Author + information
- Received June 6, 2018
- Revision received December 3, 2018
- Accepted December 14, 2018
- Published online October 7, 2019.
- Amardeep Ghosh Dastidar, MBBSa,b,
- Anna Baritussio, MBBS, MD, PhDa,b,
- Estefania De Garate, MBBSa,b,c,
- Zsofia Drobni, MBBSa,
- Giovanni Biglino, PhDa,b,
- Priyanka Singhal, MBChBa,b,
- Elena G. Milano, MBBS, MDa,b,
- Gianni D. Angelini, MD, MCha,b,c,
- Stephen Dorman, MBBSa,
- Julian Strange, MBBS, MDa,
- Thomas Johnson, BSc (Hons), MBBS, MDa,b and
- Chiara Bucciarelli-Ducci, MBBS, MD, PhDa,b,c,∗ ()
- aBristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol, United Kingdom
- bSchool of Clinical Sciences, Faculty of Health Sciences, University of Bristol, Bristol, United Kingdom
- cBristol National Institute of Health Research, Biomedical Research Centre, Bristol, United Kingdom
- ↵∗Address for correspondence:
Dr. Chiara Bucciarelli-Ducci, CMR Unit, Bristol Heart Institute, Upper Maudlin Street, Bristol BS2 8HW, United Kingdom.
Objectives This study sought to assess the prognostic impact of cardiac magnetic resonance (CMR) and conventional risk factors in patients with myocardial infarction with nonobstructed coronaries (MINOCA).
Background Myocardial infarction with nonobstructed coronary arteries (MINOCA) represents a diagnostic dilemma, and the prognostic markers have not been clarified.
Methods A total of 388 consecutive patients with MINOCA undergoing CMR assessment were identified retrospectively from a registry database and prospectively followed for a primary clinical endpoint of all-cause mortality. A 1.5-T CMR was performed using a comprehensive protocol (cines, T2-weighted, and late gadolinium enhancement sequences). Patients were grouped into 4 categories based on their CMR findings: myocardial infarction (MI) (embolic/spontaneous recanalization), myocarditis, cardiomyopathy, and normal CMR.
Results CMR (performed at a median of 37 days from presentation) was able to identify the cause for the troponin rise in 74% of the patients (25% myocarditis, 25% MI, and 25% cardiomyopathy), whereas a normal CMR was identified in 26%. Over a median follow-up of 1,262 days (3.5 years), 5.7% patients died. The cardiomyopathy group had the worst prognosis (mortality 15%; log-rank test: 19.9; p < 0.001), MI had 4% mortality, and 2% in both myocarditis and normal CMR. In a multivariable Cox regression model (including clinical and CMR parameters), CMR diagnosis of cardiomyopathy and ST-segment elevation on presentation electrocardiogram (ECG) remained the only 2 significant predictors of mortality. Using presentation with ECG ST-segment elevation and CMR diagnosis of cardiomyopathy as risk markers, the mortality risk rates were 2%, 11%, and 21% for presence of 0, 1, and 2 factors, respectively (p < 0.0001).
Conclusions In a large cohort of patients with MINOCA, CMR (median 37 days from presentation) identified a final diagnosis in 74% of patients. Cardiomyopathy had the highest mortality, followed by MI. The strongest predictors of mortality were a CMR diagnosis of cardiomyopathy and ST-segment elevation on presentation ECG.
Acute coronary syndrome (ACS) is one of the leading causes of mortality and morbidity worldwide (1). Definite diagnosis of ACS is crucial for ensuring appropriate patient management. As per the international guidelines, patients presenting with ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation-ACS (NSTE-ACS) proceed to immediate or inpatient coronary angiography, respectively, with the aim to identify and treat a culprit coronary artery occlusion or stenosis (2,3). In 1% to 14% of these patients, however, no significant coronary obstruction is identified, and thus these cases are classified as myocardial infarction with nonobstructive coronary arteries (MINOCA) (3). MINOCA represents a diagnostic dilemma, with subsequent uncertain clinical management. A recent registry study has shown beneficial effects of treatment with statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers on outcome in patients with MINOCA (4).
