Abstract
Introduction
Identifying an Infarct-related artery (IRA)in Non-STEMI is sometimes tricky. Besides, myocardial infarction with non-obstructive coronary arteries (MINOCA) mimickers are often labeled as myocardial infarction. Late Gadolinium enhancement (LGE) on cardiac MRI can help in identifying IRA besides MINOCA mimickers.
Aims
To study the role of LGE on cardiac MRI(CMR) in NSTEMI.
Material Methods
It was a prospective observational, double-blinded study. 70 NSTEMI patients were prospectively enrolled over two years. CMR was done before coronary angiography (CAG) during the index hospitalization. Matching was done between IRA selected by CAG and IRA as determined by LGE on MRI.
Results
Mean age was 58 ± 15 years. CAG could not identify IRA in 38.6% (n = 27) patients. In this patient group, LGE-CMR identified IRA in 48.1% (n = 13) & a new non-CAD diagnosis was identified in 18.5% (n = 5) patients. IRA was identified in 61.4% (n = 43) by CAG & in this patient group, LGE-CMR identified a different IRA in 6.9% (n = 3) patients. LGE-CMR also identified a new non-CAD diagnosis in 11.6% (n = 5) of patients from this group. Overall, LGE-CMR led to a new IRA diagnosis in 23% (n = 16) patients & a diagnosis of non-ischemic pathogenesis in 14% (n = 10) patients. Non-Ischemic diagnosis on CMR included stress cardiomyopathy in 3, myocarditis in 6, and infiltrative disorder in 1 patient.
Conclusion
CMR leads to new IRA diagnoses or non-ischemic pathogenesis in one-third of the cohort.
Keywords: Infarct-related artery, Late gadolinium enhancement, Non-ischemic
Abbreviations
- NSTEMI
Non ST Elevation Myocardial Infarction
- CT
Computerized tomography
- MRI
Magnetic resonance Imaging
- CAD
Coronary artery disease
- STEMI
ST elevation Myocardial infarction
- ECG
Electrocardiography
- IRA
Infarct Related Artery
- RCA
Right Coronary artery
- LCX
Left circumflex artery
- MINOCA
Myocardial infarction with non-obstructed coronary arteries
- LGE
Late gadolinium enhancement
- URL
Upper reference Limit
- CABG
Coronary artery bypass graft
- CAG
Coronary angiography
- BSA
Body surface area
- GFR
Glomerular filtration rate
- MI
Myocardial Infarction
- ANOVA
Analysis of variance
- CKD
Chronic Kidney Disease
- ACEI
Angiotensin Convertin Enzyme Inhibitors
- ARBS
Angiotensin Receptor Blockers
- CCBs
Calcium channel blockers
- LVEF
Left Ventricular ejection fraction
- SVD
Single Vessel disease
- 2VD
Two vessel Disease
- MVD
Multivessel Disease
1. Introduction
Non-ST Elevation Myocardial Infarction (NSTEMI) represents a heterogeneous group of patients with lesions ranging from normal coronary arteries to severe multivessel disease. Various non-invasive testing modalities for evaluating these patients are Electrocardiography (ECG), biomarkers, early stress testing, echocardiography, coronary CT Angio & Cardiac MRI.
