Library

Notes: Mapping of Ventricular Tachycardia. Introduction: Although direct ventricular tachycardia (VT) surgery has been shown to be effective for treatment of inferior myocardial infarction (MI), the differences in the arrhythmia substrates compared to anterior MI have not been systematically delineated. We sought to compare operative procedures and VT substrates between anterior and inferior MI locations. Methods and Results: Computerized mapping was performed in 30 patients with a 128-electrode system using epicardial sock and transatriat left ventricular endocardial balloon arrays, followed by combined endocardial resection and cryoablation. At surgery, there were 51 and 34 different VTs in 18 patients with anterior Ml and 12 patients with inferior MI, respectively. The proportion of aneurysms was lower in inferior MI (25% vs 78%, P = 0.008). Total activation times accounted for 65%± 23% and 50%± 22% of the VT cycle length in anterior and inferior infarcts, respectively (P = 0.005). Complete superficial reentry was identified in 12 VTs related to anterior infarcts and in only two VTs associated with inferior infarction (P = 0.038). Involvement of papillary muscles occurred in two patients with inferior MI. Patients with inferior infarcts received more cryolesions and required epicardial cryolesions or mitral valve replacement more frequently, and their operative mortality was greater (2/12 vs 0/18). Noninducibility rate (89.3%) and 2-year survival (76%± 8%) did not differ according to infarct location.Conclusion: VT associated with inferior MI can be ablated successfully; however, the substrate is more complex, with frequent participation of intramural layers rendering the ablative procedure more difficult.

Notes: Background:The prognosis and treatment of patients with prolonged asystole during head-up tilt test (HUT) remain controversial. The aim of this study was to identify factors predicting a favorable outcome in patients with unexplained syncope who have an asystolic response during HUT. Methods:Passive HUT was performed at 60° for up to 45 minutes in 329 patients (162 women and 167 men, mean age 38 ± 22 years). Isoproterenol was given in escalating doses when passive HUT was negative. Asystole was defined as a ventricular pause 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:1082720X:ANEC377:ges" location="ges.gif"/〉 5 seconds. Results:Among the 173 patients with positive HUT, 21 developed syncope related to asystole (mean duration 13 ± 7.5 seconds). According to our initial experience, beta-blocker therapy was used as a first line treatment. At repeat HUT on beta blockers, 16 patients (group I) were partially (n=5) or totally (n=11) controlled by beta blockers, as opposed to 5 patients (group II) in whom asystole remained inducible. Three of them required implantation of a pacemaker and the two others refused. When compared to group I patients, group II patients were older (50 ± 9 vs 24 ± 10 years, P 〈 0.001) and had a longer asystole duration (22 ± 7 vs 10 ± 5 seconds, P 〈 0.005) during initial HUT, while spontaneous clinical manifestations were identical. The diagnostic accuracy to predict failure of beta blockers was 83% for age 〉 40 years, 80% for asystole 〉 15 seconds and 100% for both. After a follow-up of 35 ± 11 months, the two patients of group II who refused pacemaker, experienced recurrence of syncope, while the three others remained free of symptoms. Concerning group I, patients successfully managed were asymptomatic, and few episodes of recurrent presyncope were observed in only four of those partially controlled by beta blockers. Conclusions: Prolonged asystole (〉 15 seconds) and an older age (〉 40 years) both predict a poor response to beta-blocker therapy in patients with vasovagal syncope referred to as malignant. Satisfactory HUT under beta blockers predict a favorable clinical outcome. A.N.E. 1999;4(4):377–384

Notes: Differential Drug Effects on Anisotropic Conduction. Introduction:Anisotropic conduction characteristics, expressed as the ratio of conduction velocities in the longitudinal (Vl) and transverse (Vt) fiber directions, may play a role in the mechanism of some ventricular tachycardias and is influenced by pharmacologic interventions. Discrepancies exist among the reported orientation-dependent effects of available Class I antiarrhythmic drugs. The aim of this study was to assess the respective effects of quinidine (Class IA), flecainide (Class IC), and cibenzoline (not subclassifled) on the anisotropic conduction of porcine hearts, in corroboration of their effects on ventricular action potentials. Methods and Results: We studied the actions of 3 and 10 μM quinidine, 1 and 3 μM flecainide, and 0.3 and 1 μM cibenzoline on Vl and Vt determined from 128 electrograms recorded with a plaque electrode on the anterior left ventricle of isolated perfused hearts (spacing 2.5 mm). Vl and Vt were computed from isochronal maps displaying ellipsoid activation during stimulation from the center of the plaque. The effects on the maximal rate of depolarization (V˙max) of action potentials were obtained from ventricular muscle exposed to the same drugs. Flecainide [1 μM] and cibenzoline [0.3 μM] did not alter Vl, and Vt, significantly. Quinidine [3 μM] predominantly depressed Vl at rapid pacing rates, hut the Vl/Vt ratio was not significantly altered. Quinidine [10 μM] and flecainlde [3 μM] reduced Vl and Vt in a frequency dependent fashion. Conversely, cibenzoline [1 μM] mostly decreased Vl and thus decreased the Vl/Vt ratio and increased the Vl/Vt at all pacing rates. This different effect was not related to a greater depressant effect on V˙max. Conclusion: Quinidine and flecainide act similarly on the anisotropic pattern of conduction (both drugs increase the Vl/Vt ratio), whereas cibenzoline exerts opposite effects. Orientation dependent effects are different among Class I antiarrhythmic drugs and may be of importance in their therapeutic efficacy or proarrhythmic potential.

