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20 October 2021: Clinical Research  

Analysis of Characteristics of Patients with Non-ST-Segment Elevation Myocardial Infarction by Cardiac Magnetic Resonance Imaging

Shujuan Dong 1ACE* , Yunbo Liu 2E* , Wenjing Sun 1BE* , Chunqiu Wang 3BD* , Yan Wang 3C , Wenbo Zhao 1F , Shenghui Zhao 1F , Yingjie Chu 1G*

DOI: 10.12659/MSM.933220

Med Sci Monit 2021; 27:e933220

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Abstract

BACKGROUND: In this study, cardiac magnetic resonance imaging was used to investigate the characteristics of patients who have total coronary occlusion but manifest with non-ST-segment elevation myocardial infarction (NSTEMI), and we assessed the extent of infarct transmurality and myocardial necrosis size in NSTEMI patients.

MATERIAL AND METHODS: We enrolled all patients diagnosed at our hospital with subtotal or total occlusion of the culprit artery (TOCA), based on the coronary angiography, who successfully underwent PCI within 12 h of admission, and who had CMR imaging performed within 2 days after the PCI.

RESULTS: Based on 12-lead ECG findings, 48% of patients were categorized as having STEMI and 52% as having NSTEMI. TOCA was detected by coronary angiography in 43% of NSTEMI patients, and in 60% and 33% of normal ST segment and ST-segment depression MI patients, respectively. The transmural segments were found in 78% of STEMI patients and 31% of NSTEMI patients (P<0.05). Transmural infarction segments were found in 64% of NSTEMI patients with TOCA and in 8% of NTOCA patients (P<0.05). Moreover, the number of transmural segments in ST-segment depression MI patients was the lowest (P<0.05). Infarct size in STEMI patients was significantly larger than in patients with NSTEMI (P<0.05), whereas there was no statistically significant difference in patients with normal ST segment and ST-segment depression MI patients (P>0.05).

CONCLUSIONS: Identification TOCA by coronary angiography and transmural infarction by DE-MRI can be challenging in AMI patients with non-ST-segment elevation. In approximately 30% of non-ST-segment elevation MI patients, transmural infarction was detected by DE-MRI. Therefore, TOCA accompanied by transmural infarction in non-ST-segment-elevation MI patients is not uncommon.

Keywords: Coronary Angiography, Electrocardiography, Magnetic Resonance Imaging, Myocardial Infarction

Background

Acute myocardial infarction (AMI) is the leading cause of morbidity and mortality in people with cardiovascular disease. The spectrum of AMI consists of ST-segment elevation MI (STEMI) and non-ST-segment elevation MI (NSTEMI) [1]. Twelve-lead-electrocardiogram (ECG) has a key role in discriminating NSTEMI from STEMI. Patients with STEMI present with chest pain and persistent ST-segment elevation on the initial ECG leads. In addition, STEMI should be defined if the clinical presentation is compatible and the ECG trace indicates left bundle branch block (LBBB), and it is usually characterized by transmural infarction resulting from total occlusion of an epicardial coronary artery induced by a thrombus [2,3]. In patients with NSTEMI, defined as presenting with acute chest pain lasting >20 min and either elevation of cardiac biomarkers or dynamic ST-segment changes on the initial ECG without ST-segment elevation, NSTEMI is an acute partial occlusion of a coronary vessel causing an incomplete interruption of blood supply of the distal myocardial territory, which causes non-transmural (subendocardial) ischemia [4,5]. The ECG in NSTEMI patients classically shows T wave inversion and/or ST-segment depression in the absence of ST-segment elevation. However, previous studies indicated that TOCA was also detected in patients with NSTEMI. The sensitivity of ECG to detect acute ischemia influencing lateral or posterior myocardial walls is obviously reduced when the infarct-related artery (IRA) involves the left circumflex artery (LCx) [6]. In addition, patients with STEMI, whose symptoms and ECG changes completely resolve upon admission, and are given the medical therapy before hospital arrival, manifest transient ST-segment elevation that is not recorded by ECG.

The accuracy of the 12-lead ECG in detecting TOCA is limited. Recently, clinical research showed that TOCA has also been observed in patients with NSTEMI [7,8]. However, the extent of transmural ischemia in patients who have total occlusion of the culprit artery but who present with non-ST-elevation remains unclear. Moreover, whether the extent of transmural segments or infarct size in STEMI patients is larger than that in NSTEMI patients with or without TOCA is a question worth exploring.

