The Role of Cardiac Magnetic Resonance in Myocardial Infarction and Non-obstructive Coronary Arteries

Abstract

Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA) accounts for 5-15% of all presentations of acute myocardial infarction. The absence of obstructive coronary disease may present a diagnostic dilemma and identifying the underlying etiology ensures appropriate management improving clinical outcomes. Cardiac magnetic resonance (CMR) imaging is a valuable, non-invasive diagnostic tool that can aide clinicians to build a differential diagnosis in patients with MINOCA, as well as identifying non-ischemic etiologies of myocardial injury (acute myocarditis, Takotsubo Syndrome, and other conditions). The role of CMR in suspected MINOCA is increasingly recognized as emphasized in both European and American clinical guidelines. In this paper we review the indications for CMR, the clinical value in the differential diagnosis of patients with suspected MINOCA, as well as its current limitations and future perspectives.

Keywords: MINOCA; Takotsubo syndrome; cardiac MRI; myocardial injury; myocardial ischemia; myocarditis; non-obstructive coronary arteries.

Conflict of interest statement

CB-D was the CEO (part-time) of the Society of Cardiovascular Magnetic Resonance and has received speakers fees from Circle Cardiovascular Imaging, Bayer and Siemens Healthineers. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Copyright © 2022 Liang, Nakou, Del Buono, Montone, D'Amario and Bucciarelli-Ducci.

Figures

Figure 1

74-year old male presented with chest pain and troponin rise with lateral T-wave inversion on electrocardiogram. Invasive coronary angiography demonstrated non-obstructed coronary arteries. CT pulmonary angiography was also negative for pulmonary embolus. A Cardiac MRI demonstrated evidence of myocardial infarction with typical ischemic pattern of subendocardial late gadolinium enhancement (LGE) [white arrows, (A1–A3): 4 Chamber, 2 Chamber, 3 Chamber, (B) short axis] in the apical inferior and lateral segments. Areas of high signal on T2-STIR imaging (C) and T2-mapping (D) correlating to the area of infarction from LGE imaging and the ECG abnormalities, suggesting acute myocardial edema due to acute myocardial injury.

Figure 2

33-year-old presented with troponin positive chest pain and inferior ST elevation on ECG. He reported recent flu-like symptoms following mRNA COVID-19 vaccination. (A) is the post-contrast steady state free precession (SSFP) cine showing a bright signal intensity in keeping with myocardial oedema due to acute myocardial injury, which is also in keeping with the T2-STIR imaging (B) and T2 mapping (D) images which demonstrate high signal intensity in the mid lateral wall correlating with subepicardial late enhancement on gadolinium imaging (C). The pattern of myocardial injury noted is in keeping with acute myocarditis. The areas of abnormalities are indicated by white arrows.

Figure 3

90-year-old patient presenting to the emergency department with chest pain, ST segment elevation in the anterior leads at electrocardiogram and elevated troponin levels. Urgent coronary angiography excluded obstructive coronary artery disease. Three Tesla cine Steady-State Free Precession sequence (SSFP) CMR showed akinesis of the apical segments with hypercontractility of the basal segments (A), absence of LGE (B) and elevated native T1 mapping [1,400–1,550 msec (local reference range: 1,086–1,292 msec)] (C) and elevated T2 mapping values [50–55 msec (local reference range: 30–45 msec)] (D) in correspondence with the area of apical akinesia. Based on the clinical context and imaging findings, the patient was diagnosed with apical ballooning in the context of Takotsubo syndrome.

Figure 4

CMR findings in a 76 year old man with asymmetric hypertrophic cardiomyopathy who presented with atypical chest pain and non-sustained ventricular tachycardia on a recent ECG-Holter. (A1–A3) Steady-state free precession sequence (SSFP) cine imaging showing asymmetrical hypertrophy of the basal anterior wall and mild apical hypertrophy (white arrows). (B1–B3) Stress perfusion images showing inducible microvascular dysfunction of the hypertrophic basal anterior wall and mid-cavity and apical inferior wall (white arrows). (C1, C2) Late gadolinium enhancement imaging (LGE) showing patchy myocardial fibrosis of the hypertrophied segments (white arrows). (C3) Native T1 mapping (basal short axis view). Increased native T1 values (yellow arrow) in the basal anterior and basal anteroseptal walls (1,170 msec, normal range 1,000 ± 50 msec) matching the patchy LGE noted in panels (C1, C2).

Figure 5

The role of CMR in non-ischemic cardiomyopathies mimicking MINOCA. CMR findings in a patient with known cardiac sarcoidosis presenting with chest pain. (A) Steady state free precession sequence (SSFP) cine sequence 4 chamber (end-systole) showing preserved ventricular systolic function (B) T2 mapping (basal segments) showing high T2 values (arrow) in the basal anterior wall (T2 = 62 ms, normal values T2 < 55 ms at 1.5 T) suggestive of myocardial oedema. (C, D) Late gadolinium enhancement imaging (LGE) at the level of basal segments demonstrating prominent subepicardial to mid wall enhancement in the basal anteroseptum and anterior wall extending into the adjacent right ventricular anterior wall (arrows). The pattern of myocardial injury noted is in keeping with acute cardiac involvement in sarcoidosis.