The underlying pathophysiological mechanisms occurring in MINOCA are complex and multifactorial (5). Patients with MINOCA are thought to have a better prognosis and consequently do not receive appropriate secondary prevention medications (6); however, recent studies suggest that all-cause mortality may be as high as 4.7% at 12 months (7,8). The latest European Society of Cardiology (ESC) guidelines on the management of STEMI and the recent ESC/American College of Cardiology/American Heart Association/World Heart Federation fourth universal definition of myocardial infarction has included MINOCA, suggesting a potential role for cardiovascular magnetic resonance (CMR) in this cohort (3,9).
Confirmation or exclusion of myocardial infarction (MI) by CMR facilitates tailoring of medical therapy, ensuring appropriate long-term secondary prevention and modification of risk, and minimizing exposure to antiplatelet therapy and the associated bleeding risks for those with a noncoronary etiology for the MINOCA presentation (10). Few previous studies have shown that CMR can identify the underlying diagnosis, which is made most commonly based on acute/chronic myocarditis, acute MI with spontaneous recanalization/embolus, stress cardiomyopathy (Takotsubo), or other cardiomyopathies (11–17). Only in a small proportion of cases is no abnormality identified by CMR. The variable proportion of normal cases in the different studies may be due to the time delay between the acute presentation and CMR (18), suggesting that the time between acute presentation and CMR can play a role in identifying the early reversible abnormalities that may resolve when patients are scanned later. Recent studies have demonstrated the prognosis in the individual diagnostic categories such as myocarditis and Takotsubo cardiomyopathy (19–21); however, there is no evidence in the literature on the prognostic significance of the CMR findings and conventional risk factors in MINOCA. The only study that looked at midterm mortality was by Mittal et al. (22); however, they looked at patients presenting via the primary percutaneous coronary angiography pathway with nonobstructed coronaries. Sixty percent of the study population had normal troponin and thereby did not strictly meet MINOCA criteria. Our study aimed to assess the prognostic impact of CMR and conventional risk factors in patients with MINOCA.
In this longitudinal observational study, consecutive patients presenting with MINOCA (chest pain, elevated troponin, and nonobstructed coronary arteries) per the new ESC STEMI Guideline (3) and undergoing CMR were identified retrospectively and followed prospectively (Figure 1). We excluded patients admitted with suspected heart failure or arrhythmic events at presentation. The study was performed at a large cardiothoracic tertiary center in southwest England; data were collected on consecutive patients scanned from September 2011 to December 2015. Patients were identified either presenting with STEMI or non-STEMI. Nonobstructed coronaries were defined as thrombosis in MI III flow and <50% stenosis in any coronary artery (3). Troponin T level <14 ng/l was considered normal. The typical rise or fall of troponin T was used for the diagnosis of acute MI. (9) False-positive troponin possibilities included a single troponin elevation (<5× upper limit of normal) that was not repeated during admission or if a single elevated troponin was followed by a second normal troponin level within 24 h was excluded from study (2). The study was reviewed and approved by the local institutional review board.
CMR was performed at 1.5-T (Magnetom Avanto, Siemens Healthineers, Erlangen, Germany). A comprehensive CMR protocol was carried out, including cine, T2-weighted (myocardial edema), and early and late gadolinium enhancement (LGE) imaging (23). In particular, cine images were performed using a steady-state free-precession sequence acquired in 3 long-axis planes and a stack of short-axis images covering the left ventricle, and T2-weighted short T1 inversion recovery (T2-STIR) sequence images were acquired in the same short- and long-axis planes as the cine images with standard parameters, as previously described (24,25). Intravenous gadolinium-chelate contrast agent (gadobutrol) was administered at a dose of 0.1 mmol/kg–1 of body weight. Images were acquired 2 to 3 min after contrast injection (early gadolinium), whereas LGE images were acquired 15 to 20 min after contrast injection using a standard inversion recovery segmented gradient echo sequence, as previously described (24,25).