Cardiac magnetic resonance imaging (CMR) is a powerful non-invasive tool that provides images with high spatial resolution [9,10]. Recently, use of CMR has gained acceptance in coronary heart disease; CMR can accurately evaluate myocardial viability after acute myocardial infarction by obtaining data about viable myocardium, myocardial perfusion, and cardiac function in a single examination [11]. In particular, delayed-enhancement magnetic resonance imaging (DE-MRI) and first-pass myocardial perfusion are ideal tools for observing the extent of transmural infarction, infarct size, and microvascular dysfunction [12–14]. We performed the present study to evaluate the transmural extent of myocardial necrosis and myocardial infarct size using CMR for unrecognized myocardial infarction determined by ECG, and to assess the difference in MACE between patients with STEMI and NSTEMI.

Material and Methods

PATIENTS:

This was a retrospective analysis of 248 AMI patients who were enrolled between September 2016 and August 2018 in Henan Provincial People’s Hospital, and were followed up for 180 days (6 months). All patients who presented to our hospital with chest pain, ECG changes, and troponin-positive results were eligible for study inclusion. All patients were diagnosed with partial or total occlusion of the infarct-related artery based on the coronary angiography, and successfully underwent PCI within 12 h of hospital admission. Patients also had CMR imaging performed within 1 week after the PCI. Exclusion criteria were chronic MI, acute myocarditis, NYHA class-IV heart failure, and contraindications to CMR. All patients gave written informed consent to study protocols approved by our hospital ethics committee.

CMR PROTOCOL: All patients were examined using a Philips Ingenia 3.0 T CX 3.0 T clinical scanner (Philips Medical Systems Nederland B.V. Best, the Netherlands) with a gradient field strength of 80 mT/m and gradient switching rate of 200 mT/m/ms, equipped with a Q- BODY coil (SENSE XL TORSO COIL 3.0 T) for signal reception. The CMR protocol has been previously described [9]. Delayed-enhancement imaging was performed 10–15 min after intravenous injection of gadolinium diethylenetri-amine penta-acetic acid (Gd-DTPA; 0.1 mmol/kg) using PSIR_TFE_BH sequence with repetition time/echo time 6.1/3.0 ms, flip angle 25°, spatial resolution 3.5×3.5×10 mm, inversion time set to null signal from normal myocardium, and slice thickness 8 mm.

CMR ANALYSIS: The presence and location of hyper-enhanced tissue were determined by visual inspection using the conventional American Heart Association (AHA) 17-segment model (Figure 1) [15]. The transmural extent of myocardial infarction in each segment was graded with a 0-IV score: 0=normal; I=1–25% transmural extent; II=26–50%; III=51–75%; IV=76–100%. Endocardial and epicardial borders in hyperenhancement images were traced manually on all short-axis slices. Myocardial necrosis size was calculated as a percentage of LV volume.

CORONARY ANGIOGRAPHY:

Two experienced, blinded, interventional cardiologists performed emergency coronary angiography in the cardiac catheterization unit of our hospital. The ‘culprit lesion’ was determined based on angiographic characteristics, location of ECG changes, and segmental wall motion abnormality. Significant CAD was defined as single or multivessel stenoses of >80% luminal narrowing in a main coronary vessel.

ECG: All patients underwent standard 12-lead ECG on admission. According to ECG changes, patients were classified as having ST-segment elevation, normal ST segment, or ST-segment depression. Based on AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram [16], ST-segment elevation was defined as 2 or more contiguous ECG leads with ST-segment elevation (ST-segment elevation ≥2 mm in the chest leads, ST-segment elevation ≥1 mm in limb leads); normal ST segment as no significant ST shift; and ST-segment depression was considered to be ST-segment depression of at least 1 mm in 2 standard limb leads or in 2 contiguous chest leads.

FOLLOW-UP AND OUTCOME: All patients were enrolled between September 2016 and August 2018 and were followed up until the time of an event or, in the case of no event, February 2019. The primary outcome was defined as major adverse cardiac events (MACEs), including cardiovascular mortality or non-fatal MI. The secondary outcomes were cardiovascular mortality, non-fatal MI, unstable angina pectoris requiring revascularization, hospitalization for heart failure, and fatal arrhythmia [17,18].