In NSTEMI, identifying the Infarct related artery (IRA) can be challenging because patients are more likely to present with either multivessel coronary artery disease (CAD) or insignificant CAD.1 Unlike STEMI, where Electrocardiography (ECG) localization of the primary IRA is quite reliable, it is difficult to localize the IRA in NSTEMI patients by ECG, especially when the ischemic changes are present in the inferior leads only.2 Echocardiography is suboptimal in NSTEMI patients with subendocardial infarctions involving <20% of the wall thickness.3 In addition, multivessel CAD, seen in up to 55% of NSTEMI patients, have echocardiographic abnormalities in multiple perfusion territories; patients with previous infarction & overlapping perfusion territories of RCA & LCX can make localization of the IRA difficult on echocardiography. Coronary CT angio can recognize or exclude the presence of epicardial CAD & help identify the diseased vessel(s). Still, it comes with its attendant radiation toxicity in comparison to CMR. CMR generates high-resolution maps of infarcted myocardium and is considered an in vivo gold standard for imaging MI(myocardial infarction). Previous studies have shown that cardiac MRI effectively determines the presence, location, and extent of MI in acute and chronic settings.4, 5, 6
Myocardial infarction with non-obstructed coronary arteries (MINOCA) accounts for about 5–15% of all patients presenting with acute myocardial infarction (MI) undergoing invasive coronary angiography.7, 8, 9, 10Accurate identification of MINOCA, or alternative diagnosis in patients presenting with myocardial injury and unobstructed coronary arteries, significantly impacts both acute and chronic clinical management and outcomes. CMR allows high accuracy to differentiate between true MINOCA and MINOCA mimics (myocarditis, Takostubo cardiomyopathy).11
The late gadolinium enhancement (LGE) technique is crucial in determining if myocardial damage is ischemic or non-ischemic. Only one study so far has studied IRA localization in NSTEMI by LGE on CMR.12 We designed this study to evaluate the role of cardiac MRI in localizing IRA in NSTEMI and assess its role in identifying MINOCA mimics.
2. Methods
70 NSTEMI patients were prospectively enrolled over two years. Informed consent was taken from all the patients & the institutional ethics/review board approved the study. NSTEMI was defined as per the third universal definition of MI, i.e., evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia (typical chest discomfort or angina equivalent) & absence of ST-segment elevation. Myocardial necrosis was detected by rise &/or fall in cTn (Troponin) by conventional assays with at least one value above the 99th percentile URL. High-sensitivity troponins were not used in the study.
2.1. Exclusion criteria
All the NSTEMI patients were included in the study except patients with prior Myocardial Infarction, prior Coronary artery bypass graft (CABG), hemodynamic Instability, need for urgent coronary revascularization, GFR <30 ml/min/1.73m2 BSA, contraindication for coronary angiography (CAG) &/or Cardiac MRI (CMR) & a substantial likelihood of non-ischemic pathogenesis.
2.2. Study design
All included patients were subjected to comprehensive history, physical examination & serial evaluation of troponins. CMR was done before CAG during the index hospitalization; however, the results were not used for clinical decision-making. It was a prospective observational, double-blinded study whereby the interventional cardiologist was informed about the diagnosis of NSTEMI but was blinded to the patient's identity & CMR results.
2.3. Cardiac MRI(CMR)
CMR was performed on a 1.5T scanner. LGE images were taken using a segmented inversion-recovery gradient-echo sequence 10–15 min after an intravenous bolus of 0.15 mmol/kg body weight of gadolinium contrast (gadolinium diethylenetriamine penta-acetic acid). Cine images were taken in multiple short-axis & long-axis views using a steady-state free-precession sequence. The presence & location of hyper-enhanced tissue was determined by visual inspection using the conventional American Heart Association 17-segment model.13 In addition, the hyperenhancement pattern was assessed to classify myocardial damage as consistent with MI or various non-ischemic disorders.14, 15, 16
2.4. Coronary angiography
Significant CAD on CAG was defined as >50% luminal narrowing of at least one major epicardial artery.17 The culprit lesion was determined based on the interventionalist's experience. The interventional cardiologists were blinded to CMR results.
2.5. Matching
The myocardial perfusion territory supplied by the IRA as identified by CAG was mapped onto a standard 17-segment model. The IRA perfusion territory was localized to up to half of the LV myocardium by selecting ≤8 segments on the 17-segment model.12 The IRA by CAG was considered to match the CMR if the number of segments with hyperenhancement within the CAG IRA perfusion territory was greater than or equal to the number of segments with hyperenhancement outside the CAG IRA perfusion territory.18 Further, if the hyperenhancement consistent with MI was found in ≥2 separate coronary artery territories, a match with CAG was considered present if either of the hyperenhancement territories met the above criteria. This method was used rather than the assignment of fixed territories for coronary arteries to account for variations in left/right dominance.
2.6. Statistical analysis
Continuous data were expressed as mean ± Standard deviation. Comparisons of continuous data between groups were made using a 1-way or 2-way ANOVA test as appropriate. The chi-square test was used for group comparisons of discrete data. All statistical tests were 2-tailed, and a p value < 0.05 was taken as significant.
