However, superimposed coronary vasospasm, in addition to regional wall motion abnormalities, may lead to an erroneous diagnosis of myocardial infarction. To our knowledge, this is the first report to describe several features of ECG changes mimicking myocardial infarction, severe multivessel coronary spasm, and regional wall motion abnormalities without an increase in wall thickness in the acute setting of giant cell myocarditis. Coronary angiography confirmed normal coronary arteries, whereas the provocative test with intracoronary injections of ergometrine at 3-min intervals in each coronary artery (20 to 40 to 60 μg) induced a >90% constrictor response in both the proximal right coronary artery and the mid-left anterior descending artery, accompanied by chest discomfort, which strongly suggested myocardial infarction secondary to multivessel coronary spasm ( Figure 1B).Īcute myocarditis presents similarly to myocardial infarction with chest pain, high cardiac biomarkers, and ECG abnormalities. There was no evidence of increased wall thickness, intracardiac thrombi, or pericardial effusion ( Figure 2, Videos 1 and 2). Echocardiography revealed diffuse hypokinesis, excluding the basal inferolateral segments of the left ventricle. PR-segment depression in the inferior leads was observed. There was coved-type ST-segment elevation in leads V 1 and V 2, and an upward concave shape of the ST-segment with QRS notching in the inferior leads, with ST-segment depression in the lateral leads (i.e., reciprocal change). Electrocardiography (ECG) ( Figure 1A) demonstrated Q-waves in the inferior and anterior precordial leads, along with a low QRS voltage and wide QRS complex. Laboratory examinations revealed a troponin level of 12,683 pg/ml (normal range: ≤15.6 pg/ml), a brain natriuretic peptide level of 487 pg/ml (normal range: ≤18.4 pg/ml), and a C-reactive protein level of 3.00 mg/dl (normal range: ≤0.14 mg/dl).
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