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A Challenging and Unexpected Case of MINOCA Using Multimodality Imaging

We describe a challenging case of a patient with MINOCA due to isolated right ventricular myocardial infarction with microvascular obstruction identified on cardiac magnetic resonance imaging. This case highlights that even a comprehensive, guideline-based assessment of these patients can initially fail to detect the underlying pathology. (Level of Difficulty: Beginner.)

A 66-year-old man developed sudden-onset severe central chest and epigastric pain at rest. The electrocardiogram (ECG) performed by the paramedics showed ST-segment elevation in V 1 to V 5 and II, III, and aVF ( Figure 1). His observations revealed hypertension (180/100 mm Hg) and a heart rate of 60 beats/min. On arrival, he had ongoing chest pain, was diaphoretic and clammy, and appeared acutely unwell. The rest of the cardiorespiratory examination was unremarkable. There was no history of a recent viral illness.

PAST MEDICAL HISTORY
The patient had a history of Miller Fisher syndrome, hypertension, and dyslipidemia.

DIFFERENTIAL DIAGNOSIS
Given the findings of severe central chest pain and ST-segment elevation, the most likely differential

LEARNING OBJECTIVES
To recognize that, in patients presenting with myocardial infarction with nonobstructive coronary arteries, an exhaustive search for the underlying cause should be undertaken, as per the 2019 AHA Scientific Statement. To recognize that early CMR is a key investigation in patients with MINOCA. To be aware that RV microvascular obstruction is a rare complication of RV myocardial infarction and can be misinterpreted as normal myocardium. To recognize that repeat CMR examination in the chronic phase can be helpful in selected high-risk patients in whom initial diagnostic tests have been unsatisfactory. To recognize that comprehensive intracoronary imaging is recommended in cases of suspected MINOCA.

INVESTIGATIONS
Initial high-sensitivity troponin T level was 50 ng/l, which peaked at 1,229 ng/l (normal range <14 ng/l). C-reactive protein (CRP) was <5 mg/l (normal range <6.0 mg/l). The only other abnormality on blood tests was a metabolic acidosis, with a venous lactate of 6.0 mmol/l (normal range 0.5 to 2.2 mmol/l). Cardiac magnetic resonance (CMR) was performed 1 day following the presentation ( Figure 3).
This revealed normal LV systolic function with no regional wall abnormalities. However, there was marked systolic flattening of the interventricular septum, and the RV was mildly dilated with impaired ejection fraction (EF) (49%) and severe hypokinesia/ akinesia of the mid to apical RV free wall. T2-short tau inversion recovery (STIR) imaging was normal, and there was no late gadolinium enhancement (LGE) to suggest any acute edema or acute MI. In addition, the  Mild diffuse disease of the right coronary artery (A to C) and the mild-to-moderate plaque disease in the left coronary system (D to F).
Williams et al.   MVO is seen following coronary reperfusion in patients who have had significant periods of ischemia.
Its appearances on CMR are caused by the inability of gadolinium contrast material to pass through the myocardial microvasculature, as reperfused myocytes become edematous because of osmotic overload and occlude the capillaries (9). This leads to a focal, welldefined area of absent signal within an area of highsignal infarction or acute ischemia (8). Myocardium with microvascular obstruction is less likely to regain function and leads to ventricular wall scarring and remodeling when compared with patients who have no microvascular obstruction (10). The presence of microvascular obstruction is associated with higher rates of cardiovascular events in the first 2 years following an MI and a poorer prognosis.

FOLLOW-UP
Our final diagnosis was a transmural, nonviable, RV MI. The patient was contacted to explain the diagnosis and was restarted on aspirin 75 mg, clopidogrel 75 mg, and appropriate secondary prevention.
The presumed culprit lesion was an ostial RV branch occlusion, which could not be identified on angiography. Subsequent ECGs (Supplemental Figures 1 and 2) demonstrated findings consistent with a transmural infarction.
The role of antiplatelet therapy in MINOCA is controversial. In our case, we thought that the most likely underlying pathophysiology was an ostial plaque rupture event, and so we decided to treat the patient as a nonreperfused STEMI, as per the 2017 ESC guidelines (11).