3. Results
3.1. Baseline characteristics
The baseline characteristics of the population are described in Table 1. The mean age of the entire cohort was 58 ± 15 years. The most common risk factor in our study population was hypertension in 58.6% (n = 41) patients, followed by smoking & dyslipidemia in 44.3% (n = 31) & 41.4% (n = 29) patients, respectively. Hypertension was detected first time in 26.8% (n = 11) patients from our study group after hospitalization for NSTEMI, whereas the remaining 73.2% (n = 30) patients were on some form of antihypertensive treatment before admission. 28.6% (n = 20) of patients had diabetes. In addition, 20% (n = 14) patients had a family history of CAD in first-degree relatives. 2.9% (n = 2) patients had CKD; however, their eGFR was >30 ml/min/1.73 m2 BSA, which was our exclusion criteria & who gave informed consent for both invasive CAG & LGE-CMR. 1.4% (n = 1) of patients had a history of Ischemic stroke. Overall, 34.3% (n = 24) of patients in our study were on statins. 30% (n = 21) were on beta-blockers, and 20% (n = 14) were on aspirin. 14.3% (n = 10) patients were on ACE-I/ARBs & 7.4% (n = 8) were on CCBs. ECG, troponins & echocardiography were done at admission in all the patients.100% (n = 70) of patients had positive troponins done by the qualitative method. 71.4% (n = 50) patients had ST depressions >0.5 mm, whereas 28.6% (n = 20) patients did not have any >0.5 mm ST depressions & there were only non-diagnostic ST/T changes in this patient group. Mean LVEF done by Simpson's biplane method on echocardiography done was 49 ± 10% in the entire group & it was 47 ± 7% & 51 ± 6% in the group where CAG identified IRA & where IRA was not identified by CAG respectively.
Table 1.
Baseline Characteristics of patients.
| Characteristics | Entire group (n = 70) | IRA identified by CAG (n = 43) | IRA not identified by CAG (n = 27) | p value |
|---|---|---|---|---|
| Age (yr) | 58 ± 15 | 60 ± 13 | 57 ± 14 | >0.05 |
| Male gender | 60% (n = 42) | 60.5% (n = 26) | 59.3% (n = 16) | 1.0 |
| Diabetes mellitus | 28.6% (n = 20) | 32.6% (n = 14) | 22.2% (n = 6) | 0.422 |
| Hypertension | 58.6% (n = 41) | 65.1% (n = 28) | 48.1% (n = 13) | 0.214 |
| Active smoking | 44.3% (n = 31) | 39.5% (n = 17) | 51.9% (n = 14) | 0.335 |
| Dyslipidemia | 41.4% (n = 29) | 41.9% (n = 18) | 40.7% (n = 11) | 1.0 |
| Family history of CAD | 20% (n = 14) | 20.9% (n = 9) | 18.5% (n = 5) | 1.0 |
| CKD | 2.9% (n = 2) | 2.3% (n = 1) | 3.7% (n = 1) | 1.0 |
| History of CVA | 1.4% (n = 1) | 2.3% (n = 1) | 0.0% (n = 0) | 1.0 |
| Statin | 34.3% (n = 24) | 41.9% (n = 18) | 22.2% (n = 6) | 0.123 |
| Beta-blockers | 30% (n = 21) | 27.9% (n = 12) | 33.3% (n = 9) | 0.789 |
| Aspirin | 20% (n = 14) | 20.9% (n = 9) | 18.5% (n = 5) | 1.0 |
| ACE-I/ARBs | 14.3% (n = 10) | 11.6% (n = 5) | 18.5% (n = 5) | 0.493 |
| CCBs | 7.4% (n = 8) | 16.3% (n = 7) | 3.7% (n = 1) | 0.140 |
(IRA-Infarct related artery,CAD-Coronary artery - disease, CKD-Chronic kidney disease, CVA-Cerebrovascular accident, ACE-I-Angiotension converting enzyme inhibitor, ARB- Angiotension receptor blocker, CCB-Calcium channel blocker).
