Latarbelakang: Kondisi atrium kanan yang terdiri dari berbagai struktur yang kompleksmenyebabkan timbulnya variasi sifat elektroiisiologis yang memberikan kemudahantimbulnya aritmia. Aritmia atrium kanan merupakan jenis aritmia yang panting karenaprevalensi yang tinggi dan konsekunsi klinis yang berbahaya. Akan tetapi epidemiologiaritmia atrium kanan beserta karakteristik eleklrofisiologinya di Indonesia belum pemahdilaporkan. Krista terminalis yang merupakan garis hambatan konduksi posterior padakepak atrium (KA), dan sumber trbanyak takikardia atrium (TA), nierupakan strukturunik dengan karakteristik elektrofisiologis yang belum diungkap secara luas. Di lainpihak, berkembangnya pemahaman mekanisme KA, menimbulkan masalah diagnosiskarena adanya kemiripan morfologi gelombang kepak antar berbagai jenis KA yangmekanismenya berlainan, dan adanya variasi morfologi gelombang kepak pada KA yangsejenis. Oleh karena itu akan dilakukan rangkaian penelitian untuk menjawab beberapamasalah mekanisme dan diagnosis aritmia atrium kanan.Metode: Dilakukan studi elektrofisiologi baik secara konvensional maupun denganpanduan sistem pemetaan non-kontak Ensite pada subyek dengan KA dan TA. Pada KAyang melibatkan ismus kavotrikuspid (KA-IKT) dilakukan entrainment untuk konfirmasidiagnosis. Pada ULR, lokasi dan lebar taut konduksi ditentukan atas dasar perubahankonvergensi propagasi impuls setelah melalui krista temiinalis. Pola aktivasi sumber TAdianalisis meinalcai propagasi impuls dan elektrogram unipolar virtual. Nilai 30% darivoltase negatif puncak dipakai sebagai pembeda daerah parut dari jadngan sehat. Analisisrnorfologi gelombang kepak pada EKG 12-sadapan dilakukan oleh dua orang ahli elektrofisiologi yang bebas. Suatu algoritme diagnosis KA yang sederhana akan dibuatatas dasar EKG permukaan. Ablasi frekuensi radio (AFR) dilakukan pada sumber atausirkuit reentry aritmia atrium kanan dengan memakai teknik yang sudah baku.Hasil: KA tipikal merupakan kasus KA terbanyak di Pusat Jantung Nasional HarapanKita, dan Iebih dari 60% subyek KA mempunyai penyakit jantung struktural. Rcratapanjang siklus takikardia (PST) ialah 261,8 ± 42,84, 226,5 ± 41,23, dan 195,4 ± 9,19mdet masing-masing untuk KA tipikal, tipikal terbalik dan atipikal (p = 0,016).Morfologi EKG pada KA tipikal terdiri dari 3 tipe gelombang kepak yaitu F-/f+ disadapan inferior dan P+ atau F+/f- di V, (tipe 1); F- di sadapan inferior dan P+ di V1 (tipe2); dan f-/F+ di sadapan inferior dan F+ di V1 (tipe 3). Pada KA tipikal terbalikdidapatkan 2 tipe rnorfologi yaitu P+ di sadapan inferior dan F- di V1 (tipe 1); dan P+ disadapan inferior dan isoeiektrik di V; (tipe 2). Akan tetapi tidak didapatkan perbedaanbermakna aktivasi atrium kanan pada variasi morfoiogi KA-IKT. Tidak didapatkankonduksi transversal Krista terminalis pada 90% KA-IKT, sebaliknya didapatkankonduksi transversal pada seluruh ULR. Pada saat ULR, KKL lebih cepat dari pada KK-r(1,228 ± 0,43 vs. 0,73 ± 0,30 m/det, p < 0,001). Rasio KK;/KKT ialah 1,95 ± 0,77 yangberbanding terbalik dengan lebar taut krista terminalis (1,57 ± 6,8 mm) (p < 0,00l).Algoritme diagnosis baru atas dasar morfologi dan amplimdo gelombang kepak disadapan I mempunyai akurasi 90 hingga 97%, sensitivitas S2 hingga 100% danspesifisitas 95% dalam membedakan KA tipikal terbalik dari ULR. TA fokal mayoritasberasal dari krista terminalis dan memperlihatkan adanya jalur konduksi istimewa.Dengan teknik konvensional, keberhasilan AFR pada IKT, taut krista terminalis padaULR dan TA fokal berturut-turut mencapai 96 % , 90% dan 91,7%.Kesimpulan: KA tipikal merupakan KA terbanyak pada populasi penelitian ini, denganmayoritas menderita penyakit janlung struktural. Tidak terdapat perbedaan aktivasiatrium kanan pada variasi morfologi gelombang kepak pada KA-IKT. Mayoritas tautkonduksi krista terminalis bersifat fungsional dan selalu didapatkan pada saat ULR. Suatualgoritme diagnosis baru, akurat untuk membedakan KA tipikal terbalik dari ULR.Impuls TA fokal menyebar ke seluruh atrium setelah melalui jalur konduksi istimewa.AFR efektif