Site-dependent intra-atrial conduction delay. Relationship to initiation of atrial fibrillation.

BACKGROUND: Atrial dysrhythmia patients have exaggerated intra-atrial conduction delays and prolonged relative refractoriness in response to atrial premature depolarizations (APDs). Furthermore, atrial fibrillation (AF) is more readily inducible by APDs from the high right atrium (HRA) than the coronary sinus (CS). In this study, we postulated that site-specific intra-atrial conduction delays can explain why AF is initiated more from the HRA than from the CS. METHODS AND RESULTS: We examined 17 patients (age, 49 +/- 22 years) without a history of atrial flutter, AF, or structural heart disease. Programmed stimulation was carried out from the HRA and distal CS, and bipolar recordings were made at the HRA, His bundle, posterior triangle of Koch, and CS. More prolongations in conduction and relative refractoriness in all intra-atrial sites were observed during HRA than CS APDs. AF was induced in 8 patients after HRA and not CS stimulation. During HRA stimulation, patients with AF inducibility exhibited significant prolongation of conduction to the posterior triangle of Koch and marked broadening of the posterior triangle of Koch electrogram compared with CS stimulation. In patients without AF inducibility, the posterior triangle of Koch electrogram width was the same during HRA and CS stimulation. CONCLUSIONS: The existence of site-dependent intra-atrial conduction delays and site-dependent dispersion of refractoriness appears to be a common property of the atrial myocardium and does not necessarily forecast AF inducibility. However, the presence of nonuniform anisotropic characteristics of the posterior triangle of Koch may be critical for AF induction.

Aortic leaflet perforation during radiofrequency ablation.

A 15-year-old girl underwent successful radiofrequency ablation of an accessory pathway. Following ablation, a new III/VI diastolic murmur was noted. Echocardiography revealed a perforated aortic leaflet, with a small amount of adherent valvular tissue and trivial aortic insufficiency by color Doppler. The patient remains asymptomatic. We are not aware of any similar complication from electrophysiological study, catheter ablation, coronary angiography, or percutaneous transluminal coronary angioplasty. We speculate that the current state of catheter technology contributed significantly to this complication. This case illustrates the need for using care in crossing the valve, continued advances in catheter technology to reduce the incidence of complications, and careful physical examination prior to and following attempts at ablation.

Progression of methotrexate-induced leukoencephalopathy in children with leukemia.

From 1972-1974, 228 children began treatment for acute lymphocytic leukemia and were prospectively assessed for neurologic complications. After CNS irradiation (2,400 rad) and intrathecal methotrexate (MTX), they received weekly intravenous maintenance therapy with MTX alone (40-60 mg/m2; 20 patients) or MTX (10-30 mg/m2) with other drugs (208 patients). Signs of leukoencephalopathy appeared in 11 children (nine without CNS leukemia) after 4-15 months of IV MTX alone, and included lethargy, seizures, spasticity, paresis, drooling, and dementia. Before or during the clinical onset, EEG frequencies slowed (all ten patients tested). Radionuclide scans showed periventricular accumulation of 99mTc (9/11 patients) and remained abnormal for greater than or equal to six months in eight patients. Cranial computed tomograms or neuropathology findings (five patients each) demonstrated leukoencephalopathy (nine patients) and radiation-related microangiopathy (ten patients). Severe neurologic and neuropsychologic dysfunctions were present in four long-term survivors.

Long-term neurological implications of somnolence syndrome in children with acute lymphocytic leukemia.

A longitudinal study of 49 children with acute lymphocytic leukemia (ALL) assessed the long-term effects of central nervous system (CNS) prophylaxis on brain function. From 10 to 12 electroencephalograms (EEGs) were done before and at intervals during after 30 months of treatment that included 2,400 rads of CNS irradiation plus intrathecal methotrexate therapy. None of the children had CNS leukemia, and all remained in first complete remissions. All 49 had abnormally slow EEG background frequencies during the four-year study, and 29 (60%) developed somnolence syndrome six to eight weeks after CNS prophylaxis. During this syndrome, EEG background frequencies decreased more than 3 standard deviations below the expected mean values for normal children. Thereafter, 7 of the 29 began to show signs of learning disabilities and 7 developed recurrent seizures. Of the 20 children who did not have the syndrome, none showed later evidence of CNS dysfunction. Somnolence may be an early indicator of long-term neurological sequelae after cranial irradiation.

Oxidative metabolism in cord-blood polymorphonuclear leucocytes.

Polymorphonuclear leucocytes were isolated from cord-blood samples collected from healthy, term infants. Oxidative metabolism was assessed in these cells by hexose monophosphate shunt activity and chemiluminescence. Basal levels of oxidative metabolism were spontaneously increased in resting (nonphagocytic) cord-blood cells as compared to adult controls. As a response to phagocytosis, cord-blood cells initiated the expected increase in oxidative metabolism and reached normal peak values of activity. However, these cells were unable to maintain the high metabolic rate for as long a time as adult controls. This aberration of leucocyte function may indicate a deficiency of metabolic reserve and could be related to the increased susceptibility of newborns to bacterial infections.