• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • br Methods br Results Among patients


    Results Among 36 patients with 37 long RP tachycardias, there were 22 patients with 23 ATs (62%) and 14 patients with 14 non-ATs (10 uncommon AVNRTs and 4 PJRTs). Age, sex, and AV Wenckebach rxr receptor length at baseline in the EP study were not significantly different between the 2 groups (Table 1). Tachycardia cycle length had a tendency to be longer in AT patients (p=0.06). Among the 23 ATs, all but 1 was a focal AT, whereas the remaining AT cases were macro-reentrant AT. The locations of the 22 focal ATs were right atrial in 18 of 22 (82%) cases, and left atrial in 4 of 22 (18%) cases. Right atrial sites included the crista terminalis (n=6), right septum (n=5), tricuspid annulus (n=3), coronary sinus ostium (n=2), in proximity to the sinus node (n=1), and the superior vena cava (n=1). Left atrial sites included the posterior wall (n=2), ostium of the right pulmonary vein (n=1), and the left atrial appendage (n=1). In the 4 patients with PJRT, the retrograde decremental accessory pathway was located in the right (n=3) and left posteroseptal regions (n=1). In 7 out of 37 long RP tachycardias (19%), intravenous isoproterenol infusion was administered to induce the tachycardia in 4 patients with AT and 2 with non-AT (18% vs. 14%, P=1.00). Catheter ablation was successfully performed in all patients with both AT and non-AT with no complications. However, 1 patient with AT and 2 non-AT patients had recurrence of arrhythmia after catheter ablation (P=0.544). The procedure times were 168±55min in the AT group and 175±59min in the non-AT group (P=0.76). Fluoroscopic times were 50±27min in the AT group and 45±22min in the non-AT group (P=0.73).
    Discussion The main findings were as follows: (1) AT accounted for nearly two thirds of long RP tachycardia; (2) the RP/PR ratio was higher in the AT group than in the non-AT group; (3) a negative P wave in the inferior leads was observed less frequently in the AT group; (4) the P-wave duration during tachycardia was longer in the AT group; (5) the combination of any 2 ECG features (including RP/PR≥1.65, absence of negative P wave in the inferior leads, and P-wave duration >96ms) had a specificity and positive predictive value of 100% for AT.
    Conflict of interest
    Case report A 47-year-old woman (height: 165cm, weight: 52.8kg) was transported to the hospital following syncope. According to the automated external defibrillator, she experienced ventricular fibrillation (VF), which was treated with a direct current shock. The patient had a history of cardiac surgery for an atrial septal defect in childhood. Echocardiography and cardiac computed tomography (Fig. 1A) revealed a severely dilated right atrium and right ventricle, and Ebstein’s anomaly of the tricuspid valve. On the other hand, the size and contraction of the left ventricle were almost normal (left ventricular ejection fraction, 57%) and her B-type natriuretic peptide level was 63.7pg/mL. Amiodarone (200mg/day) and carvedilol (10mg/day) were administered to prevent lethal ventricular arrhythmia. Initially, electrophysiological testing and cardiac catheterization were performed to identify the substrate of VF and to investigate the appropriate site for the positioning of an implantable cardioverter-defibrillator (ICD) lead. Coronary angiography revealed no significant stenosis in the coronary arteries. Left ventriculography showed normal wall motion in the left ventricle. Consistent with the echocardiographic findings, right atriography showed a significantly dilated right atrium and displacement of the tricuspid valve (Fig. 1B). Ventricular tachyarrhythmia was not induced by a programmed stimulation with up to three extrastimuli. Electroanatomical activation mapping (CARTO® system, Biosense Webster, Diamond Bar, CA, USA) clearly showed an atrialized right ventricle (Fig. 2A). Atrial electrocardiogram [Fig. 2A-(1)], normal atrioventricular node conduction delay [Fig. 2A-(2)], and ventricular electrocardiogram [Fig. 2A-(3)] were confirmed in the right atrium. Both atrial and ventricular potentials were observed near the atrioventricular groove [Fig. 2A-(2)]. At the border of the anatomical RA and atrialized RV, the ventricular potential was defined as the local activation potential. Even though electroanatomical voltage mapping showed a wide low amplitude area, especially around the atrialized ventricle, the electrograms at the septal site were relatively preserved and were recognized as an optimal lesion for ICD lead implantation (Fig. 2B). Based on these findings, a transvenous dual-chamber ICD (TELIGEN 100 F111, Boston Scientific Inc., St. Paul, MN, USA) was implanted for the prevention of sudden cardiac death. The atrial lead (DEXTRUS 4136/53cm, Boston Scientific Inc.) and ICD lead (ENDOTAK RELIANCE G 0296/64cm, Boston Scientific Inc.) were successfully implanted (Fig. 2C). P-wave and R-wave sensing was satisfactory at 3.2mV and 9.5mV, respectively. Adequate capture threshold values were measured at the right atrium (pacing threshold: 0.5V, 0.4ms) and right ventricle (pacing threshold: 0.5V, 0.4ms). Induced ventricular fibrillation was successfully terminated by a 9J direct current shock.