Myocardial infarction is rare in children but frequently occurs unexpectedly with atypical presentation. It can cause a progressive lethal course unless prompt treatment is initiated.

Paediatric cases of myocardial infarction diagnosed by the presence of ischaemic myocardial insults and symptomatic ventricular dysfunction were reviewed retrospectively.

Eighteen patients (5 days to 14 years of age; median 3 months) with myocardial infarction were studied. The aetiology was variable, including congenital coronary anomalies: anomalous left coronary artery from pulmonary artery (five patients), pulmonary atresia with intact ventricular septum with right ventricle-dependent coronary circulation (four), anomalous aortic origin of left coronary artery (three), and Williams syndrome with supravalvar aortic stenosis (one). Two acquired coronary anomalies occurred in one patient with undiagnosed Kawasaki disease with complete thrombotic obstruction of the left coronary artery and another with post-transplant cardiac allograft microangiopathy. Three patients developed thromboembolic coronary artery incidents in normal coronary anatomy. Fourteen patients were less than 1 year of age (78%). Electrocardiographic abnormalities were noted in all patients. Four patients required extracorporeal membrane oxygenation support for severe ventricular dysfunction, none of whom survived. Five patients underwent heart transplant. Five patients died during the same hospitalisation, and one patient died after discharge (overall mortality 33%). Transplant-free survival was 39%.

Most myocardial infarction occurred in infants who presented with abrupt onset of non-specific clinical manifestations with progressively deteriorating haemodynamic status resulting in poor transplant-free survival rate. Early diagnosis and treatment are essential to prevent catastrophic outcomes.

Anomalous left coronary artery from the pulmonary artery is a rare congenital heart disease (CHD) with diverse clinical presentations despite the same anatomy. Factors determining this heterogeneous presentation are not well understood.

We retrospectively investigated 14 patients (12 females) who underwent surgical repair of anomalous left coronary artery from the pulmonary artery. These patients were divided into three groups based upon the severity of initial presentation: (1) severe, life-threatening condition (n = 5), (2) mild-to-moderate distress (n = 6), and (3) asymptomatic (n = 3). All patients presented with left ventricular dilation and retrograde flow in left coronary artery by echocardiogram. Eight patients in (1) and (2) presented with severe left ventricular dysfunction. All but one showed abnormal ECG consistent with myocardial ischemia or infarction. Asymptomatic patients had preserved left ventricular systolic function despite ischemic findings on ECG. In 13 patients after surgical repair, all but one normalised left ventricular geometry and systolic function, suggesting nearly full myocardial recovery upon improvement of myocardial perfusion; 8 patients had residual echogenic papillary muscle with variable degree of mitral regurgitation.

Evidence of myocardial ischemic injury was present in all patients with anomalous left coronary artery from the pulmonary artery regardless of their initial presentation. Retrograde flow in left coronary artery, implying collateral vessel development from right coronary artery to left coronary artery, was noted in all patients, yet only few patients had preserved systolic function at the time of diagnosis. The balance between effective myocardial perfusion and a deleterious fistulous flow provided by these collaterals and the simultaneous haemodynamic status are what determine the clinical diversity of anomalous left coronary artery from the pulmonary artery.