All CMR studies were analyzed and reported by a consultant with >15 years of CMR experience and with ESC CMR level 3 certification (C.B.D.). Diffuse and focal myocardial edema was analyzed using both the early gadolinium and the T2-STIR images. Myocardial edema was considered present when the ratio of signal intensity between the myocardium and the mean signal intensity of the skeletal muscle was >2 on T2-STIR images, according to the Lake Louise criteria (26). Early gadolinium enhancement ratio used for assessment of hyperemia was evaluated as previously described (26). Patients were grouped into 4 categories based on their CMR characteristics: MI (embolic/spontaneous recanalization), myocarditis, cardiomyopathy, and normal CMR. The latter corresponded to a structurally normal heart, defined as no regional wall motion abnormality (RWMA) (except for dyssynchrony secondary to bundle branch block), no myocardial edema, and no myocardial LGE (scarring) (except nonspecific LGE in left ventricular [LV]/right ventricular [RV] insertion points). Myocarditis was diagnosed based on fulfilling 2 of 3 Lake Louise Criteria: T2-STIR sequences detecting myocardial edema; early gadolinium sequences detecting hyperemia; or epicardial or mid-myocardial LGE, as previously described (26). MI was diagnosed based on territorial subendocardial or transmural LGE. Takotsubo cardiomyopathy was diagnosed based on the T2-STIR images detecting myocardial edema and regional wall motion in the mid-cavity or apical distribution with no myocardial LGE, all in accordance with the modified Mayo Clinic criteria (27). Dilated cardiomyopathy, hypertrophic cardiomyopathy, and cardiac amyloidosis were detected based on specific tissue characterization characteristics, and all were grouped under cardiomyopathy together with Takotsubo cardiomyopathy (15). The extent of LGE and myocardial edema was quantified by calculating the number of segments involved (20).
Study primary endpoint
The endpoint of the present study was all-cause mortality. Patient-related data were collected directly from medical records. Follow-up was performed centrally by analyzing the mortality data obtained from the National Health Service summary care records. Data were collected and interpreted by 1 of the primary investigators (A.G.D., A.B., E.D.G., or G.B.) in all cases.
Baseline patient characteristics, conventional risk markers, and CMR findings are described according to the diagnostic groups. Data for continuous variables are presented as mean ± SD or median as appropriate. Categorical variables are presented as frequencies and percentages. Normally distributed continuous variables were compared using 1-way analysis of variance with Bonferroni correction for multiple comparisons. Continuous variables that were not normally distributed were compared by Kruskal-Wallis tests. In univariate analyses, the association of time variables to mortality was assessed using Kaplan-Meier curves and the log-rank test. Univariable and multivariable associations of risk covariates with mortality were assessed using Cox proportional hazard regression analyses. Only variables with p < 0.05 in univariable analyses were used in multivariable model. SPSS version 23 (IBM Corp., Armonk, New York), was used for statistical analysis. Probability values were 2-sided, and values of p < 0.05 were considered significant. Because of a paucity of mortality data on the MINOCA subgroups, post hoc power calculation was performed based on the study findings.
A total of 11,757 patients underwent emergency or urgent coronary angiography during the recruitment period, of which 410 patients with suspected MINOCA underwent CMR assessment. Two percent (n = 8) were excluded because of incomplete protocol and 3% (n = 14) because of coronary artery disease that was deemed >50% stenosis, thereby leaving a study sample size of 388. CMR was able to identify a cause for the troponin rise in 74% of cases. Clinical characteristics of the overall population (n = 388) and for separate patient groups based on the CMR diagnosis are summarized in Table 1. There was a low prevalence of cardiovascular risk factors (hypertension, diabetes, hyperlipidemia, smoking, and family history), with no difference across groups. The median time delay between acute presentation and CMR was 37 days. Thirty-seven of our patients underwent a scan within 2 weeks of presentation. In a median follow-up of 1,262 days (3.5 years), the overall all-cause mortality was 5.7%.
Conventional risk factors
The mean age of the total population was 56 ± 17 years. Kaplan-Meier curves were drawn showing the risk of mortality according to the different age categories (<40, 40 to 59, 60 to 79, and >79 years). There was a strong association between increasing age and mortality (log-rank test: 23.2; p < 0.001) (Figure 2).
Women comprised 48% of the total cohort and 98% of the patients diagnosed with Takotsubo cardiomyopathy were women. There was no significant association between sex and mortality in the overall cohort (log-rank test: 2.5; p = 0.10).
Electrocardiogram at presentation (STEMI or NSTE-ACS)
Nineteen percent of our study population presented with ST-segment elevation on the 12-lead electrocardiogram (ECG). Kaplan-Meier curves were drawn showing the risk of mortality according to the ECG presentation as ST-segment elevation or no ST-segment elevation. There was a strong association between ECG presentation as ST-segment elevation and mortality (log-rank test: 7.4; p = 0.007) (Figure 3).
