proBNP level was inversely associated with GRPS (r=−0.421, P<0.001), GCPS (r=−0.490, P<0.001), and GLPS (r=0.358, P<0.001) (Figure 4A). There was also a negative correlation between an increased LV infarct extent (all P<0.001) and global PS in all three directions (Figure 4B). Further, the GRPS, GCPS, and GLPS were significantly correlated with LVEF (r=0.797, 0.872, and 0.526, respectively, all P<0.001) (Figure 4C). However, the global PS in the three directions was not significantly associated with the Gensini score (all P>0.05) (Figure 4D).

Figure 4 The relationship between LV global strains and serum myocardial enzymology indexes (A), and infraction parameters (B), and LVEF (C), and Gensini score (D). GCPS, global circumferential peak strain; GLPS, global longitudinal peak strain; GPS, global peak strain; GRPS, global radial peak strain; LV, left ventricular; LVEF, left ventricular ejection fraction; NT-proBNP, N-terminal pro-B-type natriuretic peptide.

After adjusting for some confounding factors in the AMI subgroups, the NT-proBNP level remained an independent influencing factor of impaired GLPS (β=−0.379, P=0.015), and the diseased vessels remained an independent determinant of impaired GRPS (β=−0.431, P=0.046) and GLPS (β=−0.434, P=0.017) in the MINOCA group. In the MIOCA group, the NT-proBNP level remained an independent determinant of impaired GRPS (β=−0.496, P<0.001), GCPS (β=−0.508, P<0.001), and GLPS (β=−229, P=0.034). Moreover, in the MINOCA and MIOCA groups, infarct size was an independent determinant of global PS in all three directions (GRPS: β=−0.356 and −0.401, GCPS: β=−0.399 and −0.317, and GLPS: β=−0.282 and −0.41, all P<0.01) (Table 4).

Table 4

Determinants of impaired LV strains in the AMI patient group

Determinants GRPS GCPS GLPS
Univariable Multivariable Univariable Multivariable Univariable Multivariable
r β r β r β
Module 1
   Age, years N/A N/A N/A N/A −0.201§ N/A
   BMI, kg/m2 −0.198§ N/A −0.076§ N/A N/A N/A
   HDL, mmol/L N/A N/A 0.071§ 0.346* N/A N/A
   Hypertension, % N/A N/A N/A N/A −0.275§ N/A
   NT-proBNP −0.273§ N/A −0.322§ N/A −0.405§ −0.379*
   Diseased vessels, n −0.146§ −0.431* N/A N/A −0.204§ −0.434*
   Gensini score −0.163§ −0.436* N/A N/A N/A N/A
   Infarct size, g% of LV −0.265§ −0.356* −0.376§ −0.399* −0.272§ 0.282*
Module 2
   Hypertension, % −0.145§ N/A N/A N/A N/A N/A
   NT-proBNP −0.506§ −0.496** −0.593§ −0.508** 0.293§ −0.229*
   Infarct size, g% of LV −0.535§ −0.401** −0.431§ −0.317* 0.416§ −0.41**

Model 1: univariable and multivariable linear regression analysis of LV global peak strain in patients with MINOCA; Model 2: univariable and multivariable linear regression analysis of LV global peak strain in patients with MIOCA. β is the adjusted regression coefficient. NT-proBNP is log-transformed before being included in the regression model. Factors with P<0.1 in the univariable analyses were included in the stepwise multiple liner regression model. *, P<0.05 in the stepwise multiple liner regression model; **, P<0.001 in the stepwise multiple liner regression model; §, P<0.1 in the univariable analyses. AMI, acute myocardial infarction; BMI, body mass index; GCPS, global circumferential peak strain; GLPS, global longitudinal peak strain; GRPS, global radial peak strain; HDL, high-density lipoprotein; LV, left ventricular; MINOCA, myocardial infarction with nonobstructive coronary arteries; MIOCA, myocardial infarction with obstructive coronary arteries; N/A, not applicable; NT-proBNP, N-terminal pro-brain natriuretic peptide.

Statistical analysis of inter- and intra-observer variability

Table 5 shows the intraobserver and interobserver variabilities for LV deformation and LGE analysis results. The intraclass correlation coefficients for intraobserver and interobserver variabilities were 0.721–0.872 and 0.726–0.902, respectively, for LV deformation, and 0.851–0.865 and 0.876–0.883, respectively, for LGE parameters. Thus, both CMR measurement methods were in agreement.

