Acute perimyocarditis masquerading as acute coronary syndrome with spontaneous resolution of increased left ventricular wall thickness.

Dear Editor, A 20-year-old normotensive male presented with sudden onset of near syncope, chest discomfort and dyspnoea. The patient has no known cardiovascular risk factors, including history of smoking, diabetes mellitus, dyslipidaemia and positive family history of ischaemic heart disease. Electrocardiogram (ECG) showed ST-elevation in the anterior and inferior leads (Panel A). Total white blood cell count was elevated at 16.9 x 109/L with predominance of neutrophils (13 x 109/L). Serum cardiac markers were also elevated: creatine kinase, 342 U/L; MB fraction, 24.3 ug/ L; troponin T, 1.01 ug/L. Initially, myocardial infarction (MI) was suspected. Emergent coronary angiography was performed and it was normal. Echocardiography revealed increased left ventricular (LV) wall thickness, hypokinesia in the inferior and inferolateral walls, preserved ejection fraction (EF) and mild pericardial effusion (Panel B). The patient was treated with anti-platelet therapies and investigated for possible causes of young MI. In addition, he was questioned for the possible use of cocaine which he denied. Serum levels of Lp(a), fibrinogen, anti-cardiolipin antibodies, anti-thrombin III, lupus anticoagulant and screen, protein C and S activities and activated protein C resistant test were normal. Four days later, cardiovascular magnetic resonance (CMR) showed an undilated LV with increased myocardial thickness of 12 mm at the inferolateral wall at end-diastole (Panel D). LV mass index was elevated at 109 g/m2 and LVEF was preserved (74%). Late gadolinium enhancement was documented in the subepicardial lateral wall and mid interventricular septum (Panel E). There was moderate pericardial effusion. These findings were consistent with acute perimyocarditis. There was no sub-endocardial late gadolinium enhancement. The patient was discharged without any medication. Investigations for infective aetiologies including mycoplasma serology, urine for legionella and stool for enterovirus were negative. At 8 weeks, with spontaneous clinical improvement, CMR documented normalisation of wall thickness to 8 mm and LV mass index of 61 g/m2. There was no residual myocardial late gadolinium enhancement. Echocardiography (Panel C) and ECG also normalised. The patient then resumed vigorous activity. Acute Perimyocarditis Masquerading as Acute Coronary Syndrome with Spontaneous Resolution of Increased Left Ventricular Wall Thickness