CMR characteristics and diagnosis
The CMR characteristics are described according to diagnosis groups (Table 2).
MI was the most prevalent diagnosis (25%, 97 of 388 patients), followed by myocarditis (25%, 96 of 388) and cardiomyopathy 25%, whereas 26% had a structurally normal heart and were grouped into the normal CMR category.
In the overall cohort, the mean indexed end-diastolic volume (iEDV) was 81 ml/m2. On Bonferroni correction, the iEDV in the cardiomyopathy was significantly higher than the MI and normal CMR categories.
LV ejection fraction
The mean left ventricular ejection fraction (LVEF) for the entire cohort was 61%. On Bonferroni correction, the LVEF in the cardiomyopathy was significantly lower than the MI, myocarditis, and normal CMR categories. In addition, the LVEF in the myocarditis category was significantly lower than the normal CMR category.
Overall, 39% of patients had RWMA. The normal CMR category had RWMA secondary to bundle branch block on ECG.
The overall prevalence of focal myocardial edema was 34% based on T2 STIR or early gadolinium enhancement. Focal myocardial edema was absent in patients with normal CMR. Additional analysis of the normal CMR cohort revealed no evidence of diffuse myocardial injury in any of the patients.
LGE was present in 58% of the entire cohort. Six percent of patients with normal CMR had evidence of LGE in the LV/RV insertion points only, which currently is considered a nonspecific finding.
Cardiomyopathy subgroup analysis
In the cardiomyopathy group, 43% had Takotsubo cardiomyopathy, 29% dilated cardiomyopathy, and 18% hypertrophic cardiomyopathy. The remaining had infiltrative cardiomyopathy (amyloidosis; n = 4), hypertensive heart disease (n = 4), and valvular heart disease (n = 2) and were grouped as other. There was no statistically significant difference in the mean age and presentation as STEMI; however, there was a significant difference in sex among the different cardiomyopathy subgroups. There was also a significant difference in the CMR parameters among the different cardiomyopathy subgroups (Table 3).
Treatment before CMR
Aspirin, other antiplatelets, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, beta-blocker, and statin use in the overall cohort was 93%, 61%, 66%, 65%, and 57%, respectively. There was no significant difference in the use of medications among the different diagnostic categories (Table 4).
Prognosis in different CMR categories
In a median follow-up of 1,262 days (3.5 years), the overall all-cause mortality was 5.7%, with worst prognosis identified in the cardiomyopathy group (15% mortality). The mortality rate in the different groups was: cardiomyopathy 15%; MI group 4%; myocarditis group 2%; and normal 2% (p = 0.001).
Kaplan-Meier curves were drawn showing the risk of mortality according to the different CMR diagnoses, showing a strong association between CMR categories and mortality (log-rank test: 19.9; p < 0.001) (Figure 4A). An additional Kaplan-Meier curve was drawn for Takotsubo cardiomyopathy, showing a significantly higher mortality in Takotsubo group compared with any other diagnosis (log-rank test: 7.3; p = 0.011) (Figure 4B).
Predictors of all-cause mortality
Age, presentation with ST-segment elevation on ECG, iEDV, log troponin, LVEF, and CMR diagnosis of cardiomyopathy were significant univariable predictors of mortality (p < 0.05 considered significant for univariate analysis). In a multivariable model, only CMR diagnosis of cardiomyopathy (hazard ratio: 3.0; 95% confidence interval: 1.08 to 8.37; p = 0.034) and ECG presentation with ST-segment elevation (hazard ratio: 3.10; 95% confidence interval: 1.27 to 7.68; p = 0.013) remained significant (Table 5).
Mortality risk markers (ECG presentation with ST-segment elevation + CMR diagnosis)
A risk assessment tool for predicting mortality was constructed on the basis of 2 variables: CMR diagnosis of cardiomyopathy and ECG presentation with ST-segment elevation. The first group was defined as 242 patients with any other CMR diagnosis except cardiomyopathy and presentation as NSTE-ACS. The second group consisted of 122 patients with only 1 of the factors altered (i.e., either a CMR diagnosis of cardiomyopathy or ECG presentation with ST-segment elevation). Finally, the third group included 24 patients with CMR diagnosis of cardiomyopathy and ECG presentation with ST-segment elevation. The mortality rates in these 3 groups were 1.6% (4 of 242), 10.6% (13 of 122), and 20.8% (5 of 24), respectively. Kaplan-Meier curves were drawn showing the risk of mortality in these 3 groups, showing a strong association between number of risk markers and mortality (log-rank test: 23.6; p < 0.001) (Figure 5).