menyembuhkan KA-IKT, KA non-IKT dan TA.;Background: Complex structures with variable electrophysiological properties in rightatrium facilitate arrhythmias occurrence. The right atrial arrhythmia is one of clinicallyimportant anrhythmias as it has high prevalence and significant clinical consequences.However, clinical and electrophysiological characteristics of iight atrial arrhythrnias havenot been elaborated in Indonesia. The crista terrninalis has been shown as a posteriorobstacle line during atrial flutter (AFL), and as a major source of focal atrial tachycardia(AT). However, as a unique structure of right atrium, little has been known about Cristaterrninalis electrophysiological properties as a substrate of right atrial arrhythmias. Abetter understanding of AFL mechanisms yielded a diagnostic problem, since the flutterwave of different AFL has similar rnorphologies and the variable morphologies of thesame AFL. Therefore, we conduct several interconnected study to overcome thosediagnostic and mechanisms issues in right atrial arrhythmias.Methods: Atrial flutter and AT subjects underwent electrophysiology study usingconventional and/or noncontact mapping Ensite system. Entrainment pacing wasperformed to confirm the diagnosis of cavotricuspid isthmus (CTI) dependent AFL. InULR subjects, location and width of gap conduction was determined by the change ofconvergent wavefront as it is passed the crista terminalis. Careful wavefront and virtualunipolar electrogram analysis was performed during focal AT. A value of 30% of peaknegative voltage was used to differentiate low voltage zone and normal tissue. Twoindependent electrophysiologist analyzed the morphology and polarity of flutter wave in standard 12-lead ECG. Radiofrequency ablation was peformed at the origin and/orreentry circuit of right atrial arrhythmias using a standard technique.Results: Typical APL is predominant AFL cases in National Cardiovascular CenterHarapan Kita. More than 60% of all AFL cases suffered from structural heart disease.Mean tachycardia cycle length of typical, reverse typical and atypical AFLS were 261.8 ±42.84, 226.5 ± 41.23, and 195.4 ± 9.19 msec, respectively (p = 0.0l6). Typical AFLshowed 3 types flutter wave morphologies comprised of F-/f+ at inferior and P+ or F+/f-at V1 (type 1); F- at inferior and F+ at V, (type 2); and f-/F+ at inferior and P+ at V1 (type3). Reverse typical AFL showed 2 types flutter wave morphologies comprised of F+ atinferior and F- at V, (type 1); and P+ at inferior and isoelectric at V1 (type 2). However,there were no significant different of right atrial wavefront activations between thoseAFL morphologies types. Ninety percent of CTI dependent AFL demonstrated notransversal conduction at crista terminalis, on the contrary all ULR demonstratedtransversal conduction. During ULR, CVL was faster than CVT (1.23 ± 0.43 vs. 0.73 ±0.30 m/sec, p < 0.00l). The ratio of CVL/CVt (1.95 :t 0.77) had inverse correlation withthe gap width (1.57 ± 6.8 mm) (p < 0.001). A new diagnostic algorithm based onmorphology and amplitude of flutter wave at lead I had accuracy of 90 to 97%, sensitivityof 82 to 100% and specificity of 95% to differentiate reverse typical AFL from ULR. Themajority of focal AT originated hom crista terminalis and showed a preferentialwavefront conduction before spreading to the whole atrium. The success rate ofradiofrequency ablation of CTI dependent AFL, crista terminalis gap of ULR and focalAT were 96%, 90% and 91.7% respectively.Conclusion: Typical AFL is the predominant AFL cases and majority of AFL hadstructural heart disease. There was no right atrial activation different among flutter wavemorphology types of CTI dependent AFL. The majority of crista tenninalis gap wasfunctional and always exists during ULR. A new diagnostic ECG algorithm has beendemonstrated to have excellent accuracy to differentiate typical AFL from ULR. Thewavefront of focal AT spreads out to the whole atrium after traveled in preferentialconduction. RPA was effective to eliminate CTI and non-CTI dependent