Use of Cardiac Magnetic Resonance Imaging to Distinguish Between Acute Myocarditis and Takotsubo Cardiomyopathy

A 62-year-old man was admitted to the hospital with pneumonia. The following day, he developed acute-onset chest pain and an ECG demonstrated tombstone-like ST-segment elevation in the anterior and lateral leads, without reciprocal changes (Fig. 1A ). He was intubated for acute pulmonary edema. He was treated with thrombolytic therapy for suspected ST-segment elevation myocardial infarction. Upon arrival to our institution, the ST-segment elevation had resolved. He was hemodynamically unstable, requiring vasopressor support. His troponin T level was 7000 ng/L, peaking at 15,300 ng/L after 5 days (normal: < 14 ng/L), and his creatinine kinase level was 3600 U/L, peaking on admission (normal: 52-256 U/L). He underwent coronary angiography, which revealed nonobstructive coronary artery disease in the right coronary artery and no evidence of plaque rupture. His ventriculography (left ventricular [LV] gram) and transthoracic echocardiography (TTE) revealed mid-apical akinesis and ballooning (Fig. 1, B and C; Video 1 , view video online); a pattern commonly seen in Takotsubo cardiomyopathy (TC). The left ventricular ejection fraction was 40%-45%. His initial ECG, demographics, and profound biomarker elevation were atypical for TC; therefore, he underwent cardiac magnetic resonance imaging (CMR) for diagnostic clarification (Fig. 1, D and E; Fig. 2). The CMR findings were not in keeping with TC, but they were consistent with extensive acute myocarditis.

TC is a reversible condition in which a transient LV dysfunction is present that is characterized most commonly by basal hyperkinesis and mid to apical LV ballooning and hypokinesis. The clinical presentation of TC is often similar to that of an acute coronary syndrome with chest pain, cardiac biomarker elevation, and ECG changes. Typically, the preceding history includes a physical or emotional stressor, including acute illness. Although TC is often suspected on LV gram or TTE, the Mayo Clinic diagnostic criteria recommend that CMR imaging be performed to exclude alternate pathologies such as myocarditis. Two major advantages of CMR over other imaging modalities are myocardial edema detection and tissue characterization. The pattern of myocardial edema, seen as a hyperintense T2-weighted signal or an increase of native T1 signal or high extracellular volume, is typically transmural in TC, involving the areas of wall motion abnormality, in contrast to the typical subepicardial or midmyocardial pattern seen in myocarditis. In our case, the T2 mapping, T1 mapping, and extracellular volume elevation in the mid segments were midmyocardial and epicardial, and transmural at the apex. The most striking differentiating factor in our case was the pattern and extent of late gadolinium enhancement (LGE), which often represents myocardial scar or fibrosis. Unlike in myocarditis, the literature suggests LGE is absent in classic TC, although focal or patchy LGE has been observed in a minority of cases, usually at a lower signal intensity than in acute myocarditis, owing to the absence of scar formation in transient TC. Our case illustrates the utility of CMR imaging to distinguish acute myocarditis from TC. Due to the typical mid-to-apical wall-motion abnormalities, the diagnosis might have been missed with use of only the LV gram and TTE.

Once stabilized, the patient was initiated on guideline-directed medical therapy for heart failure with reduced ejection fraction. TTE approximately 1 month later showed persistence of the apical akinesis, further evidence against TC, as it would have normalized if he had TC. A CMR was repeated 6 weeks postpresentation and demonstrated negative remodelling, and extensive LGE, in the same locations, as a result of previous myocarditis without ongoing inflammation.

The authors have no funding sources to declare.

The authors have no conflicts of interest to disclose.