MINOCA

Late gadolinium enhancement (LGE) facilitates the measurement of myocardial damage, with the capability to detect infarcted myocardium as small as 1 g. The presence of LGE in the subendocardium signifies an ischemic injury, even though it doesn’t specify the underlying mechanism.

• Atherosclerotic Causes

Include unstable nonobstructive plaques (plaque rupture or plaque erosion) with spontaneous autolysis of the associated intracoronary thrombus.

Fig 2: Ulcerated atherosclerotic plaque / vasospasm. Patient, 61 years old, with a history of nephropathy due to obstructive uropathy, with chronic kidney disease on a regular hemodialysis program since December 2021. Admitted for severe acute myocardial infarction, without ST elevation, with normal coronary angiography. Cardiac short-axis (A) and long-axis (B) LGE images. Small area of late gadolinium enhancement in the anterior basal subendocardial myocardium, with a distribution compatible with areas of focal ischemic fibrosis. In the absence of significant stenotic atherosclerotic disease of the anterior descending coronary artery, the differential diagnosis of vasospasm or an ulcerated atherosclerotic plaque is raised (an atherosclerotic calcified plaque is identified in the previous CT in the DAp/m).

• Non-atherosclerotic Causes of MINOCA

Include epicardial and microvascular coronary spasm, SCAD and distal coronary embolism/thrombosis.

Fig 3: Microvascular obstruction. A 57-year-old patient presents with oppressive retrosternal pain radiating to the upper limbs, increased troponin values and negative invasive coronary angiography. A: Short axis T2- weighted short-tau inversion recovery image, a transmural hyperintense areas with central hypointensity is seen in the inferior wall (arrowhead); B: Late gadolinium enhancement image: the hypointense areas correspond with areas of microvascular obstruction and is thought to represent myocardial hemorrhage (arrows); The cardiovascular magnetic resonance study is in accordance with acute myocardial infarction with sign of microvascular obstruction and hemorrhage.

Fig 4: Distal coronary embolism/thrombosis. A 66-year-old self-employed man with risk factors including obesity, dyslipidemia, hypertension, and smoking was admitted in January 2024 with a diagnosis of MINOCA. A - Normal angiography of the right coronary artery; B - Focal transmural enhancement in the inferior/septal apical segment (arrow); C - The previous finding corresponds to a focal area of edema in the T2 sequence (arrow). Its distribution and morphology suggest a small focal myocardial infarction, with the culprit likely being a distal septal coronary branch, probably a distal branch of the right coronary artery or left anterior descending artery.

MINOCA Mimics

• Acute Myocarditis

In the context of myocarditis, the patterns discerned through CMR typically manifest as intra-myocardial or subepicardial LGE. Distinct from the subendocardial or transmural enhancement seen in ischemic etiologies. During the acute phase, the myocardium may exhibit significant oedema, which could lead to a temporary increase in wall thickness. Additional supportive indicators, such as the presence of pericardial effusion and abnormalities in the left ventricular (LV) wall motion, may also be observed.

Fig 5: Myocarditis. Male, 43 years old. Presents with chest pain after a flu-like prodrome of 5 days. Troponin elevation up to 492 ng/L. Slight ST elevation in aVL. Coronary angiography without changes. A - 4 chamber view, observing several foci of intramural enhancement in the free ventricular wall. B - cardiac short axis with intramural enhancement (arrow) corresponding to a small area of hyperintensity in T2 weighted sequence (Arrow). Aspects compatible with acute myocarditis.

• Takotsubo's Syndrome

Takotsubo’s Syndrome (TTS) is a type of acute systolic heart failure that is frequently precipitated by a physical or emotional event. This occurs in the absence of an obstructive lesion in the epicardial coronary artery. The left ventricular (LV) regional wall motion abnormalities seen in TTS typically surpass the area supplied by a single epicardial coronary artery, exhibiting a circumferential pattern that does not correspond to the epicardial coronary distribution. The most commonly observed anatomical variant is known as “apical ballooning.” This is characterized by hypo/akinesianof the apical region and compensatory hyperkinesia of the basal region.

Fig 6: Apical ballooning. A 58-year-old woman with chronic kidney disease due to autosomal dominant polycystic kidney disease. Undergoing hemodialysis. Sudden typical chest pain with nausea and vomiting. Coronary angiography without changes. In the CMR, hyperdynamic basal segments and concentric hypokinesia of the mesoapical segments are visualized, associated with myocardial edema of the apical segments, compatible with apical Takotsubo cardiomyopathy.

It is common for patients with TTS to exhibit transmural myocardial edema, as seen on T2-weighted imaging, which is associated with the dysfunctional segments.

Fig 7: Myocardial edema in Takotsubo. Two-chamber view of the long cardiac axis showing T2 hyperintensity in a patient with basal hypokinesia and no appreciable late myocardial enhancement. Aspects compatible with Takotsubo.

• Hypertrophic Cardiomyopathy 

In patients with hypertrophic cardiomyopathy, it is common for CMR to reveal an increased signal in T2-weighted imaging. This is indicative of myocardial edema, which is often a secondary response to ischemic changes that occur due to microvascular dysfunction. CMR also has the advantage of being able to measure LV wall thickness with precision.

Fig 8: Hypertrophic Cardiomyopathy. Patient, 88 years old, partially dependent, with high blood pressure, mild aortic stenosis, atrial fibrillation, diabetes mellitus, dyslipidemia. Hospitalized after cardiac arrest with elevated troponins. Underwent coronary angiography without changes. A - Asymmetric left ventricular hypertrophy with septal predominance with a maximum thickness of 27 mm. Image B and C - Area of late gadolinium enhancement transmural with segmental morphology of the anterior/septal apical segment suggesting a small acute myocardial infarction

• Pericarditis 

Acute pericarditis frequently resembles acute coronary syndrome because of their similar symptoms, the occurrence of ischemic ECG changes, and the potential rise in troponin levels. In patients with pericarditis, CMR reveals thickened pericardial layers and pericardial effusion, which can be seen on T1-weighted CMR or cine imaging. Additionally, T2-weighted imaging shows edema in the inflamed pericardium, which is associated with pericardial enhancement on LGE sequences.

Fig 9: Pericarditis. Patient presents with pleuritic chest pain, troponin elevation, T wave inversion V2-V5, and increased PCR. EchoTT without segmental changes and preserved LVEF with slight pericardial effusion. A - two-chamber view LGE. B - short cardiac axis LGE. Pericardium with regular diffuse thickening with linear gadolinium enhancement arrow.

• Cardiac Sarcoidosis

Cardiac sarcoidosis, a systemic granulomatous disease, can manifest as chest pain, ischemic ECG alterations, and ventricular arrhythmias. Typical CMR characteristics include septal thinning, ventricular enlargement, systolic impairment, and pericardial effusions. A non-ischemic LGE pattern is often observed, predominantly affecting the anteroseptal and inferolateral walls, but other segments, including the right ventricle, can also be involved. Notably, the existence of LGE is acknowledged as a mortality and ventricular arrhythmia risk factor, even in patients maintaining a normal ejection fraction.