P3-50

ELECTROPHYSIOLOGIC CHARACTERISTICS IN AN ANDERSENSYNDROME PATIENT WITH KCNJ2 MUTATIONSatoshi Nagase, MD, Kengo Fukushima Kusano, MD,Nobuhiro Nishii, MD, Kimikazu Banba, MD, AtsuyukiWatanabe, MD, Kazufumi Nakamura, MD, Hironori Saitou,MD and Tohru Ohe, MD. Okayama University GraduateSchool of Medicine and Dentistry, Okayama, Japan.

Andersen syndrome (AS) is a rare, inherited disorder characterized byperiodic paralysis, long QT syndrome (LQTS) with ventricular arrhythmias(VA), and skeletal developmental abnormalities. Recently, it is reportedthat reduced current amplitudes of the inward rectifying K� channels(Kir2.1) contributed to the development of delayed afterdepolarization(DAD) and might be related to the arrhythmic development. However, theprecise mechanism of QT prolongation and the development of VA havenot been fully examined in human. Here, we present a case of a patient withAS with VA who received electrophysiological study (EPS). Patient was a19-year-old female with a history of familial periodic paralysis. She hadexperienced exertional palpitation for several years. Non-sustained poly-morphic ventricular tachycardia (bi-directional morphology) during exer-cise was detected by Holter monitoring. Then she was reffered to ourhospital. A 12-lead ECG showed a normal QT interval and an abnormal TUcomplex, that is a prominent U wave at the precordial leads. Mutationanalysis revealed a missense mutation in KCNJ2, Thr192Ala (T192A), thatis a component of Kir2.1. Therefore, she was diagnosed as AS. In the EPS,monophasic action potentials (MAP) were recorded at three sites (rightventricular apex, outflow tract and left ventricle) of the ventricular endo-cardium simultaneously. MAP duration at 90% repolarization (MAPD90)and effective refractory periods (ERP) at each site were similar to thecontrol patients at baseline condition and after adrenaline infusion. How-ever, adrenaline injection exaggerated both DADs at the left ventricularMAP and U wave amplitude in the surface ECG. Importantly, these DADswere always coincided with the U waves in the surface ECG. SpontaneousPVCs were observed after adrenaline injection and its initiation was alwayscoincided with both increased DAD and U wave. These findings suggestthe evidence that reduction of Kir2.1 current contributes to DAD formationand subsequently VA development without affecting action potential du-ration in human. AS may be a distinct from other forms of inherited LQTS.

P3-51

EFFECT OF OMEGA-3 FATTY ACIDS ON RECURRENCES OFPAROXISMAL ATRIAL ARRHYTHMIASFrancesco Biscione, MD, Alessandro Totteri, MD, AntonioDe Vita, MD, Francesco Lo Bianco, MD and GiulianoAltamura, MD. UTIC - Osp. S. Giacomo, Roma, Italy.

Omega-3 fatty acids (n-3) reduce ventricular arrhythmias and suddendeath; fewer data exist regarding the effects of n-3 on atrial arrhythmias.Object of this report is to evaluate the reduction of atrial arrhythmias aftertreatment with n-3 in pts with DDD pace-makers (PM).Methods: we examined 40 pts with paroxismal atrial arrhythmias (PAA)recorded at the periodic (every four months) PM controls. The PMs wereimplanted more than 1 year earlier for AV block (14 pts), synus bradicardia(8 pts), bradi-tachy syndrome (16 pts) and CHF (2 pts). All pts had bipolaratrial and ventricular leads with proper sensing function; the PMs wereprogrammed in DDD or DDDr mode with minimum rate of 70 to 85 bpm.At the study entry, all pts were treated with n-3 (1 gr/d); no changes in PMprogrammation and in the previous pharmacological therapy were allowed.The PM memories were interrogated after 4 months of treatment to eval-uate the number and burden of PAA episodes; the percentual reduction ofPAA burden was calculated. At this time, the treatment was discontinuedand the pts were evaluated 4 months later. Statistical analysis were per-formed with the T-Student test.Results: 2 pts discontinued the treatment complaining of adverse drugeffects. They were included in the intention-to-treat analysis. The overallpatient population showed a dramatic reduction in episodes and burden of

PAA during the treatment period. The PAA episodes in the pre- treatmentperiod resulted 444�1161, and the PAA burden 3,89% of time; in thetreatment period resulted respectively 181�436 (p�0,034) and 1,06%(p�0,029), with a mean PAA burden reduction of 67%. After the with-drawal of drug, the PAA episodes raised to 552�1717 (p�0,065) and thePAA burden to 2,69% (p�0,003). Even after the exclusion from analysisof the 6 pts with non sustained-PAA (�30 sec), the treatment showedreduction of the PAA episodes (483 vs 177, p�0,034) and burden (4,54%vs 1,21%, p�0,028).Conclusions: Our data suggest a powerful effect of n-3 in reduction ofPAA in these pts, without significant adverse effects.