AFL, and focalAT. Background: Complex structures with variable electrophysiological properties in rightatrium facilitate arrhythmias occurrence. The right atrial arrhythmia is one of clinicallyimportant anrhythmias as it has high prevalence and significant clinical consequences.However, clinical and electrophysiological characteristics of iight atrial arrhythrnias havenot been elaborated in Indonesia. The crista terrninalis has been shown as a posteriorobstacle line during atrial flutter (AFL), and as a major source of focal atrial tachycardia(AT). However, as a unique structure of right atrium, little has been known about Cristaterrninalis electrophysiological properties as a substrate of right atrial arrhythmias. Abetter understanding of AFL mechanisms yielded a diagnostic problem, since the flutterwave of different AFL has similar rnorphologies and the variable morphologies of thesame AFL. Therefore, we conduct several interconnected study to overcome thosediagnostic and mechanisms issues in right atrial arrhythmias.Methods: Atrial flutter and AT subjects underwent electrophysiology study usingconventional and/or noncontact mapping Ensite system. Entrainment pacing wasperformed to confirm the diagnosis of cavotricuspid isthmus (CTI) dependent AFL. InULR subjects, location and width of gap conduction was determined by the change ofconvergent wavefront as it is passed the crista terminalis. Careful wavefront and virtualunipolar electrogram analysis was performed during focal AT. A value of 30% of peaknegative voltage was used to differentiate low voltage zone and normal tissue. Twoindependent electrophysiologist analyzed the morphology and polarity of flutter wave in standard 12-lead ECG. Radiofrequency ablation was peformed at the origin and/orreentry circuit of right atrial arrhythmias using a standard technique.Results: Typical APL is predominant AFL cases in National Cardiovascular CenterHarapan Kita. More than 60% of all AFL cases suffered from structural heart disease.Mean tachycardia cycle length of typical, reverse typical and atypical AFLS were 261.8 ±42.84, 226.5 ± 41.23, and 195.4 ± 9.19 msec, respectively (p = 0.0l6). Typical AFLshowed 3 types flutter wave morphologies comprised of F-/f+ at inferior and P+ or F+/f-at V1 (type 1); F- at inferior and F+ at V, (type 2); and f-/F+ at inferior and P+ at V1 (type3). Reverse typical AFL showed 2 types flutter wave morphologies comprised of F+ atinferior and F- at V, (type 1); and P+ at inferior and isoelectric at V1 (type 2). However,there were no significant different of right atrial wavefront activations between thoseAFL morphologies types. Ninety percent of CTI dependent AFL demonstrated notransversal conduction at crista terminalis, on the contrary all ULR demonstratedtransversal conduction. During ULR, CVL was faster than CVT (1.23 ± 0.43 vs. 0.73 ±0.30 m/sec, p < 0.00l). The ratio of CVL/CVt (1.95 :t 0.77) had inverse correlation withthe gap width (1.57 ± 6.8 mm) (p < 0.001). A new diagnostic algorithm based onmorphology and amplitude of flutter wave at lead I had accuracy of 90 to 97%, sensitivityof 82 to 100% and specificity of 95% to differentiate reverse typical AFL from ULR. Themajority of focal AT originated hom crista terminalis and showed a preferentialwavefront conduction before spreading to the whole atrium. The success rate ofradiofrequency ablation of CTI dependent AFL, crista terminalis gap of ULR and focalAT were 96%, 90% and 91.7% respectively.Conclusion: Typical AFL is the predominant AFL cases and majority of AFL hadstructural heart disease. There was no right atrial activation different among flutter wavemorphology types of CTI dependent AFL. The majority of crista tenninalis gap wasfunctional and always exists during ULR. A new diagnostic ECG algorithm has beendemonstrated to have excellent accuracy to differentiate typical AFL from ULR. Thewavefront of focal AT spreads out to the whole atrium after traveled in preferentialconduction. RPA was effective to eliminate CTI and non-CTI dependent AFL, and focalAT. |