trial tachycardia (AT) originating focally from diverse anatomical structures in both atria has been well described. [1][2][3][4][5][6][7][8] Focal AT is distinguished from macroreentrant AT by its electrophysiological characteristics and electropharmacological responses, and by the approaches to mapping and ablation of the tachycardia. 7,8 The underlying mechanism of focal AT is thought to be automaticity, triggered activity or atrial microreentry. 7,8 Recently, Tsai et al reported an unusual form of focal atrial fibrillation (AF) triggered by ectopic beats originating from the superior vena cava (SVC), and radiofrequency (RF) ablation of the triggering SVC focus was safe and highly effective in eliminating the focal AF. 9 Theoretically, it is possible that focal electrical firing in the SVC could initiate AT in addition to AF; however, the mechanism of this type of focal AT remains unclear. In this study, we describe the distinct electrocardiograms and electrophysiological characteristics in 3 patients with focal AT originating from various parts of the SVC. The location of the successful RF site in the SVC was proven by multi-plane SVC angiography. All 3 patients underwent uneventful ablations of their SVC foci within a few seconds of RF current application.
Methods
PatientsThe study group were 3 patients with drug-refractory atrial tachyarrhythmias who were admitted for electrophysiological study and RF ablation therapy. Each patient had a focal AT originating from the SVC that had been diagnosed and confirmed by the electrophysiological study, SVC angiography and RF ablation. Two (cases 1 and 2) of the 3 patients did not have significant organic heart diseases detectable by physical examination, chest roentgenograms, echocardiography, and coronary angiography. The other patient (case 3) had one-vessel coronary artery disease. The definition of focal AT was based on previously established criteria. 7,10-12
Electrophysiological Study and RF AblationThe electrophysiological study was performed in a postabsorptive state after each patient gave written informed consent. All antiarrhythmic drugs except amiodarone were discontinued for at least 5 half-lives before the study. Two 6F quadripolar electrode catheters with a 5-mm interelectrode spacing were positioned at the high right atrium and the right ventricular apex, respectively, for pacing and recording. Another 6F quadripolar electrode catheter with a 10-mm interelectrode spacing was positioned across the tricuspid annulus to record the His bundle potential. A 6F decapolar electrode catheter with a 2-10-2-mm interelectrode spacing (Daig Corp) was positioned in the coronary sinus for recording and pacing. A 7F deflec-
Electrophysiological Characteristics and Radiofrequency Ablation of Focal Atrial Tachycardia Originating From the Superior Vena CavaKuan-Cheng Chang, MD; Yu-Chin Lin, MD; Jan-Yow Chen, MD; Hsiang-Tai Chou, MD, PhD; Jui-Sung Hung, MDThe initiation of focal atrial tachycardia (AT) from the superior vena cava (SVC) remains unclear. In 3 patients (2...
SUMMARYInflammation and genetics may play a role in the pathogenesis of rheumatic heart disease (RHD). The aim of this study was to test whether interleukin (IL)-1β, IL-1 receptor antagonist (IL-1Ra), IL-4, or IL-10 gene polymorphisms could be used as markers of susceptibility to or severity of RHD among the Chinese population in Taiwan.A group of 115 patients with RHD diagnosed by echocardiography, and 163 age-and sex-matched normal control subjects were studied. IL-1β promoter, IL-1β exon 5, IL-1Ra, IL-4 promoter, IL-4 intron 3, and IL-10 gene polymorphisms were identified by polymerase chain reaction-based restriction analysis.There was no significant difference in the distribution of genotypes and allelic frequencies between RHD cases and controls for IL-1β promoter, IL-1β exon 5, IL-1Ra, IL-4 promoter, IL-4 intron 3, and IL-10 gene polymorphisms. Further categorization of the RHD patients into mitral valve disease and combined valve disease subgroups also revealed no statistical difference in these gene polymorphisms when compared with controls.These findings suggest that the IL-1β, IL-1Ra, IL-4, or IL-10 gene polymorphisms are not suitable genetic markers for RHD in Taiwan Chinese. (Int Heart J 2005; 46: 397-406)
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