Notes: Between March 1995 and June 1997, 128 leads were extracted from the hearts of 28 women and 50 men, 69 ± 15 years of age (mean ± SD, range 22–92 years). The indications for the procedure were: Accufix lead in 18 patients (14%), dysfunction or incompatibility with ICD in 16 (12%), endocarditis on the lead in 41 (32%), pulse generator pocket infection in 28 (22%), and pulse generator and/or lead erosion in 25 patients (19%). The extraction was performed with a snare (lasso), via a femoral vein as a first approach in 116 leads, and as an alternate approach, after extraction from the original site of implantation had failed, in 12 leads. The leads had been implanted for 62 ± 48 months (range 1–205 months). A Cook sheath was used in 7, and a femoral approach traction in 20 instances. Of the 128 leads, 122 (95%) were completely extracted, and 2 (2%) were partially extracted (the distal electrode remaining attached to the myocardium), and 4 (3%) could not be removed. Four complications occurred: 2 tears of the tricuspid valve without clinical consequences, one separation of the lead's distal electrode which migrated into the hypogastric vein, and one hemorrhage at the femoral puncture site. There was no death or serious complication caused by lead extraction in this series.

Notes: A 63-year-old man with an ischemic dilated cardiomyopathy previously implanted with an implantable cardioverter defibrillator (ICD) received a triple chamber pacemaker as an ultimate therapeutic resort for end-stage congestive heart failure. After implant, the tolerance to physical exercise increased and NYHA class decreased from III to II. Echocardiography assessed ventricular contraction resynchronization during DDD biventricular pacing as compared to VVI pacing. No major pacemaker-ICD interaction was noted during testing or follow-up. We conclude that sequential biventricular pacing is feasible in the presence of an ICD.

Notes: We report an implantable cardioverter defibrillator (ICD) implanted with a single lead inadvertently introduced in the great cardiac vein. No venous lesion was caused by the shocks and the position of the lead remained stable. This case emphasizes the usefulness of different fluoroscopic views during ICD implantation.

Notes: Transvenous pacing has become widespread in the pediatric population, but related pacemaker lead infection in young patients has rarely been reported. To determine prevalence and optimal management of pacemaker lead infection in children and young adults, the authors reviewed their pacing database including 4,476 patients who previously had pacemaker implantations from 1975 to 2001. A pacemaker was implanted in 304 patients under the age of 40. Of these patients 217 of them had congenital heart disease: 108 with structural defect, 109 without (mainly complete AV blocks). Among patients with congenital heart disease, 12 developed a pacemaker lead infection (5.5%, 6 patients with structural defect, 6 without). This incidence was significantly higher than in patients 〈 40 years at first implantation without congenital heart disease (2.3%) and in 〉 40-year-old patients (1.2%, P 〈 0.001) . However, the number of reinterventions at the pulse generator site was higher in patients having had their first implantation before the age of 40. In patients with structural cardiac defect: two died after surgical lead extraction and one died before the scheduled lead extraction. The three remaining patients had successful surgical (n = 1) or percutaneous (n = 2) lead extractions. In patients without structural cardiac defect successful percutaneous extraction (5/6) or surgical extraction (1/6 with vegetation 〉 25 mm) was performed. One patient with percutaneous extraction developed chronic cor pulmonale during follow-up. One infection recurred in one patient with structural cardiac defect although complete removal of the pacing material had been performed. The prevalence of pacemaker lead infection is higher in younger patients, perhaps in part due to a higher number of procedures at the pacemaker site than in the general population of patients with a pacemaker. Patients with structural cardiac defect who underwent surgical lead removal were at high risk for death. Patients with percutaneous lead extraction may develop cor pulmonale. (PACE 2003; 26[Pt. I]:1489–1493)

Notes: The aim of this study was to analyze the onset mechanisms of atrial tachyarrhythmias using a dedicated diagnostic system in 83 recipients of DDDR pacemakers implanted for standard clinical indications. The pulse generator was programmed in DDD mode, at 60 beats/min, and the diagnostic instrument was programmed to document atrial tachyarrhythmic episodes at rates 〉200 beats/min. Onset mechanism was defined as the combination of ambient rhythm and trigger. Various underlying rates and rhythms patterns, including tachycardia, increasing frequency of premature atrial complex (PAC), underlying heart rate increase, restart, and no specific underlying rhythm, and various triggers, including single, multiple, or short runs of PACs, sudden rate decrease, and sudden onset of atrial tachyarrhythmia were included in the combined classification. Atrial tachyarrhythmic episodes were documented on one follow-up interrogation in 48 of the 83 patients. The pacing indications consisted of high degree atrioventricular block in 19 patients, bradycardia-tachycardia syndrome in 22, and isolated sinus node dysfunction in 6 patients. The onset mechanisms of 318 episodes were recorded and analyzed. A variety of triggers were observed in 33 of the 48 patients, and 39 patients had various ambient rhythms. Among 20 documented onset mechanisms, the most common were increasing frequency of PAC + short runs (17%), no specific ambient rhythm + sudden onset (24%), and increasing frequency of PAC + sudden onset (12%). There were wide intra- and interpatient variations in onset mechanisms, suggesting that state-of-the-art pacemakers should represent versatile diagnostic tools and offer flexible pacing methods to refine the management of atrial tachyarrhythmias. (PACE 2003; 26:1336–1341)

Notes: Venous thrombosis is one of the most frequently encountered obstacles when reintervening on endocardial leads. We report on two patients with a ventricular defibrillator requiring lead replacement in whom a subclavian vein thrombosis was documented prior to the intervention. We recanalized the vein and replaced the lead through the same path to preserve the venous access.