Inappropriate Sinus Tachycardia After Radiofrequency Ablation of Para-Hisian Accessory Pathways

Inappropriate Sinus Tachycardia After Catheter Ablation. Introduction : Inappropriate sinus tachycardia (IST) has been observed following radiofrequency ablation (RFA) of the AV nodal fast pathway. This study was aimed to prospectively analyze the incidence and clinical significance of IST following RFA of para-Hisian accessory pathways (APs).
Methods and Results : Twenty-eight patients (pts) with para-Hisian APs underwent RFA. An AP was defined as para-Hisian whenever its atrial and ventricular insertions were associated with a His-bundle potential ≥ 0.1 mV. RF current was always delivered at the atrial aspect of the tricuspid annulus. to a site where the His-bundle potential was < 0.15 mV. Time- and frequency-domain analysis of heart rate variability was performed in 22 patients, before and after RFA. Abolition of AP conduction was obtained in all pts, and no AV conduction alteration occurred. Six pts (21.4%) presented with IST 45 to 240 minutes after the ablation procedure. In 5 of them, IST disappeared spontaneously within 72 hours, whereas in 1 pt β-blockers were required for 2 months. The atrial potential amplitude (1.217 ± 0.264 mV vs 0.882 ± 0.173 mV, P = 0.009) and A/V potential amplitude ratio (2.633 vs 1.686, P = 0.05) were significantly higher in pts who developed IST than in those who did not. A marked decrease in heart rate variability was observed only in pts who developed IST.
Conclusion : IST is a relatively frequent complication after RFA of para-Hisian APs: it is generally short-lasting and usually does not require any treatment. IST after catheter ablation is likely to depend upon transient parasympathetic denervation of the sinus node.     

Wavelength Index at Three Atrial Sites in Patients with Paroxysmal Atrial Fibrillation

PADELETTI, L., et.al .: Wavelength Index at Three Atrial Sites in Patients with Paroxysmal Atrial Fibrillation . The purpose of this study was to evaluate the wavelength index (WLI) at three atrial sites in a group of 23 patients with recurrent episodes of lone paroxysmal atrial fibrillation (LPAF) and a control group (n = 20). All patients underwent programmed atrial stimulation (paced cycle length = 600 ms) at high, medium, and low lateral right atrial wall. P wave duration, sinus cycle length, and corrected sinus node recovery time were not significantly different between the two study groups. WLI was calculated according to the following formulas: atrial effective refractory period (AERP)/duration of atrial extrastimulus electrogram (A₂) or AERP/A₂+ atrial latency; and atrial functional refractory period (AFRP)/A₂. WLI was significantly shorter in LPAF than in the control group at each of the paced atrial sites independently of the formula used. Duration of premature atrial electrogram appeared to play the major role in determining the difference in WLI between patients with paroxysmal atrial fibrillation and the control group.     

Atypical chronic lymphocytic leukaemia witht(ll;14)(ql3;q32): karyotype evolution and prolymphocytic transformation

Summary. In order to define better the cytological and clinical features of atypical B-cell chronic lymphocytic leukaemia (B-CLL) with t(ll;14)(ql3;q32), sequential morphologic immunological and cytogenetic studies were performed in seven patients belonging to a series of 72 consecutive cases presenting with a diagnosis of CLL or atypical CLL according to the FAB criteria. Cytologic diagnosis in these seven patients with t(ll;14) was typical CLL in two cases presenting with < 10% large lymphocytes (LL) and prolymphocytes (PL) and atypical CLL in five cases in which LL and PL comprised between 10% and 55%. The diagnosis was supported by histologic findings on bone marrow biopsy (five cases) or splenectomy specimens (two cases). A progressive increase of peripheral LL and PL was observed, resulting in a switch of FAB diagnosis over a 6-60-month period from typical CLL into atypical CLL in two cases and from atypical CLL into prolymphocytic leukaemia in five cases. Immunophenotyping showed a mature B-cell phenotype with CD19, CD22, CD24 positivity and CD10 negativity in all patients. A bright-staining pattern for surface immunoglobulins (SIg) was detected in 6/7 cases, CD5 positivity in 6/7 cases, and CD23 positivity in 1/7 cases. The FMC-7 monoclonal antibody was positive in >40% cells in 5/6 cases. Chromosome changes in addition to t(11; 14) were seen in five cases; in two cases unbalanced translocations involving the 3q21 chromosome region, resulting in partial trisomy for the long arm of chromosome 3, were detected early in the course of the disease. Karyotype evolution that was associated with disease progression occurred in 3/6 assessable patients. Comparison of these findings with similar data from 65 B-CLL patients without t(ll;14) showed that atypical morphology, switch of FAB diagnosis during the course of the disease, and karyotype evolution were more frequently seen in cases with t(ll;14) (5/7 v 15/65 cases, P = (V015, 7/7 v 7/65 cases, P < 0-0001, and 3/6 v 5/45 assessable cases, P= 0-04, respectively). The frequency of positivity for CD2 3 and bright SIg staining differed significantly in the two groups. It is concluded that t(ll;14) identifies a cytologically atypical subset of B-CLL, characterized by frequent cytologic and cytogenetic evolution and by a distinct immunological profile, sharing some biological features with mantle cell lymphoma.     

Inhibition of Endogenous Acetylcholine Release by Blockade of Voltage-dependent Calcium Channels in Enteric Neurons of the Guinea-pig Colon

Abstract— The effects on acetylcholine release from the guinea-pig colon of the N-type calcium channel blocker ω-conotoxin GVIA (ω-conotoxin), the L-type calcium channel blocker nifedipine and the putative blocker of T-type channels, flunarizine, have been investigated. Endogenous basal acetylcholine release and electrically (1 Hz, 1 ms, 450 mA)-evoked overflow in the presence of cholinesterase inhibitor were studied. ω-Conotoxin (1–10 nM) and nifedipine (0·03–3 μm ) dose-dependently inhibited basal and electrically-evoked acetylcholine release. Maximal inhibition of basal or electrically-evoked acetylcholine release was about 40% for nifedipine and about 75% for ω-conotoxin. The potency of nifedipine was inversely related to the external calcium concentration: its EC50 value in low-calcium medium (0·5 Mm ) was as low as 12 Nm . Flunarizine inhibited acetylcholine release only at concentrations higher than 0·2 μm . Our results are consistent with an involvement of N- and L-type calcium channels in the control of the endogenous acetylcholine release from the guinea-pig colon.     

Feasibility and performance of post-mortem examination to determine the aetiology of congenital anomalies in a population of 1019 foetal and perinatal deaths

We assess the feasibility and the performance of a post-mortemexamination protocol including Polaroid® photographs, radiographs,karyotyping, gross and microscopic necropsy, and genetic expertise.This protocol was applied to the 1019 consecutive foetal orperinatal deaths that occurred between January 1984 and June1987 in the Marseille district (France). The feasibility forthe routine use of such a protocol was low; all five componentsof the protocol were completed in only 9% of the cases. Grossautopsy was performed in 85% of the cases, histologic examinationin 48%, successful karyotyping in 17%, radiography in 52% andgenetic expertise in all the cases. Of the 1019 consecutivecases reviewed, 227 lethal congenital anomalies were detected(22.3%). Each element's contribution to the establishment ofthe aetiology of congenital anomalies was assessed. Alone orcombined with the information given by other elements of theprotocol, gross necropsy gave the cause of death in 58% of allcases, karyotyping in 38%, radiography in 3% and genetic expertisein 38%. If the protocol had been applied to malformed Infantsonly, it would have detected 86% of the aetiologies of congenitalanomalies.