Left atrial tachycardia after circumferential pulmonary vein ablation for atrial fibrillation Electroanatomic characterization and treatment

ObjectivesThe purpose of this study was to evaluate the electroanatomic characteristics of left atrial tachycardia (AT) in a series of patients who underwent circumferential pulmonary vein ablation (CPVA) and to describe the ablation strategy and clinical outcome.BackgroundCircumferential pulmonary vein ablation is an effective treatment for atrial fibrillation. A potential midterm complication is the development of left AT. There are only isolated reports describing mapping and ablation of such arrhythmias.MethodsThirteen patients (age 57.4 ± 8.9 years, five female) underwent mapping and ablation of 14 left ATs via an electroanatomic mapping system a mean of 2.6 ± 1.6 months after CPVA.ResultsThree patients were characterized as having focal AT (cycle length: 266 ± 35.9 ms). Of 11 macro–re-entrant tachycardias studied in the remaining 10 patients (cycle length: 275 ± 75 ms), 5 showed single-loop and 6 dual-loop circuits. Re-entrant circuits used the mitral isthmus, the posterior wall, or gaps on previous encircling lines. Such gaps and all three foci occurred anterior to the left superior pulmonary vein or at the septal aspect of the right pulmonary veins. Thirteen of 14 tachycardias (93%) were successfully ablated.ConclusionsLeft AT after CPVA can be due to a macro–re-entrant or focal mechanism. Re-entry occurs most commonly across the mitral isthmus, the posterior wall, or gaps on previous ablation lines. Such gaps and foci occur most commonly at the anterior aspect of the left superior pulmonary vein and at the septal aspect of the right pulmonary veins. These arrhythmias can be successfully mapped and ablated with an electroanatomic mapping system

La scheda di acquisizione di immagini da telecamera di area TVM 770. Descrizione generale

Attivit parzialmente finanziata con fondi del Progetto Finalizzato Sistemi Informatici e Calcolo Parallelo del CNRConsiglio Nazionale delle Ricerche (CNR). Biblioteca Centrale / CNR - Consiglio Nazionale delle RichercheSIGLEITItal

Idiopathic hypereosinophilic syndrome (HES) with FIP1L1-PDGFRA rearrangement can be effectively treated with Imatinib

We studied 141 patients with HES, of which 55 primary HES (39%) defined as a peripheral blood eosinophilia greater than 1,500 cells/µL for longer than 6 months, absence of other apparent aetiologies for eosinophilia and symptoms of organ involvement. All patients were studied by molecular analysis for PDGFRB-TEL, FGFR1-BCR and BCR-ABL transcripts, frequently associated with HES/CMML/MDS syndrome: all these transcripts were absent in our series. We also sought for the recently reported involvement of PDGFR, cryptically translocated with FIP1L1 in some HES pts responsive to Imatinib therapy: 13 pts (23%) were positive for the FIP1L1-PDGFRA rearrangement and all of them showed previously unreported, abnormal-sized fusion transcripts. Curiously, all FIP1L1-PDGFRA positive pts were male. We enrolled in a national clinical trial 31 (55%) primary HES pts, including all 13 (23%) FIP1L1-PDGFRA positive, with imatinib mesylate (100 to 400 mg/day). Median follow up of treatment was 4,5 moths (range 2–28). Rapid and complete haematological responses to imatinib therapy were recorded only in all FIP1L1-PDGFRA positive pts (100%) after one months of therapy and partial response in only one cases with HES without FIP1L1-PDGFRA fusion transcript. Complete molecular response without evidence of FIP1L1-PDGFRA transcript by qualitative RT-PCR was also recorded in all responding pts after median 2 months of therapy. We conclude that FIP1L1-PDGFRA rearrangement may be useful molecular marker of myeloproliferative HES, a predictor of imatinib-responsiveness and as a means to follow therapy in this subgroup of pts