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Catheter ablation has become the first line of therapy in patients with symptomatic, recurrent, drug-refractory atrial fibrillation. However, catheter ablation of persistent atrial fibrillation is still a challenge. Various rather complex ablation strategies exist and their results are not very favorable. Therefore, the aim of our study was to evaluate a well-defined reasonable approach to catheter ablation of persistent atrial fibrillation. The strategy consisted of a circumferential pulmonary vein ablation in combination with a potential-guided segmental approach to achieve complete pulmonary vein isolation and a linear lesion at the roof of the left atrium. A total of 43 patients (30 men, 13 women; mean age 55 years (SD ± 9 years)) with symptomatic persistent atrial fibrillation were enrolled in this study. All patients underwent catheter ablation of persistent atrial fibrillation using the above-mentioned approach (with the CARTO or the NAVX system). Additionally, catheter ablation of the mitral isthmus and the right atrial isthmus was performed in selected cases. In all patients, cardiac MRI or multi-detector spiral computed tomography was performed prior to the ablation procedure and a surface rendered model of the left atrium was created. After discharge, patients were scheduled for repeated visits at the arrhythmia clinic at 1, 3, 6, 9, and 12 months after the ablation procedure. The ablation procedure could be performed as planned in all 43 patients. Nine patients had to undergo a repeat ablation procedure, so that a total of 52 procedures were evaluated. An additional linear lesion was created at the mitral isthmus in three patients (7%) during the initial procedure and in one patient (2.3%) during the second procedure. Catheter ablation of the right atrial isthmus was performed in 11 patients (25.6%) during the first procedure and in four additional patients during the redo procedure (9.3%). Twenty-four out of 43 patients (55.8%) experienced an arrhythmia recurrence within the first 3 months after ablation requiring an electrical cardioversion. At 1-year follow-up, analysis of a 7-day Holter monitoring revealed no evidence for an arrhythmia recurrence in 26 of 43 patients (60.5%). In nine of 43 patients (20.9%), only short episodes of paroxysmal atrial fibrillation were documented. In eight patients (18.6%), a recurrence of persistent atrial fibrillation (>48 h) was revealed by the long-term recordings. A duration of persistent atrial fibrillation >3 months was the most powerful predictor for arrhythmia recurrences at 1-year follow-up. A subgroup analysis revealed a markedly higher rate of stable sinus rhythm at 1-year follow-up in patients with a short duration of atrial fibrillation (≤3 months) compared to patients with a longer duration of AF (>3 months) prior to the procedure (72.0% versus 44.4%). There were no major complications. Catheter ablation of persistent atrial fibrillation can be performed safely and effectively using this ablation strategy (especially in patients with short-lasting persistent atrial fibrillation (≤3 months)).

Wir berichten von einem Patienten mit ventrikularen Tachyarrhythmien, die wahrend einer manifesten Sepsis nach schwerer Brandverletzung in einen elektrischen Sturm mundeten. Das Oberflachen EKG in der Akutphase zeigte Zeichen von zwei moglichen Ursachen fur diesen lebensbedrohlichen Zustand: 1.) Brugada-Syndrom 2.) kardiale Ischamie. In Angesicht der komplexen klinischen Situation (manifeste Sepsis, Brandverletzungen) differierte unser Behandlungsansatz vom ublichen Management des elektrischen Sturms: unter der primaren Annahme eines fieber-induzierten Brugada-Syndroms initiieren wir eine aggressive Normalisierung der Korpertemperatur anstelle von einer antiadrenergen und antiarrhythmischen Behandlung beziehungsweise einer Koronarangiographie zum Ausschluss einer kardialen Ischamie als Trigger des elektrischen Sturms.

The aim of the present study was to elucidate whether the duration of a technical follow-up (FU) of a pacemaker (PM)/implantable cardioverter defibrillator (ICD) has an impact on cost-effectiveness in the outpatient clinic. We determined the time required for a complete FU of devices from three different manufacturers. In 130 patients (70 VVI/DDD-PM, 60 VVI/DDD-ICD) with either a PM (Phylos, Chorum/Talent, Kappa, EnPulse) or an ICD (Belos, Alto or GEM) the time was recorded for a complete FU including determination of lead impedance, sensing and pacing threshold. The time for activation of individual menue buttons was excluded. On the basis of time required for FU, cost-units (CU) were calculated for 2000 FU/year and for a presumed device longevity (PM 7 years, ICD 5 years). For VVI-PM, the duration of FU was almost identical for devices from different manufacturers (105+/-11 s to 125+/-8 s; p=n.s.). However, analysis of DDD-PM revealed marked differences (140+/-25 s vs 282+/-23 s, p

Chromanol 293B and dofetilide are inhibitors of IKs and IKr, i.e., of the slow and the rapid component of the delayed rectifier potassium current. The specificity of these drugs was tested by investigating their effects on the delayed rectifier potassium current in vascular smooth muscle, regulating the tone of blood vessels. Using depolarizing step protocols with asymmetrical potassium concentrations (135/4.5 mM K+ in pipette/bath), voltage-dependent K+ currents (IKv) of enzymatically dispersed guinea pig portal vein cells were studied in the whole-cell patch-clamp technique. Peak currents were obtained within 20 ms (at +50 mV) after activation. During a 10 s test pulse to +60 mV, these currents exhibited a relatively fast inactivation with time constants of 384 ms (Tfast) and 4505 ms (Tslow). Dofetilide was totally ineffective in modulating currents; in contrast, after application of chromanol 293B, a steady-state block of IKv developed within 135 s. The block was concentration-dependent with an IC50 of 7.4 microM. Chromanol did not produce any shift in the normalized steady-state activation and inactivation curves and the recovery from inactivation was not significantly changed. Chromanol 293B similarly inhibited delayed rectifier K+ channels whether in their closed or open state, and produced an "apparent" acceleration of inactivation, i.e., the drug accelerated the faster time constant of inactivation during a 10 s test pulse from 384 ms (control) to 149 ms (100 microM chromanol). In recent studies, chromanol was described as a specific blocker of slowly activating delayed rectifier potassium channels (IKs) in cardiomyocytes. The results of this study, however, extend the inhibitory spectrum of the drug and demonstrate block of closed and open state delayed rectifier K+ currents in portal vein vascular smooth muscle. Such a block could possibly contribute to the generation of portal hypertension.