3.2. Comparison of invasive CAG & LGE-CMR for identification of IRA
CAG could not identify the IRA in 38.6% (n = 27) patients. In this patient group, LGE-CMR identified IRA in 48.1% (n = 13) patients & a new non-CAD diagnosis was identified in 18.5% (n = 5) patients. Further, 33.3% (n = 9) of patients had no enhancement on LGE-CMR. IRA was identified in 61.4% (n = 43) patients by CAG & in this patient group, LGE-CMR identified a different IRA in 6.9% (n = 3) patients. LGE-CMR also identified a new non-CAD diagnosis in 11.6% (n = 5) of patients from this group. 9.3% (n = 4) patients had no enhancement on LGE-CMR. The remaining 72% (n = 31) of patients had the same IRA on CAG & LGE-CMR. Overall, LGE-CMR led to a new IRA diagnosis in 23% (n = 16) patients & a diagnosis of non-ischemic pathogenesis in 14% (n = 10) patients. 18.5% (n = 13) of patients had no enhancement on LGE-CMR. In the entire study group, IRA was identified more frequently by LGE-CMR than by CAG [67.1% (n = 47) vs. 61.4% (n = 43)]. We could not identify the IRA in 38.6% (n = 27) & 32.9% (n = 23) patients by Invasive CAG & LGE-CMR, respectively. The typical images of different subgroups identified are shown in Fig. 1, Fig. 2, Fig. 3, Fig. 4, Fig. 5.
Fig. 1.
Concordant IRA On CAG & LGE-CMR.45 years old male with single vessel CAD, with 2nd Obtuse marginal cut off. LAD & RCA are normal. LGE-CMR image shows enhancement in LCX territory
Fig. 2.
Discordant IRA on LGE-CMR & CAG.65 years old male with tight 90% stenosis in mid LAD on CAG, with non-obstructive plaquing in LCX & normal RCA. LGE-CMR showed transmural enhancement in LCX territory.
Fig. 3.
IRA identified by LGE-CMR in presence of no identifiable IRA on CAG.75 years old female with normal coronaries on CAG has a subendocardial enhancement in anteroseptal & anterior wall on LGE-CMR suggestive of ischemic pathology.
Fig. 4.
Non-CAD diagnosis on LGE-CMR in presence of CAD on CAG. 55 years old male with NSTEMI like presentation having 80% stenosis in mid LAD & normal LCX & RCA on CAG. LGE-CMR shows subepicardial enhancement in anteroseptal & inferoseptal areas suggestive of myocarditis.
Fig. 5.
Non-CAD diagnosis on LGE-CMR in absence of CAD on CAG.41 years old male with a NSTEMI like presentation with CAG showing normal coronaries. LGE-CMR showed subepicardial enhancement in inferoseptal area suggestive of focal myocarditis.
3.3. CAD patterns in our study population
CAG showed single vessel CAD in 22.9% (n =16) patients, two vessel CAD in 21.4% (n =15) patients, multivessel CAD in 18.6% (n =13) patients & non-significant CAD in 37.1% (n =26) patients. Table 2 shows different CAD patterns in our study population & the vessels diseased. Overall, LAD (Left anterior descending) artery was the most common vessel involved, followed by RCA (Right coronary artery) & LCX (Left circumflex) artery. As shown in Table 2, in patients with single vessel & two vessels CAD, CAG selects the IRA in 100% (n =16) of the patients. In patients with multivessel disease, CAG selects IRA only in 53.9% (n =7) patients only. Further, in those with non-significant CAD, CAG selects IRA in only 19.2% (n =5) patients.
Table 2.
Identification of IRA in Single, two vessel and multivessel disease by CAG.
| Parameter | Entire group | IRA selected by CAG | IRA not selected by CAG |
|---|---|---|---|
| Sample size | 70 | 43 | 27 |
| SVD on CAG (LAD = 50% (n = 8), RCA = 31.3% (n = 5), LCX = 18.7% (n = 3) | 16 | 16 | 0 |
| 2VD on CAG (LAD = 40% (n = 6), RCA = 33.33% (n = 5), LCX = 26.67% (n = 4) | 15 | 15 | 0 |
| MVD on CAG (LAD = 100% (n = 13), RCA = 100% (n = 13), LCX = 100% (n = 13) | 13 | 7 | 6 |
| Non-significant CAD on CAG | 26 | 5 | 21 |
SVD: Single vessel Disease, 2VD: Two vessel Disease, MVD: Multivessel Disease, CAD: coronary artery disease, CAG: Coronary angiography. LAD: Left anterior descending artery, LCX:Left circumflex artery, RCA: Right coronary artery.
