Acute myocardial infarction is a cause of neonatal collapse. The diagnosis is suggested by ischaemic electrocardiography, raised cardiac enzymes and deteriorating cardiac function and should be considered in severe neonatal cardiac dysfunction without other identifiable causes. This paper presents four cases of neonatal myocardial infarction treated with veno-arterial extracorporeal membrane oxygenation (VA ECMO) for cardiorespiratory support. The paper illustrates that left ventricular function may recover after neonatal myocardial infarction if it can be supported for long enough, and that early ECMO referral may be of benefit.

In a fetus at 20 weeks gestation, we found a large fistula from the left coronary artery to the left atrium in association with tetralogy of Fallot. Postnatally, the therapeutic issues were complex because of prematurity, low birth weight, decreased flow of blood to the lungs, and volume overload of the left ventricle because of the huge fistula. At three months, the baby underwent repair of tetralogy of Fallot, with surgical ligation of the fistula, but the baby died postoperatively.

A SIXTEEN-YEAR-OLD BOY PRESENTED WITH abdominal pain, and physical examination revealed absence of both femoral pulses. Blood pressure measured 200 over 110 millimetres of mercury in the right arm, and 99 over 66 millimetres of mercury in the left leg. Because magnetic resonance imaging showed obliteration of the descending aortic lumen, but failed to demonstrate collateral vessels or exclude cerebral aneurysms, we performed multidetector computed tomography of the head and trunk, combined with 3-dimensional volume rendering. This showed the detailed anatomy of the cerebral, thoracic and abdominal vasculature, including numerous large collateral arteries, a tight coarctation distal to the left subclavian artery, and otherwise normal cerebral and abdominal vessels (Fig. 1). For comparison, the intra-operative findings are shown in Figure 2.The latest generation of multi-detector computed tomographic scanners gives a lower dose of radiation than that received during paediatric cardiac catheterization, and with 3-dimensional volume rendering, provides more detailed information about extracardiac structures than conventional angiography. In our case, it also provided more accurate imaging of the arterial vessels than was obtained with magnetic resonance imaging. Its rapid acquisition allows completion of the study under sedation rather than general anesthesia, which is a major advantage when imaging children. Figure 1. Figure 2.

The majority of arrhythmias presenting in infancy cardiovert readily or rapidly respond to conventional medical therapy. A small number prove highly refractory to anti-arrhythmic medications. Myocardial performance may be severely compromised by the combination of fast heart rate and negatively inotropic drugs. Some babies die. We have recently supported 2 babies with refractory arrhythmias on ECMO, both to pursue drug therapy and eventually, to support the circulation during radiofrequency ablation, with very successful results. The first patient was a 2.5 kg neonate presenting with collapse secondary to atrial ectopic tachycardia with a rate of 300/minute. Myocardial function was severely impaired. The arrhythmia was adenosine resistant and after iv amiodarone loading had no effect, esmolol infusion was started. This produced profound hypotension and the arrhythmia rapidly recommenced after DC cardioversion. In the face of such severe haemodynamic disturbance, VA ECMO was instituted. Further anti-arrhythmics were tried on-circulatory support, but the arrhythmia was incessant despite multiple DC cardioversions. Therefore radiofrequency ablation of the atrial ectopic focus was attempted on ECMO support. This was achieved uneventfully and the myocardial function rapidly improved, with decannulation 24 hours later. Unfortunately the arrhythmia recurred 2 weeks later, but was successfully treated by further ablation without ECMO. The child remains well with normal development on no medication. An 11-month-old baby presented to the GP with acute onset of lethargy and poor feeding and a heart rate of 350 bpm was noted! This was a broad complex tachycardia with independent p wave activity (confirmed with adenosine); ie ventricular tachycardia. Although initially well tolerated, the tachycardia resisted DC “cardioversion” even up to 60 J. Progressive and severe myocardial dysfunction and hypotension ensued, exacerbated by any attempts at drug therapy. The patient was therefore placed on VA ECMO. Some slowing of the ventricular rhythm was achieved with amiodarone and flecainide. The patient was then decannulated but the rapid arrhythmia recurred and ECMO was reinstituted. Electro-physiological mapping was then undertaken on ECMO support. NAVEX mapping identified a right ventricular outflow tract focus. This was resistant to conventional RF energy but was eventually successfully ablated with a “Cool-tip” catheter. Myocardial function improved rapidly, the patient was decannulated after 48 hours observation and there has been no recurrence of the arrhythmia since discharge. Although viewed as a very invasive technique, VA ECMO support here has prevented two otherwise unavoidable deaths in babies with conditions readily treated by radio-frequency techniques in older children. Not only did ECMO permit institution of aggressive drug therapy but also safely supported catheter interventions in very small patients. ECMO support should be considered early for small patients with refractory arrhythmias, before irreversible neurological compromise ensues. It could also be used electively to permit radiofrequency ablation in children whose size causes concern for safe catheter manipulation.