Analysis of T wave changes by activation recovery interval in patients with atrial septal defect

• Published in: International journal of cardiology 2000-07, Vol.74 (2), p.115-124
• Main Authors: Izumida, Naomi, Asano, Yuh, Wakimoto, Hiroko, Nishiyama, Mitsunori, Doi, Shouzaburoh, Tsuchiya, Shirou, Hosaki, Junro, Kawano, Seiko, Sawanobori, Tohru, Hiraoka, Masayasu
• Format: Article
• Language: English
• Subjects: Activation recovery interval; Atrial septal defect; Biological and medical sciences; Cardiology. Vascular system; Child, Preschool; Congenital heart diseases. Malformations of the aorta, pulmonary vessels and vena cava; Electrocardiography; Female; Heart; Heart Septal Defects, Atrial - diagnosis; Humans; Male; Medical sciences; Probability; Reference Values; Right ventricular overload; Sensitivity and Specificity; T wave change; Ventricular Dysfunction, Right - diagnosis
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/S0167-5273(00)00248-5

We examined the distributions of the activation recovery interval (ARI), which is correlated with the local action potential duration (APD), to clarify the origin of the repolarization changes in ASD. The ECGs, QRST isointegral maps and ARI isochronal maps of 21 children with ASD from 3 to 5 years old in age were studied in comparison with 21 age-matched normal children. A conventional and 87 unipolar body surface ECG were simultaneously recorded. The ARIs were determined from the first derivatives of the ECG waveforms. Abnormal ST-T patterns were observed in 11 of 21 ASD, but only in two normal children. The QRST maps of a split positive area pattern were seen in 15 of ASD but none of the normal. In the ARI maps, all the normal children exhibited a short-ARI area on the left and a long-ARI area on the right side of the chest. In 19 of ASD, the ARI distribution revealed a leftward extension of the long-ARI area on the anterior chest, a relative shortening on the right anterior chest, and a localized prolonged ARI on the left anterior chest. The results suggest that right ventricular (RV) volume overload in ASD produces a localized prolongation of the APD on the RV epicardium.