Table 5

Reproducibility about intragroup correlation coefficients of LV global strains via CMR tissue-tracking technique

Coefficients Intra-observer Inter-observer
ICC 95% CI ICC 95% CI
PS, %
   GRPS 0.872 0.751–0.973 0.868 0.767–0.951
   GCPS 0.721 0.602–0.812 0.742 0.684–0.835
   GLPS 0.771 0.668–0.835 0.726 0.560–0.803
PSSR, 1/s
   Radial 0.794 0.673–0.823 0.817 0.757–0.890
   Circumferential 0.846 0.726–0.908 0.902 0.832–0.968
   Longitudinal 0.745 0.645–0.883 0.827 0.736–0.924
PDSR, 1/s
   Radial 0.852 0.788–0.880 0.838 0.758–0.874
   Circumferential 0.841 0.760–0.874 0.763 0.699–0.862
   Longitudinal 0.744 0.669–0.775 0.809 0.695–0.861
LGE
   Infarct size, g 0.865 0.761–0.868 0.883 0.772–0.937
   Infarct size of LV, % 0.851 0.740–0.856 0.876 0.658–0.914

CI, confidence interval; CMR, cardiac magnetic resonance; GCPS, global circumferential peak strain; GLPS, global longitudinal peak strain; GRPS, global radial peak strain; ICC, intraclass correlation coefficient; LGE, late gadolinium enhancement; LV, left ventricular; PDSR, peak diastolic strain rate; PS, peak strain; PSSR, peak systolic strain rate.


Discussion

Our study investigated clinical and CMR’s imaging characteristics in patients with MINOCA and MIOCA. The major findings were as follows: (I) patients with MINOCA were less likely to present with hypertension, hyperlipidemia, and diabetes than those with MIOCA; (II) patients with MINOCA had a smaller MI area and lower incidence rates of wall motion abnormalities, complex infarct type, and multiple infarct territories; (III) patients with MINOCA had significantly lower LV volumetric and strain parameters than those with MIOCA; (IV) the LV global strains reduced progressively with increased NT-proBNP levels and infarct extent. Notably, the NT-proBNP level was an independent determinant of GLPS in MINOCA patients.

Epidemiology of patients with MINOCA and MIOCA

Our results found that compared with patients with MIOCA, patients with MINOCA were younger and less likely to have hypertension, hyperlipidemia, and diabetes and had lower fasting blood glucose and HbA1c levels. The results proved to be partly similar to previous studies and deserved further research (15,18-21). A systemic review revealed no clinical characteristics or risk factors that can easily distinguish patients with MINOCA from those with MIOCA (18). The differing characteristics in MINOCA patients, such as smooth coronary arteries or minor stenosis (22,23), may lead to inconsistencies in baseline characteristics between AMI subgroups, attributed to other pathogeneses such as coronary artery spasm, spontaneous coronary dissection, and microvascular causes (24). As the epidemiology of MINOCA significantly varies, this recently established disease remains controversial, and it can be easily misdiagnosed (25). Thus, clinicians should provide early interventions for patients with angina pectoris even if they are young and at low risk and have good CAG findings.

Latent MI between patients with MINOCA and those with MIOCA

Cine and contrast-enhanced CMR imaging is widely used to evaluate myocardial structure and function with unusual precision (26-28). Acute infarct size is directly related to LV remodeling and strongly predicts future events (24). In our study, the incidence rates of wall motion abnormalities in the patients of the MINOCA were lower than those of the MIOCA. The patients with MINOCA had smaller MI area and lower incidence rates of multiple infarct territories and complex infarct types. Therefore, patients with MINOCA present with early coronary arterial endothelial dysfunction and atherosclerosis, which is consistent with those with MIOCA. In addition, the coronary artery of patients with MINOCA is less affected, and the condition may be in the early stages (22). Reynolds et al. noticed that the myocardium dominated by coronary plaque rupture had more edema area and less infarct size using CMR monitoring. Therefore, the coronary blood flow is restored immediately after plaque rupture in patients with MINOCA (29,30). Although CAG was not positively detected, MI had already occurred. Therefore, based on these results, patients with MINOCA presented with a specific etiology, and routine CMR imaging is essential as it is sensitive in detecting myocardial dysfunction and small infarctions and can provide effective information for preventing large infarctions and adverse outcomes.