P3-52

EFFICACY OF DOFETILIDE IN PATIENTS WITH PAROXYSMALATRIAL FIBRILLATION AND NORMAL LEFT VENTRICULARFUNCTIONAndrew Mykytsey, MD, Tanveer Akbar, MD, Sorin Danciu,MD, Marcial Santos, MD, Mansour Razminia, MD, TerryZheutlin, MD, Ted Wang, MD, Jose Nazari, MD, PradeepMaheshwari, MD, Edward Telfer, MD, Jerry Bauman,PharmD and Richard Kehoe, MD. Advocate Illinois MasonicMedical Center, Chicago, IL and University of Illinois atChicago, Chicago, IL.

Background: ACC/AHA/ESC guidelines recommend using dofetilide (DF)as second tier therapy to maintain sinus rhythm in pts with paroxysmalatrial fibrillation (PAF) and normal LV function. Our study was undertakento define the safety and efficacy of DF use in this setting.Methods: We conducted a retrospective chart review in 4 area hospitals.The safety and overall efficacy were evaluated in pts who fulfilled the studyinclusion criteria of symptomatic PAF, normal LV function. The primaryendpoint was overall efficacy defined as complete suppression of symp-tomatic PAF .A secondary endpoint was cumulative efficacy defined assubjective symptomatic improvement in PAF burden or complete supres-sion of AF while on DF.Results: 34 pts (23 M, 11 F; mean age of 62.2 yrs, PAF duration 6.5�6.7years) were included. All pts failed previous antiarrhythmic therapy: ami-odarone 14(41%), sotalol 16 (47%), class IC drugs 10 (29%). Of 34 pts, 31(91%) were discharged on DF (mean dose 436�111mg). In 3 pts, DF wasdiscontinued prior to discharge (incessant PSVT, 1 pt; QT prolongation, 2pts). DF was stopped in 13 of 31 pts (42%)due to: serious proarrhythmia3 pts (sustained monomorphic VT, 1; polymorphic VT, 1; and non-sus-tained VT, 1); supraventricular tachycardia 2 pts; QT prolongation 1 pt;dizziness 1 pt; inefficacy 6 pts. At one year, overall efficacy was noted in6 of 31 pts (19%) and cumulative efficacy in 18 of 31 pts (58%).Conclusion: Based on above we conclude: 1) DF can be safely initiated ina majority of pts; 2) DF is a valuable therapeutic option for pts with drugrefractory PAF and preserved LV function with overall efficacy 19% andcumulative efficacy 58%; and 3)Despite careful inpatient drug titration andmonitoring, serious proarrhythmia can occur during long term follow-up.

P3-53

RESULTS OF A NEW LEFT ATRIAL LINEAR ABLATIONAPPROACH COMPARED TO ANTRAL PULMONARY VEINISOLATION FOR CURE OF PERSISTENT ATRIAL FIBRILLATIONDouglas Gibson, MD, Uma Srivatsa, MD, Bobbi Hoppe, MD,Dan Muhtar, MD, Navinder Sawhney, MD, Vincent Chen,MD and *Gregory K. Feld, MD. University of California,San Diego, CA.

Background: Left atrial (LA) linear ablation (LALA) is more likely to curepersistent atrial fibrillation (pAF) than antral PV isolation (APVI). How-ever, posterior LA ablation may cause lethal LA-esophageal fistula. There-fore, we studied a new LALA approach avoiding the posterior LA (Fig. 1)in pts with pAF lasting �24 hours and requiring cardioversion.Methods: In consecutive pts with pAF, 20 (15M/5F) underwent APVI, and20 (16M/5F) underwent LALA using our new approach. In AVPI pts mean

S191Poster 3