Paradoxical embolism through patent foramen ovale as a cause of myocardial infarction

A 42‐year‐old man presented with acute onset substernal chest pain. His only cardiac risk factor was mild, medicated dyslipidaemia and he was a lifelong non‐smoker. He had a healthy body mass index and exercised regularly. There was no history of previous thromboembolic events or known haematological disease. On arrival to the emergency department, he was haemodynamically stable. Electrocardiogram initially showed sinus rhythm with biphasic anterior lead T wave inversion that resolved before angiogram (Box 1). Cardiac high sensitivity troponins were positive, peaking at 2479 ng/L (reference range, < 20 ng/L), while the remaining laboratory tests, including white cell count and inflammatory markers, were unremarkable. Telemetry throughout admission did not identify arrhythmia. Coronary angiography to investigate the source of the troponin leak showed normal coronary arteries (Box 2). Subsequent cardiac magnetic resonance imaging scan revealed localised hypokinesia of mid‐anteroseptum and apical cap with non‐contiguous subendocardial late gadolinium enhancement in mid‐septum and distal cap (Box 3), raising the possibility of embolic events. Transthoracic echocardiogram demonstrated regional wall motion abnormalities with mid‐anteroseptal and apical hypokinesis, with an early positive agitated saline bubble study and evidence of right‐to‐left shunt suspicious of patent foramen ovale (PFO). Subsequent transoesophageal echocardiogram confirmed moderate sized PFO with shunt present both at rest and after Valsalva manoeuvre. Ultrasound of the lower limbs showed superficial saphenous vein thromboembolism (unprovoked) but no deep vein thrombosis. Remaining investigations, including a thrombophilia screen, were unremarkable. After discussion with the patient, he was commenced on anticoagulation for 2 months until he underwent successful percutaneous PFO closure, at which point he was transitioned to antiplatelet therapy.