ETHICS APPROVAL:

Clinal experiments were reviewed and approved by the Clinical Medicine Research Center Ethics Committee of Henan Provincial People’s Hospital (approval date 2015, code 23).

STATISTICAL ANALYSIS:

All statistical analyses were carried out using SPSS version 22.0 (IBM, Armonk, NY, USA). All continuous data are described by mean±SD. The difference between STEMI and NSTEMI patients was determined by chi-square test or by Fisher’s exact test, as appropriate, and the Mann-Whitney U test. A two-sided P<0.05 was considered statistically significant.

Results

STUDY POPULATION: Baseline clinical characteristics are presented in Table 1. The mean age was 56±11.8 years, and 67% of patients were male. Based on the AHA/ACCF/HRS criteria, 48% (120/248) of patients were diagnosed with STEMI and 52% (128/248) with NSTEMI. NSTEMI included patients with normal ST segment (41%, 52/128) and/or ST-segment depression (59%, 76/128). Patients with STEMI had significantly higher levels of hypertension and blood glucose compared to NSTEMI patients (P<0.05). No significant differences were found in age, EF (%), smoking history, drinking history, or dyslipidemia (P>0.05).

COMPARISON OF CORONARY ARTERY CHARACTERISTICS BETWEEN STEMI AND NSTEMI: Coronary artery characteristics are shown in Table 2. Based on coronary angiography, the culprit lesion location and disease distribution of coronary artery in all 248 AMI patients were the following: left anterior descending coronary artery (LAD) and right coronary artery (RCA) were the most common infarct-related arteries in the ST-segment elevation group and ST-segment depression group, while left circumflex artery (LCx) was more common in the normal ST segment group (P<0.05). The infarct sites in the ST-segment elevation and ST-segment depression groups were mostly located in the proximal and middle segments, while those in the normal ST segment group were commonly located in the middle and distal segments (P<0.05). The proportion of occlusive lesions in the ST-elevation group and normal ST segment group was higher than that in the ST-segment depression group (P<0.05). The proportion of single-vessel disease in the ST-segment elevation group and normal ST segment group was higher than that in the ST-segment depression group (P<0.05).

CMR FINDINGS: CMR characteristics are shown in Tables 3–5. Myocardial necrosis hyperenhancement was observed in 99% (239/248) of patients. Among them, 99% (118/120) of patients with ST-elevation were identified by DE-MRI, 94% (49/52) with normal ST segment, and 95% (72/76) with ST-segment depression. In 113 (47%) cases, hyperenhancement was observed in the anterior wall; in 59 (25%) patients it was observed in the lateral wall, and in 67 (28%) it was observed in the inferior wall. Among patients with STEMI, 93/120 (78%) had transmural myocardial infarction and 27/120 (22%) had non-transmural infarction.

COMPARISON OF EXTENT OF TRANSMURAL INFARCTS IN STEMI AND NSTEMI PATIENTS WITH OR WITHOUT TOCA: The transmural infarction extent as assessed by DE-MRI in 93/120 (78%) of ST-segment elevation patients was more than 75% of at least 1 segment (Table 3). Transmural infarcts in patients with normal ST segment and in ST-segment depression patients with TOCA were detected in 22/56 (39%) and 14/56 (25%), respectively (Table 4), in 38/72 (53%) of patients with normal ST segment, and in less than 50% of ST-segment depression patients without TOCA (Table 5). In addition, using the AHA 16-segment model, transmural infarcts were detected in 689 of the 1920 segments (36%) in ST-segment elevation patients, in 87 of the 496 segments (17.5%) in patients with TOCA with normal ST segment, and in 63 of 400 segments (15.7%) in ST-segment depression patients with TOCA, as determined by DE-MRI. Our results indicated that the number of transmural segments was higher in patients with STEMI compared to NSTEMI patients (P<0.05). In addition, there were more transmural infarction segments in NSTEMI patients with TOCA than in those without TOCA (P<0.05). There was a minor, not statistically significant, difference in necrosis transmurality in patients with normal ST segment in comparison with those with ST-segment depression (P<0.05). Interestingly, transmural infarcts in the NSTEMI population were predominantly located in the inferior and anterior wall, as detected by DE-MRI (Figure 2).