Post hoc power calculation
Using mortality of 15% in the cardiomyopathy group versus 3% for the rest of the cohort with an alpha of 0.05, our study demonstrated 95% power.
This is the largest cohort to date of patients with MINOCA assessed with CMR, and the first study to our knowledge to assess the prognostic role of CMR and conventional risk factors in patients with MINOCA. The main findings are as follows: 1) CMR can identify a diagnosis in 3 of 4 patients presenting with MINOCA and suitable for CMR assessment; 2) CMR diagnosis of cardiomyopathy (imaging) and ECG presentation with ST-segment elevation (conventional risk marker) were the strongest predictors of mortality; and 3) a combined risk assessment tool using the 2 parameters (cardiomyopathy and ECG presentation with ST-segment elevation) provides further risk stratification in these patients.
Diagnostic role of CMR in MINOCA
It is important to identify a cause for MINOCA to guide ongoing management and provide patient guidance. As a noninvasive imaging technique, CMR (done at a median of 37 days from presentation) is able to identify a diagnosis in these patients in up to 3 of 4 cases. The diagnostic role of CMR in this patient group has been demonstrated in a small number of previous studies with smaller sample sizes (11–17); however, the diagnostic yield of CMR in the literature was disparate, ranging from as low as 30% to as high as 90% (11–17). The variation in the diagnostic yield in the literature can be explained by the use of incomplete CMR protocol (edema imaging was not always included) as well as the timing of the test, which sometimes occurs several months after the acute event, leading to the resolution of the reversible cardiac abnormalities (13,18).
In our cohort, the most common diagnosis was MI (25%, n = 97), closely followed by myocarditis (25%, n = 96) and cardiomyopathy (25%); however, the literature suggests that myocarditis is much more common than MI (10–13,15), contrary to our result. The mean age in our study was much higher compared with the other studies on MINOCA, which may have contributed to the higher prevalence of MI (14,15). Another possible explanation could be the use of established criteria (Lake Louise Criteria) for diagnosing myocarditis (26), in addition to an inclusion cutoff of <50% coronary artery stenosis (10–15).
Prognostic role of CMR in MINOCA
Of all the CMR parameters examined (including LV, LV, and LV mass; myocardial edema; LGE; and the overall CMR diagnosis), a CMR diagnosis of cardiomyopathy was associated with the worst prognosis (15% mortality). On a multivariable analysis involving both traditional markers and CMR characteristics, CMR-derived diagnosis of cardiomyopathy remained significant as an independent predictor of mortality.
Among the other CMR parameters assessed, LVEF and LV indexed end-diastolic volume were significant univariable predictors of mortality, but not in multivariable analysis. These findings are particularly useful in justifying the role of CMR tissue characterization in MINOCA.
The cardiomyopathy group in our study was a heterogenous group, with Takotsubo cardiomyopathy being the most common (43% of the cardiomyopathy group). Takotsubo cardiomyopathy had the worst prognosis over a median follow-up of 3.5 years (15% overall mortality) when compared with any other CMR diagnosis. The findings are comparable to the recent study by Templin et al. (21) in which Takotsubo cardiomyopathy had a mortality of 5.6% per patient-year in long-term follow-up. CMR not only helps diagnose, it may also help identify the high risk Takotsubo cardiomyopathy cases by delineating the amount of myocardial edema, RV involvement, thrombus, and LV outflow tract obstruction. CMR-derived apico-basal myocardial edema gradient may be used as a marker of malignant arrhythmia risk (28).
Conventional risk factors for prognosis assessment
Of all the risk factors assessed, ECG presentation with ST-segment elevation was an independent predictor of mortality. Age and log-peak troponin were univariable predictors of mortality, but not in multivariable analysis. Gender was not associated with mortality. The finding on peak troponin is particularly important because it is in contrary to the regular practice. High peak troponin level is often used as an arbitrary prognostic marker because of its evidence from ACS trials (29). The importance of the presentation ECG is a novel finding because it is often overlooked while managing patients with MINOCA.
