Antiarrhythmic Treatment (antiarrhythmic + treatment)

Distribution by Scientific Domains

Selected Abstracts

The Effect of Induction Method on Defibrillation Threshold and Ventricular Fibrillation Cycle Length

Introduction: Since no clinical data are available on the comparison of the "shock on T-wave" and "high frequency burst" ventricular fibrillation (VF) induction modes during defibrillation threshold (DFT) testing, we aimed to compare these two methods during implantable cardioverter defibrillator implantation. Methods: The DFT was determined with a step-down protocol using biphasic, anodal polarity (100%, 40%, 20% voltage control) shocks. Patients were randomized: VF was induced by 50 Hz burst in group B (n = 45) and T-wave shock in group T (n = 41). The DFT was defined as the lowest energy level that terminated VF; confirmed DFT (DFTc) was defined as the minimal energy level that consecutively terminated VF twice. Success rate of DFTc was calculated during an intraindividual test for the alternate induction method. Results: A total of 546 episodes of VF were induced: n = 278 (B) vs n = 268 (T). Incidence of VT during inductions was 9.9% (B) vs 2.7% (T), P < 0.05. Neither the DFT, 8.8 ± 4.0 J (B) vs 9.7 ± 4.2 J (T), nor the DFTc, 10.6 ± 5.1 J (B) vs 10.8 ± 4.2 J (T), proved to be significantly different. A significant correlation was found between VF cycle length (CL) and the concomitant DFT (r = 0.298, P < 0.05) in group T only. Subgroup analysis of patients under chronic class III antiarrhythmic treatment showed no increase of the DFT in either group and significantly lower incidence of VT induction in group T regardless of antiarrhythmic treatment. Conclusion: The DFT and the VFCL proved to be independent of the VF induction method. The T-wave shock was more unlikely to induce VT during DFT testing. These results suggest that both methods are reliable in DFT determination, though T-wave shock application is a more reliable method for DFT testing. [source]

Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fihriliation

DE SISTI, A., ET AL.: Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fibrillation . In patients with sinus node dysfunction (SND) with or without associated paroxysmal atrial fibrillation (AF), the effectiveness of atrial pacing in reducing the incidence of AF is not definitive. In addition, despite several studies involving large populations of implanted patients, little attention has been paid to the electrophysioiogicai (EP) atrial substrate and the effect of permanent atrial pacing. The aim of this study is to correlate EP data and the risk of AF after DDD device implantation. We reviewed FP data of 38 consecutive patients with SND. mean age 70 ± 8 years, who were investigated free of antiarrhythmic treatment, for the evaluation of the atrial substrate. We also considered as control group 25 subjects, mean age 63 ± 14 years, referred to our EP laboratory for unexplained syncope or various atrioventricular disturbances. Following pharmacological washout and at a drive cycle length of 600 ms. effective and functional refractory periods (ERP, FRP), Sl-Al and S2-A2 latency, Al and A2 conduction duration, and latent vulnerability index (EHP/A2) were measured. AF induction was tested with up to three extrastimuli at paced cycle lengths of 600 and 400 ms in 20 patients. Induction of sustained AF (> 30 seconds) was considered as the endpoint. P wave duration on the surface ECG in lead II/Vl was also measured. DDD pacing mode was chosen in all patients with the minimal atrial rate programmed between 60 and 75 beats/min (mean 64 ± 4 beats/min). After implantation, the patients were followed-up for 29 ± 17 months and clinically documented occurrence of AF was determined. When comparing patients with SND and subjects of the control group, we did not find any significant statistical differences in terms of ERP (237 ± 33 vs 250 ± 29 ms), FRP (276 ± 30 vs 280 ± 32 ms) and Sl-Al (39 ± 16 vs 33 ± 11 ms) and S2-A2 latency (69 ± 24 vs 63 ± 25 ms). In contrast, we observed significant differences regarding Al (55 ± 19 vs 39 ± 13 ms; P < 0.001), A2 (95 ± 34 vs 57 ± 18 ms; P < 0.001) and P wave duration (104 ± 18 vs 94 ± 15 ms; P < 0.05), and ERP/A2 (2.8 ± 1.2 vs 4.8 ± 1.6; P < 0.001). When comparing patients with (n = 11) or without (n =27) postpacing AF occurrence, we did not find any difference with reference to ERP, FRP. Sl-Al, S2-A2, Al duration, or follow-up duration. In patients with postpacing AF occurrence, A2 was longer (116 ± 41 vs 87 ± 27 ms; P < 0.01), FRP/A2 lower (2.1 ± 0.4 vs 3.1 ± 1.4; P < 0.05), P wave more prolonged (116 ± 22 vs 99 ± 14 ms; P < 0.01), and preexisting AF history predominant (6/11 vs 5/27 patients; P < 0.05). No difference was observed between patients with (n = 8) and without (n = 12) AF induction during the EP study. In patients with SND, the atrial refractoriness appears normal and the most important abnormality concerns conduction slowing disturbances. Persistence of AF despite pacing stresses the importance of mechanisms responsible for AF not entirely brady-dependent. In this setting, more prolonged atrial conduction disturbances, responsible for a low vulnerability index, and a preexisting history of AF enable us to identify a high risk patient group for AF in the follow-up. sinus node dysfunction, atrial fibrillation, electrophysiologicai study, atrial pacing [source]