COMPARISON OF MYOCARDIAL NECROSIS SIZE IN STEMI AND NSTEMI POPULATIONS WITH OR WITHOUT TOCA: Our results revealed that myocardial necrosis size was larger in STEMI patients than in NSTEMI patients. Moreover, the necrosis size in patients with TOCA was also significantly larger as compared to those with NTOCA (Figure 3). However, no significant difference in infarct size was found between the patients with normal ST segment and ST-segment depression patients. In the NSTEMI population, myocardial necrosis size in patients with transmural hyperenhancement was significantly larger than in those with non-transmural hyperenhancement (Figure 3).

PROCEDURAL CHARACTERISTICS AND MEDICAL THERAPY OF THE PATIENTS: Patients in the 3 groups had similar procedural characteristics and medical therapy (Table 6). No significant differences were detected in the prevalence of door-to-balloon time or stent implantation in each group. In addition, no significant differences between groups were observed in MI (TIMI) flow before or after thrombolysis. Approximately 90% of patients with primary PCI had restored TIMI flow III.

OUTCOME DATA: During the follow-up of 180 days (6 months), there were 30 (12%) MACEs, including 16 (6.5%) cardiovascular deaths and 14 (5.5%) non-fatal MIs, 32 (13.0%) hospitalizations for heart failure, 24 (9.7%) unstable angina pectoris requiring revascularization, and 5 (2.1%) ventricular arrhythmias. The incidence of MACE was higher in patients with ST-segment elevation compared to patients with normal ST segment or ST-segment depression (Figure 4), However, no significant difference was observed between STEMI and NSTEMI patients (Figure 5). In univariable analysis, presence of inducible ischemia, number of segments of inducible ischemia, presence of LGE, number of segments of LGE, and LV end-diastolic and end-systolic volume index were all significantly associated with MACE (HR, 2.99 [95% CI, 1.67–5.83]; P<0.01; HR, 1.48 [95% CI, 1.32–2.01]; P<0.01; HR, 1.56 [95% CI, 1.26–1.93]; P<0.01, HR, 1.23 [95% CI, 1.15–1.38]; P<0.01; HR, 1.06 [95% CI, 0.89–1.16]; P<0.01; and HR, 1.03 [95% CI, 1.32–2.01]; P<0.01, respectively; Table 7). In a multivariable Cox regression analysis, age, presence of inducible ischemia, number of segments of inducible ischemia, presence of LGE, and number of segments of LGE were independent predictors of a higher incidence of MACE (HR, 1.07 [95% CI, 0.99–1.14]; P<0.01; HR, 3.01 [95% CI, 1.69–5.85]; P<0.01; HR, 1.50 [95% CI, 1.35–2.04]; P<0.01, HR, 1.58 [95% CI, 1.28–1.99]; HR, 1.25 [95% CI, 1.15–1.40]; and HR, 1.01 [95% CI, 0.84–1.09]; respectively; Table 8)

Discussion

STUDY LIMITATIONS:

In this study, CMR imaging was performed 2 days after admission by ECG with subsequent PCI. However, it is possible that due to coronary reperfusion and the extent of infarcts, excitation ECG changes during the acute stage did not develop into necrotic areas, which DE-MRI would then detect, which may have led to an underestimation of the extent of transmural infarction and infarct size in MI patients. Also, our observations are strongly linked with the studied patients and therapy; thus, selection bias cannot be excluded.

Conclusions

Our results suggest that MI patients with ST-segment elevation and those with normal ST segment often present a higher proportion of occlusive lesions. Furthermore, NSTEMI patients tend to have less transmural infarction, with a much smaller infarct size. However, identification of total occlusion of a coronary artery by coronary angiography and transmural infarction by DE-MRI is challenging in AMI patients with non-ST-segment elevation.