3.4. CMR in different subgroups (Table 3)
Table 3.
Role of LGE-CMR in different subsets.
| Parameter | IRA identified on CAG | IRA not identified on CAG | Same IRA on LGE-CMR | Different IRA on LGE-CMR | New IRA on LGE-CMR | Non-CAD diagnosis on LGE-CMR | No enhancement on LGE-CMR |
|---|---|---|---|---|---|---|---|
| Total study population (n = 70) | 43 (61.4%) | 27 (38.6%) | 31 (44.3%) | 3 (4.3%) | 13 (18.6%) | 10 (14.3%) | 13 (18.6%) |
| SVD on CAG (n = 16) | 16 (100%) | 0 (0.0%) | 12 (75%) | 0 (0.0%) | 0 (0.0%) | 3 (18.8%) | 1 (6.3%) |
| 2VD on CAG (n = 15) | 15 (100%) | 0 (0.0%) | 10 (66.7%) | 0 (0.0%) | 0 (0.0%) | 2 (13.3%) | 3 (20%) |
| MVD on CAG (n = 13) | 7 (53.8%) | 6 (46.2%) | 5 (38.5%) | 2 (15.4%) | 4 (30.8%) | 1 (7.7%) | 1 (7.7%) |
| Non-significant CAD on CAG (n = 26) | 5 (19.2%) | 21 (80.8%) | 4 (15.4%) | 1 (3.8%) | 9 (34.6%) | 4 (15.4%) | 8 (30.8%) |
SVD: Single vessel Disease, 2VD: Two vessel Disease, MVD: Multivessel Disease, CAD: coronary artery disease, CAG: Coronary angiography. IRA: Infarct related artery, LGE: late gadolinium enhancement, CMR: cardiac magnetic resonance imaging.
In patients with multivessel disease (n =13), CAG identifies IRA only in 53.9% (n =7) patients. However, on CMR,15.4% (n =2) of such patients have a different IRA & 30.8% (n =4) patients have a new IRA while as 5 (38.5%) had same IRA. IRA was not identified in 46.1% (n =6) patients with multivessel disease. Overall, in those with multivessel disease, LGE identified IRA in 11(84.6%) patients vs CAG which selected IRA in 7(53.9%) patients(p =0.08).
Further, it shows that in patients with non-significant CAD (n =26), IRA is identified by CAG in only 19.2% (n =5) patients while as LGE-CMR identified an IRA in 53.84%(n =14).(p =0.009)
3.5. Non-CAD diagnosis
The Non-Ischemic diagnosis of CMR in our study population included stress cardiomyopathy in 3(1 in IRA selected by CAG group and 2 in IRA not selected by CAG group), myocarditis in 6 (3in each group), and infiltrative disorder in 1(in IRA selected by CAG group) patient. There was no enhancement in 13 patients (4 in IRA selected by the CAG group and 9 in IRA not selected by the CAG group).
4. Discussion
Our study showed a significant impact of LGE on CMR in NSTEMI patients. CMR leads to new IRA diagnosis or non-ischemic pathogenesis in one-third of the entire cohort. It helped in identifying IRA in cases where CAG did not select IRA. It also helped correct and identify new IRAs in cases where CAG selected IRA but did not match with LGE. Besides, it helped in identifying non-ischemic etiologies in patients presenting as NSTEMI. Our findings have important therapeutic implications.
The fraction of Acute Coronary syndromes attributed to NSTEMI is increasing while that of STEMI is declining as a result of the more extensive use of preventive measures such as aspirin, statins & smoking cessation, an aging population with a greater prevalence of diabetes & CKD & lower rates of smoking & broader use of high sensitivity troponin assays for myocardial necrosis that shifts the diagnosis from Unstable angina to NSTEMI. Invasive CAG in these patients may reveal a single vessel, double vessel, multivessel, or no significant CAD. As the ECG is not as accurate in NSTEMI as in STEMI for IRA localization, especially in those with patients with multivessel disease, it can be challenging to identify the IRA on invasive CAG.
