Carbon monoxide (CO) poisoning is the most common cause of death and injury among all poisonings. Myocardial injury is detected in one-third of CO poisonings. In this Case Report, a previously healthy 41-year-old man was referred for CO poisoning. The initial electrocardiogram (ECG) showed 1mm ST segment elevation in leads DII, DIII, and aVF. As the patient did not describe chest pain and had no cardiac symptoms, ECG was repeated 10 minutes later and it was seen that ST segment elevation disappeared. As the patient had a transient ST segment elevation and elevated high-sensitive Tn-T (HsTn-T), the patient was transferred to the coronary angiography laboratory. The patient’s left coronary system was normal, but a thrombus image narrowing the lumen by approximately 60% was observed in the right coronary artery. Intravenous tirofiban was administered for 48 hours. Control coronary angiography showed continuing thrombus formation and a bare metal stent was successfully implanted. This is the first reported case with transient ST segment elevation associated with acute coronary thrombus caused by CO poisoning. It may be recommended that patients with CO poisoning should be followed-up with a 12-lead ECG monitor or 24-hour ECG Holter monitoring, even if they show no cardiac symptoms and echocardiography shows no wall motion abnormality. Early coronary angiography upon detection of such dynamic ECG changes in these recordings as ST segment elevation can reduce the risk of myocardial infarction (MI) and mortality in these patients.

We describe two neonates presenting with myocardial infarction, due to two different aetiologies of this extremely rare but potentially treatable condition, and discuss the management. One neonate had myocardial infarction complicating enteroviral myocarditis and recovered completely. The second had fatal myocardial infarction due to thrombosis of the left coronary artery. Although rare, the attending paediatrician should have a high index of suspicion when evaluating a neonate with acute onset of collapse. Electrocardiographic changes are diagnostic, but further echocardiographic assessment and prompt management at a tertiary cardiac centre are advised.

An 8-month-old boy presented with right hemiplegia of sudden onset after 20 days of Kawasaki disease, which was not initially treated by gamma globulin. Cranial X-ray computed tomography confirmed cerebral infarction as the cause of the right hemiplegia. In subsequent weeks, he developed multiple thromboses in coronary aneurysms. He successfully underwent intracoronary thrombolysis using tissue plasminogen activator without haemorrhagic complications. Cerebral infarction as a complication of Kawasaki disease is rare, and is a difficult clinical situation to manage.