Procainamide and Survival in Ventricular Fibrillation Out-of-hospital Cardiac Arrest

David T. Markel
Abstract Objectives:, Procainamide is an antiarrhythmic drug of unproven efficacy in cardiac arrest. The association between procainamide and survival from out-of-hospital cardiac arrest was investigated to better determine the drug's potential role in resuscitation. Methods:, The authors conducted a 10-year study of all witnessed, out-of-hospital, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) cardiac arrests treated by emergency medical services (EMS) in King County, Washington. Patients were considered eligible for procainamide if they received more than three defibrillation shocks and intravenous (IV) bolus lidocaine. Four logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CI) describing the relationship between procainamide and survival. Results:, Of the 665 eligible patients, 176 received procainamide, and 489 did not. On average, procainamide recipients received more shocks and pharmacologic interventions and had lengthier resuscitations. Adjusted for their clinical and resuscitation characteristics, procainamide recipients had a lower likelihood of survival to hospital discharge (OR = 0.52; 95% CI = 0.36 to 0.75). Further adjustment for receipt of other cardiac medications during resuscitation negated this apparent adverse association (OR = 1.02; 95% CI = 0.66 to 1.57). Conclusions:, In this observational study of out-of-hospital VF and pulseless VT arrest, procainamide as second-line antiarrhythmic treatment was not associated with survival in models attempting to best account for confounding. The results suggest that procainamide, as administered in this investigation, does not have a large impact on outcome, but cannot eliminate the possibility of a smaller, clinically relevant effect on survival. ACADEMIC EMERGENCY MEDICINE 2010; 17:617,623 © 2010 by the Society for Academic Emergency Medicine [source]

Clinical and demographic determinants of heart rate variability in patients post myocardial infarction: Insights from the cardiac arrhythmia suppression trial (CAST)

Phyllis K. Stein PH.D.
Abstract Background: Clinical and demographic determinants of heart rate variability (HRV), an almost universal predictor of increased mortality, have not been systematically investigated in patients post myocardial infarction (MI). Hypothesis: The study was undertaken to evaluate the relationship between pretreatment clinical and demographic variables and HRV in the Cardiac Arrhythmia Suppression Trial (CAST). Methods: CAST patients were post MI and had , 6 ventricular premature complexes/h on pretreatment recording. Patients in this substudy (n = 769) had usable pretreatment and suppression tapes and were successfully randomized on the first antiarrhythmic treatment. Tapes were rescanned; only time domain HRV was reported because many tapes lacked the calibrated timing signal needed for accurate frequency domain analysis. Independent predictors of HRV were determined by stepwise selection. Results: Coronary artery bypass graft surgery (CABG) after the qualifying MI was the strongest determinant of HRV. The markedly decreased HRV associated with CABG was not associated with increased mortality. Ejection fraction and diabetes were also independent predictors of HRV. Other predictors for some indices of HRV included beta-blocker use, gender, time from MI to Holter, history of CABG before the qualifying MI, and systolic blood pressure. Decreased HRV did not predict mortality for the entire group. For patients without CABG or diabetes, decreased standard deviation of all NN intervals (SDANN) predicted mortality. Clinical and demographic factors accounted for 31% of the variance in the average of normal-to-normal intervals (AVGNN) and 13,26% of the variance in other HRV indices. Conclusions: Heart rate variability post MI is largely independent of clinical and demographic factors. Antecedent CABG dramatically reduces HRV. Recognition of this is necessary to prevent misclassification of risk in patients post infarct. [source]

Effective long-term control of cardiac events with ,-blockers in a family with a common LQT1 mutation

H Wedekind
The congenital long QT syndrome (LQTS) is characterized by a prolonged QT interval on the surface electrocardiogram and an increased risk of recurrent syncope and sudden cardiac death. Mutations in seven genes have been identified as the molecular basis of LQTS. ,-blockers are the treatment of choice to reduce cardiac symptoms. However, long-term follow-up of genotyped families with LQTS has been rarely reported. We have clinically followed a four-generation family with LQTS being treated with , - blocker therapy over a period of 23 years. Seven family members were carriers of two amino acid alterations in cis (V254M-V417M) in the cardiac potassium channel gene KCNQ1. Voltage-clamp recordings of mutant KCNQ1 protein in Xenopus oocytes showed that only the V254M mutation reduced the IKs current and that the effect of the V417M variant was negligible. The family exhibited the complete clinical spectrum of the disease, from asymptomatic patients to victims of sudden death before ,-blocker therapy. There was no significant reduction in QTc (556 ± 40 ms˝ before therapy, 494 ± 20 ms˝ during 17 years of treatment; n = 5 individuals). Of nine family members, one female died suddenly before treatment, three females of the second generation were asymptomatic, and four individuals of the third and fourth generation were symptomatic. All mutation carriers were treated with ,-blockers and remained asymptomatic for a follow-up up to 23 years. Long-term follow-up of a LQT1 family with a common mutation (V254M) being on ,-blocker therapy was effective and safe. This study underscores the importance of long-term follow-up in families with specific LQT mutations to provide valuable information for clinicians for an appropriate antiarrhythmic treatment. [source]