Figures

Figure 1. The 17 myocardial segments of the left ventricle presented by AHA and their corresponding coronary artery anatomy. Figure 2. Images from 6 AMI patients. (A) ECG in leads V1–V5 manifests ST-elevation in a 57-year-old man. CMR illustrates transmural infarction in the anterior segments detected by DE-MRI. Coronary angiography revealed LAD 100% occluded proximally. (B) ST-segment elevation on ECG in leads II, III, and aVF in a 48-year-old man. CMR illustrates contrast-enhanced areas in the lateral segments characterized by DE-MRI. Coronary angiography revealed a 99% distal stenosis in the RCA. (C) A 58-year-old MI patient with a normal ST segment. CMR shows contrast-enhanced areas in the inferior segments characterized by DE-MRI. Coronary angiography revealed 100% proximal occluded RCA. (D) A 55-year-old woman with MI with a normal ST segment. CMR illustrates non-transmural hyperenhancement in the lateral segment. Coronary angiography revealed 95% middle stenosis in the LCx. (E) ECG of a 50-year-old patient showing presence ST-depression in inferior leads. CMR showed partial transmural and subendocardial necrosis in the inferior segments detected by DE-MRI. Coronary angiography revealed 100% proximal occluded RCA. (F) ECG of a 66-year-old woman presenting non-ST-segment elevation in anterior leads. CMR showed non-transmural hyperenhancement in the anterior segment detected by DE-MRI. Coronary angiography revealed 95% proximal stenosis in the LAD. DE-MRI – delayed-enhancement magnetic resonance imaging; MI – myocardial infarction; LAD – left anterior descending artery; LCx – left circumflex; RCA – right coronary artery. Figure 3. Myocardial infarction size as assessed by DE-MRI according to ST-elevation and non-ST-elevation on admission 12-lead-ECG. * P<0.05 vs ST-elevation group, ** P<0.05 vs ST-elevation group. Figure 4. MACE rate according to hospitalization for heart failure (A) and unstable angina pectoris requiring revascularization (B). Figure 5. Kaplan-Meier curves of cardiovascular mortality.

References

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16. Wagner G, Macfarlane P, Wellens H: AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: Acute ischemia/infarction: A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology: J Ame Coll Cardiol, 2009; 53(11); 1003-11

17. Bulluck H, Paradies V, Barbato E: Prognostically relevant periprocedural myocardial injury and infarction associated with percutaneous coronary interventions: A Consensus Document of the ESC Working Group on Cellular Biology of the Heart and European Association of Percutaneous Cardiovascular Interventions (EAPCI): Eur Heart J, 2021; 42(27); 2630-42

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Figures

Figure 1. The 17 myocardial segments of the left ventricle presented by AHA and their corresponding coronary artery anatomy.Figure 2. Images from 6 AMI patients. (A) ECG in leads V1–V5 manifests ST-elevation in a 57-year-old man. CMR illustrates transmural infarction in the anterior segments detected by DE-MRI. Coronary angiography revealed LAD 100% occluded proximally. (B) ST-segment elevation on ECG in leads II, III, and aVF in a 48-year-old man. CMR illustrates contrast-enhanced areas in the lateral segments characterized by DE-MRI. Coronary angiography revealed a 99% distal stenosis in the RCA. (C) A 58-year-old MI patient with a normal ST segment. CMR shows contrast-enhanced areas in the inferior segments characterized by DE-MRI. Coronary angiography revealed 100% proximal occluded RCA. (D) A 55-year-old woman with MI with a normal ST segment. CMR illustrates non-transmural hyperenhancement in the lateral segment. Coronary angiography revealed 95% middle stenosis in the LCx. (E) ECG of a 50-year-old patient showing presence ST-depression in inferior leads. CMR showed partial transmural and subendocardial necrosis in the inferior segments detected by DE-MRI. Coronary angiography revealed 100% proximal occluded RCA. (F) ECG of a 66-year-old woman presenting non-ST-segment elevation in anterior leads. CMR showed non-transmural hyperenhancement in the anterior segment detected by DE-MRI. Coronary angiography revealed 95% proximal stenosis in the LAD. DE-MRI – delayed-enhancement magnetic resonance imaging; MI – myocardial infarction; LAD – left anterior descending artery; LCx – left circumflex; RCA – right coronary artery.Figure 3. Myocardial infarction size as assessed by DE-MRI according to ST-elevation and non-ST-elevation on admission 12-lead-ECG. * P<0.05 vs ST-elevation group, ** P<0.05 vs ST-elevation group.Figure 4. MACE rate according to hospitalization for heart failure (A) and unstable angina pectoris requiring revascularization (B).Figure 5. Kaplan-Meier curves of cardiovascular mortality.

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750