Long-term follow-up of pseudoinfarction pattern in two children

Abstract

Pseudoinfarction is defined as the presence of abnormal Q-waves with or without ST-segment changes which are not associated with myocardial ischemia. In adults, different causes of pseudoinfarction pattern have been described in cardiac diseases [1] associated with cardiomyopathy [2], hyperkalemia [3] or Wolf–Parkinson–White syndrome [4], and extra cardiac causes such as acute pancreatitis [5]. There is only one report about pseudoinfarction in infancy with symptomatic congestive heart failure, which was caused by the presence of an accessory atrioventricular conduction pathway and most likely intermittent supraventricular tachycardia [6]. We report about two children who were admitted in the outpatient clinic to clarify the heart murmur and found to have ECG abnormalities without any signs of clinical impairments. First patient was a 5-day-old female infant with a small membranous ventricular septal defect (VSD). Her ECG showed sinus rhythm, right axis deviation with deep Q-waves (up to -0.5 mV) in leads II, III, aVF and in pre cordial leads V4–V6. In addition, there was a discrete ST-elevation up to 0.2 mV in leads II and aVF. At the age of 6 weeks and 3.5 months, we observed left axis deviation with deepening of above mentioned Q-wave in ECG (Fig. 1a). Her clinical status was totally normal. The echocardiography confirmed normal size and function of the heart with hemodynamically not relevant left-to-rightshunt through the small membranous VSD. The second patient was a 2.5-year-old boy also with a small membranous VSD. Although in his first years of live, the ECG’s showed normal conduction, the ECG abnormalities were observed at the age of 2 years with extreme left axis deviation and deep Q-waves (up to -0.7 mV) in leads I, aVF and pre cordial leads V4–V6 without significant ST-elevation (Fig. 1b). His clinical status showed no impairments. Physical ability was not limited and there were no episodes of chest pain or dyspnoea in the past medical history. The echocardiography confirmed also in this case normal size and function of the heart with hemodynamically not relevant left-to-right-shunt through the small membranous VSD. The blood work, including CK and CK-MB was within normal range for both patients. The echocardiogram was not thought to have completely ruled out the possibility of a coronary artery abnormality, and angiographic visualization of the coronary arteries was considered appropriate to rule out anomalous left coronary artery from the pulmonary trunk (Bland–white–Garland syndrome). In both cases, the angiography showed a normal anatomy of the heart, great vessels and the coronary arteries. The hemodynamic evaluation was also entirely normal. The already by echocardiography described small membranous VSD was confirmed in both patients. A continuous follow-up investigation revealed in first patient (latest 6 years after initial investigation) a normal ECG (Fig. 1c) with spontaneous closure of VSD and in A. Wessel K. Norozi Department of Paediatric Cardiology, Medical School Hannover, Hannover, Germany