4.1. Different patterns observed when comparing invasive CAG and LGE-MRI
Briefly, our population was younger (mean age 58 years), with the majority of males. The most common risk factors were hypertension (58%) and smoking (45%). Nearly one-third were diabetics, and 20% had dyslipidemia. The overall LVEF was preserved (49%). We noted the following different patterns when we compared invasive CAG with LGE-CMR: Concordance between IRA on LGE-CMR & CAG: In 61.4% (n = 43) patients where CAG selected an IRA, LGE-CMR found a similar IRA in only 72.1% (n = 31) patients. The rest of the patients either had a different IRA, a non-CAD diagnosis, or no enhancement on LGE-CMR. Discordance between IRA on LGE-CMR & CAG: In 4.3% (n = 3) patients, LGE-CMR identified a different IRA compared to CAG. This was primarily seen in those with multivessel disease. IRA diagnosis by LGE-CMR in the presence of a CAG with no definite IRA: The IRA could not be identified by CAG in 38.6% (n = 27) patients. In this patient group, LGE-CMR identified IRA in 48.1% (n = 13) of patients. This was primarily seen in those with non-obstructive disease on CAG. Non-CAD diagnosis on LGE-CMR in the presence of CAD on CAG: In 7.1% (n = 5) patients, LGE-CMR found a non-CAD diagnosis, despite CAG showing evidence of CAD & in 5.7% (n = 4) patients, LGE-CMR showed no enhancement. Non-CAD diagnosis on LGE-CMR in the absence of CAD on CAG. A new non-CAD diagnosis was found on LGE-CMR in 7.1% (n = 5) of patients without CAD on CAG. 12.9% (n = 9) of patients had no enhancement on LGE-CMR. Our results were comparable to Heitner et al.12 Kerensky RA et al; in the Veterans Affairs Non-Q-Wave Infarction Strategies in-hospital (VANQUISH) trial showed that 37% of patients had no identifiable culprit lesion on invasive CAG. In addition, 14% of patients had multiple apparent culprit lesions.17 McCullough PA et al, in Medicine versus angiography in thrombolytic exclusion (MATE) study, reported that in all ACS patients, including STEMI, NSTEMI & unstable angina, culprit lesions could not be identified in 45% of patients.19 Our study was consistent with it as from our 70 patients, 38.6% (n = 27) had no identifiable IRA on invasive CAG. From these 27 patients, LGE-CMR identified an IRA in 48.1% (n = 13) patients & a new non-CAD diagnosis was identified in 18.5% (n = 5) patients. The patients whose IRA was identified by LGE-CMR & not by CAG were predominantly patients with a non-significant CAD (P = 0.002) or those with multivessel disease.
An analysis of multicentre studies on acute MI reveals that culprit lesions cannot be discerned in up to 15–50 % of cases, the reasons being mainly either multivessel or insignificant coronary artery disease. Our study also emphasizes the fact that identification of IRA in NSTEMI can be challenging. We suggest a possible role of CMR in NSTEMI patients, especially in those with multivessel disease or those with insignificant CAD on CAG. Correctly identifying IRA helps in the timely and correct revascularization of IRA. This would result in favourable immediate and long-term outcomes. There has been considerable debate on whether culprit-only revascularization or complete revascularization is best for NSTEMI patients with multivessel disease, as it may not always be possible to identify IRA on CAG. The benefit of complete revascularization ensures that revascularization of IRA takes place; however, it comes at the cost of longer procedure time, higher contrast volume, and higher periprocedural complications. We suggest that if prior CMRI can correctly identify IRA, the strategy of IRA-only revascularization might have more benefit. We encourage cardiac MRI with LGE in NSTEMI patients reporting to a facility with CMR availability who are stable enough for imaging before Coronary angiography and PCI. However, the authors acknowledge the limitations of the clinical application of our study. Still, the observations made in our research can help us modify our practice in an appropriate clinical setting.
