A 10-week-old, 31-week gestation preterm boy re-presented with heart failure after an initial episode of neonatal aseptic meningitis with positive CSF enterovirus polymerase chain reaction. Investigation demonstrated global myocardial dysfunction with left ventricle posterolateral myocardial infarction. The boy's heart failure was controlled with medical treatment but his myocardial dysfunction persisted 9 months after presentation.
Between 1979 and 1989 17 patients aged two months to 12 years with acute myocardial infarction of any cause (other than after cardiac surgery) were seen at a children's hospital. Eight died from three days to three years after diagnosis (overall mortality 47%). The nine survivors, now aged 2-17 years, have been followed for one to 10 years (mean follow up five years) after infarction. The commonest causes of myocardial infarction in this series were anomalous origin of left coronary artery from the pulmonary artery (six patients (35%] and Kawasaki disease (five patients (27%]. The main symptoms of acute myocardial infarction were dyspnoea, vomiting, and difficulty feeding. Diagnosis was made in all patients by electrocardiography and confirmed by echocardiography, cardiac catheterisation, or at operation. All survivors were symptom free with excellent exercise capacity. The left ventricular ejection fraction in survivors ranged from 21% to 66%, and only one child was on regular cardiac medications. There were no cases of late sudden death. Twenty four hour Holter monitoring performed on survivors was normal (seven) or showed minor abnormalities only (one), suggesting that serious arrhythmia is rare after paediatric myocardial infarction. Myocardial infarction in children had a high early mortality; however, the incidence of serious arrhythmia was low in the survivors, who had a good exercise tolerance even when the left ventricular ejection fraction was low.
We sought to characterise patients with POS related to PFO without pulmonary hypertension. We retrospectively reviewed databases at three tertiary referral hospitals in New South Wales, Australia from 2000 to 2019. Fourteen patients with a mean age of 69614 years of age had a PFO with wide tunnel separation. Median NYHA Class was II and 7 inpatients had been confined to bed (from postural symptoms). It was 30633 days from onset of POS to diagnosis. Baseline oxygen saturations supine were 9365% and 8466% upright. 2 patients had a minor congenital heart Platypneaorthodeoxia Syndromedefect and 4 had mild parenchymal lung disease with preserved lung function. The mean aortic root diameter was 3766mm and distance between aortic root and posterior atrial wall was 1662mm. POS was preceded by surgery in 5 patients and 1 patient had mild pneumonia. Successful closure of the PFO using an Amplatzer device was performed in 11 of 14 patients. Post-closure, NYHA Class improved by 260.9 (p,0.001, n=11) and supine oxygen saturations increased by 1368% (p,0.001, n=10). POS is a debilitating condition, curable by PFO closure. Anatomical distortion of the atrial septum related to a dilated aortic root or shortening of the distance between the aortic root and posterior atrial wall may contribute to the syndrome.
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