Our findings strengthen the evidence that CMR is a clinically relevant noninvasive imaging modality for the assessment of patients presenting with MINOCA. In a previous study, we demonstrated that CMR in MINOCA leads to a change in diagnosis in 54% and change in management in 41% of patients (18). The current study reinforces the effect of CMR because a diagnosis of cardiomyopathy is associated with worst prognosis. Any other diagnosis except cardiomyopathy had a relatively low mortality (2% to 4%), thereby putting patients in a good prognostic category.
Currently, there is no risk stratification algorithm for patients presenting with MINOCA. The results of our study suggest that ECG at presentation and CMR diagnosis might be useful predictors for risk stratification. This should be explored further and confirmed in larger multicenter studies.
Several limitations merit consideration. This is a single-center study with relatively limited sample size. Although our study was designed to represent a real-world population, we potentially might have excluded higher-risk patients with contraindications to CMR (e.g., creatinine clearance <30 ml/min, intracardiac devices). Our study did, however, include a broad range of consecutive patients with MINOCA from a large catchment area, and only a limited number (2%) of patients were excluded from CMR. There may have been a referral bias because the study included patients with MINOCA, referred for a CMR by the physician providing the care; however, our regular clinical practice at the Bristol Heart Institute includes CMR in patients presenting with MINOCA. The CMR was performed at a median of 37 days from presentation; this may have affected the diagnostic pickup rate as well as the prevalence of myocardial edema because not all patients were imaged in the acute phase. Nevertheless, our study showed a significant prognostic effect irrespective of the timing of scan. Also, newer mapping techniques were not performed in this patient cohort. The normal CMR group had few patients with bundle branch block and LGE in the insertion points, which may not be classed as entirely normal; however, the presence of diffuse myocardial injury was excluded on the basis of both the early gadolinium enhancement and T2-weighted images analysis. Last, myocardial biopsy was not carried out in these patients; however, well-established and clinically validated CMR criteria were used for the diagnosis of individual cases.
In a large cohort of patients with MINOCA, CMR (median 37 days from presentation) established a diagnosis in almost 3 of 4 cases. Among the conventional risk factors and CMR characteristics, ST-segment elevation on presentation ECG and CMR diagnosis of cardiomyopathy were independent predictors of mortality. Combined analysis of CMR diagnosis and ECG at presentation may allow stratification of patients with poor outcomes.
COMPETENCY IN MEDICAL KNOWLEDGE: CMR (median 37 days from presentation) enabled establishing a diagnosis in 74% of patients presenting with MINOCA. Patients presenting with ST-segment elevation on ECG and CMR diagnosis of cardiomyopathy have worse prognoses.
TRANSLATIONAL OUTLOOK: MINOCA is common and often represents a clinical dilemma. Current ESC/American College of Cardiology guidelines suggest some diagnostic tests, but there is no recommended workup and management of MINOCA. CMR is useful for both diagnosis and prognostication in MINOCA. A large multicenter prospective trial is warranted to confirm these results and thereby enable a tailored treatment strategy in this heterogeneous cohort.
The authors thank Chris Benny Lawton (superintendent radiographer) and the team of cardiovascular magnetic resonance radiographers in the Bristol Heart Institute for their help in acquiring the cardiovascular magnetic resonance studies. They also thank Alan Davies, clinical data manager at UHBristol NHS Foundation Trust, for providing the mortality data.
Dr. Bucciarelli-Ducci is supported by the National Institute of Health Research Biomedical Research Centre at University Hospitals Bristol NHS Foundation Trust and the University of Bristol and is a consultant for Circle Cardiovascular Imaging. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research, or the Department of Health and Social Care. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- acute coronary syndrome
- cardiac magnetic resonance
- indexed end-diastolic volume
- late gadolinium enhancement
- left ventricular
- left ventricular ejection fraction
- myocardial infarction
- myocardial infarction with nonobstructed coronary artery
- non-ST-segment elevation-acute coronary syndrome
- right ventricular
- regional wall motion abnormality
- ST-segment elevation myocardial infarction
- short tau inversion recovery
- Received June 6, 2018.
- Revision received December 3, 2018.
- Accepted December 14, 2018.
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