Our study shows the immediate utility of CMRI in identifying IRA in NSTEMI patients, especially in those with multivessel disease or in those with insignificant CAD on CAG. In the NSTEMI patients with cardiogenic shock, refractory angina, and hemodynamic & electrical instability, it is a class I recommendation to follow an immediate invasive strategy & revascularize the patient. In two-vessel or multivessel CAD, it may be challenging to identify the culprit lesion accurately. Our study found that LGE-CMR identified IRA in 48% of those for whom IRA was not identified on CAG. Besides, we also found that in 7% of cases, our subjective assessment of IRA on CAG was erroneous. Thus, CMR can help identify IRA correctly, which can have obvious benefits of immediate correct revascularization. In their study, Heitner et al.12 found that in NSTEMI patients undergoing revascularization, 27% had revascularization solely of the non-culprit coronary arteries as determined by LGE-CMR.12 SMILE20 trial has shown that erroneous identification of culprit IRA leads to worse outcomes.
4.2. Role of CMR in non-ischemic diagnosis
We found that CMR identified non-CAD diagnosis in 14% (10) of patients in the entire cohort. When IRA was not identified on CAG, LGE-CMR identified a new non-CAD diagnosis in 18.5% (n = 5) patients. In the non-CAD diagnosis, stress cardiomyopathy was seen in 4.3% (n = 3), myocarditis in 8.6% (n = 6) patients, Infiltrative disorder in 1.5% (n = 1) patients & 18.6% (n = 13) patients had no enhancement on LGE-CMR. Studies have shown that the prevalence of MINOCA is 6%, with patients more likely to be younger & of the female gender. The underlying pathophysiology responsible for MINOCA includes the presence of a typical myocardial infarct on cardiac MRI in only 24% of patients, with myocarditis occurring in 33% & no significant abnormality in 26%. Coronary artery spasms in 27% of patients & thrombophilia disorders were detected in 14%.21 This emphasizes that non-significant CAD on invasive CAG can still be a typical myocardial infarct, as seen in our study. Our study showed that 50% (n = 13) of the patients with non-significant CAD on CAG had a typical myocardial infarct demonstrated on LGE-CMR. The patient may have a non-CAD diagnosis as well. Codreanu A et al; showed that non-ischemic pathogenesis exists in an otherwise NSTEMI-like presentation in 44% of patients presenting with ACS & no coronary stenosis on CAG.22 Further, Assomull RG et al; studied the role of CMR in patients with chest pain, raised troponins & unobstructed coronary arteries. From a sample size of 67, they were able to establish an identifiable cause of troponin elevation in 65% of patients, which included myocarditis in 50%, MI in 11.6% & cardiomyopathy in 3.4% of patients.23 We emphasize that non-CAD diagnosis in an NSTEMI-like presentation is not a rarity & LGE- CMR can help identify it & appropriate treatment is instituted.
4.3. Limitations
It was a single-center study. IRA identification on CAG was dependent on the interventionist's experience. However, the interventionist who read those CAGs were highly experienced high-volume operators. There is a possibility of misregistration as our definition of match relied on mapping the perfusion territory onto a 17-segment standard model. However, this matching system has been validated in international multicentre trials18. Another limitation is that we don't have the follow-up data of patients who did or did not undergo revascularization of the culprit artery as determined by CMR.
5. Conclusion
Cardiac MRI in NSTEMI patients leads to new IRA diagnosis besides elucidating new non-ischemic diagnoses in one-third of the cohort. This was mainly in cases with a non-obstructive disease on coronary angiography where identifying Infarct related artery (IRA) can be challenging. LGE on CMR can help in accurately identifying IRA, which in turn helps in appropriate revascularization of culprit vessels and avoids inappropriate revascularization, which has substantial short-term and long-term impacts on patient outcomes. Besides, LGE also helps in non-CAD diagnosis (Myocarditis, Stress cardiomyopathy), which helps in appropriate treatment.
Ethics approval and consent to participate
Ethical approval was taken from the Sherikashmir Institute of Medical sciences,Institute ethical committee.(IEC /SKIMS).
Funding
No funding received.
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgements
No acknowledgement.
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