CMR strain parameters for the accurate and early diagnosis of MINOCA

Our study found that in terms of LV volumetric and strain parameters, the LVEDVI, LVESVI, LVSVI, LVEF, GRPS, GCPS, and GLPS of the MINOCA group were superior to those of the MIOCA group but inferior to those of the control group. Leurent et al. revealed that the etiology of MINOCA is very complex without evident obstruction during CAG (31). It may be related to the recovery of coronary artery blood supply after autolysis of thrombosis or spasm relief. Hence, patients with MINOCA had a lower degree of myocardial damage than those with MIOCA. In addition, patients with AMI who presented with an LVEF of ≥40% had decreased global strains, and patients with MINOCA had decreased PSSR-C, PSSR-L, PDSR-C, and PDSR-L. This is because the subendocardial fibers were the first area to exhibit abnormal function due to critical coronary narrowing and coronary microvascular dysfunction and the injury progressed as a wavefront toward the subepicardium (30,32-34).

Results showed that the global PS in the three directions was inversely associated with the increasing NT-proBNP level, LV infarct extent, and decreasing LVEF in all patients with AMI. Multivariate linear regression analysis showed that the NT-proBNP level was only an independent determinant of GLPS, not GCPS or GRPS, in patients with MINOCA. The animal experiments revealed that longitudinal subendocardial fiber function is related to the release of natriuretic peptides (23,35). The results of the abovementioned study and the animal experiment findings confirmed that the NT-proBNP level and GLPS have a high sensitivity and consistency for detecting early subendocardial infarction in patients with MINOCA. The diseased vessels remained an independent determinant of impaired GRPS and GLPS in patients with MINOCA. It suggested again that the involvement of coronary arteries in patients with MINOCA is in the early compensatory stage (22). Several studies have found a good correlation between global strains and infarct size (32,36,37). This agrees with our results and indicates that the strains derived via CMR-feature tracking with NT-proBNP levels and infarct size are reliable parameters for monitoring cardiac dysfunction in patients with AMI with or without coronary artery occlusion. Notably, the global strain parameters in the longitudinal and circumferential directions can be a useful early biomarker of subclinical impairment before LV function can become globally impaired. Further, it can be applied to identify high-risk individuals and facilitate clinical monitoring among patients with AMI who present with an LVEF of ≥40% (23,38,39).

Limitations

This study had limitations including its single-center nature, potential biases in the results such as selection bias due to renal function cutoffs and poor image quality, and the need for further studies with a larger sample size. Additionally, medication use and troponin T and NT-proBNP levels in the control group were not assessed. Due to the retrospective nature of the study, there are inherent design limitations. The long-term survival and the prognostic action of PS in patients with AMI should be further investigated in future studies.


Conclusions

MINOCA has a specific etiology, and patients with MINOCA have better myocardial function than those with MIOCA. Strains and infarct size on CMR imaging and NT-proBNP levels are reliable for monitoring cardiac dysfunction in patients with AMI, particularly MINOCA. Global strain parameters, particularly GLPS and GCPS, can be an early biomarker of subclinical impairment in patients with MINOCA.


Acknowledgments

None.


Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1331/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1331/dss

Funding: This study was financially supported by the National Natural Science Foundation of China (Nos. 81771887, 81771897, 82371925), the 1-3-5 Project for Disciplines of Excellence of West China Hospital, Sichuan University (No. ZYGD23019) and the Sichuan Province Central Government Guide Local Science and Technology Development Project (No. 2023ZYD0100).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1331/coif). The 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. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Biomedical Research Ethics Committee of the West China Hospital, Sichuan University (No. 2019-756) and individual consent for this retrospective analysis was waived.

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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(English Language Editor: J. Jones)

Cite this article as: Shen LT, Yang ZG, Guo YK, Qian WL, Yan WF, Jiang YN, Shi K, Li Y. Clinical and cardiac magnetic resonance imaging features for differentiation between acute myocardial infarction with and without obstructive coronary arteries. Quant Imaging Med Surg 2026;16(1):49. doi: 10.21037/qims-2025-1331

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