Evaluating methods for intersectoral comparison of quality of care. A routine data analysis of elective percutaneous coronary interventions.

OBJECTIVES: To compare the quality of care regarding the use of elective percutaneous coronary interventions (PCIs) in the inpatient and outpatient setting and to evaluate different methods of confounder control in this context. METHODS: Based on data of three statutory health insurances including more than nine million insurance members, a retrospective cohort study between 2005 and 2009 was conducted. The occurrence of myocardial infarction, stroke, further coronary intervention and death was ascertained following the first PCI in the study period, which was preceded by a one-year period without a PCI. A Cox proportional hazard model was used to assess the influence of the setting of the elective PCI on the risk for complications after the PCI for each outcome separately. Age, sex, the number of diseases of the Elixhauser comorbidity measure, past acute coronary syndrome, coronary artery disease, dyslipidemia, past stroke, past coronary artery bypass surgery and the year of the PCI were included as covariables. The analyses were repeated in a propensity score matched cohort as well as in inverse probability of treatment weighted analyses. RESULTS: The cohort comprised 4,269 patients with an outpatient PCI and 26,044 patients with an inpatient PCI. The majority of the analyses revealed no statistically significant effect of the setting of the PCI on the risk of myocardial infarction, stroke and further coronary interventions, whereas a reduced mortality risk was observed for outpatient PCIs. Similar results were obtained in the propensity score analyses. CONCLUSIONS: The analysis revealed that the adjusted risk for complications following an elective PCI is similar between the inpatient and the outpatient setting. For mortality the risk differed but this might be explained by residual or unmeasured confounding. The different methods applied in this study revealed mostly similar results. Since our study only covered one aspect of quality of care in the field of PCI and did not consider drug treatment in hospital or in the outpatient setting, further studies are needed which include these aspects.

Peripheral artery occlusive disease in chronic phase chronic myeloid leukemia patients treated with nilotinib or imatinib.

Several retrospective studies have described the clinical manifestation of peripheral artery occlusive disease (PAOD) in patients receiving nilotinib. We thus prospectively screened for PAOD in patients with chronic phase chronic myeloid leukemia (CP CML) being treated with tyrosine kinase inhibitors (TKI), including imatinib and nilotinib. One hundred and fifty-nine consecutive patients were evaluated for clinical and biochemical risk factors for cardiovascular disease. Non-invasive assessment for PAOD included determination of the ankle-brachial index (ABI) and duplex ultrasonography. A second cohort consisted of patients with clinically manifest PAOD recruited from additional collaborating centers. Pathological ABI were significantly more frequent in patients on first-line nilotinib (7 of 27; 26%) and in patients on second-line nilotinib (10 of 28; 35.7%) as compared with patients on first-line imatinib (3 of 48; 6.3%). Clinically manifest PAOD was identified in five patients, all with current or previous nilotinib exposure only. Relative risk for PAOD determined by a pathological ABI in first-line nilotinib-treated patients as compared with first-line imatinib-treated patients was 10.3. PAOD is more frequently observed in patients receiving nilotinib as compared with imatinib. Owing to the severe nature of clinically manifest PAOD, longitudinal non-invasive monitoring and careful assessment of risk factors is warranted.

[Radiation therapy in patients with cardiac pacemakers or implantable cardioverter defibrillators. Interdisciplinary safety recommendations]. / Strahlentherapie bei Patienten mit Herzschrittmachern oder implantierbaren Kardioverter-Defibrillatoren. Interdisziplinäre Sicherheitsempfehlungen.

BACKGROUND: With increasing numbers of implanted pacemakers and implantable cardioverter defibrillators (ICD) and a rising incidence of malignant tumors, there is a growing probability of radiation-mediated device dysfunction. The only guidelines for the management of patients with cardiac pacemakers in the case of radiation therapy were published in 1994 and have not been updated since then. Based on the current evidence and modern device technology, the present paper aims to develop contemporary and interdisciplinary safety recommendations for the minimization of patient risk. METHODS AND RESULTS: A systematic literature research was carried out including the most relevant medical electronic databases. The search yielded 147 articles published between 1994 and 2012 of which 45 met the selection criteria and of these studies 34 presented primary data (9 in vitro and 25 in vivo studies). The impact of ionizing radiation varied significantly between implanted devices and ranged from no functional changes to complete loss of function. Important device dysfunctions included changes in sensing capability, altered pacing pulses or rate, changed or disabled tachyarrhythmia ICD therapies, early battery depletion and loss of telemetry. Modern pacemakers and ICDs are more sensitive to radiation than older models. Potentially life-threatening complications were observed after exposure of the pulse generator to comparatively low radiation doses (0.11 Gy). CONCLUSIONS: Practical recommendations for patient management and safety are presented that can be readily adopted by any institution carrying out radiation therapy.

[18-year old patient with anti-epileptic therapy and sudden cardiac death]. / 18-jährige Patientin mit antiepileptischer Therapie und KammerflimmernKasuistik eines hochmalignen LQT2-Syndroms.

An 18-year old female taking anti-epileptic medication was found unconscious in her bed early in the morning. After documented ventricular fibrillation and successful resuscitation, the patient was admitted to our emergency care unit. According to ECG criteria a long-QT syndrome of the subtype 2 was suspected. A few days later, however, the patient died because of hypoxic brain death. From previous hospital reports it turned out that the patient had repeatedly experienced syncopes in the past, which were interpreted as epileptic seizures. Her 17-year old sister and the female twin of her mother had both recently died from sudden cardiac death of unknown cause. An ECG screening in the family revealed six members with LQTS. A genetic analysis revealed in all of them a previously not described rearrangement mutation (888 delG insAA) in the LQT2 gene ( HERG) that was predicted to cause a protein truncation (360X) in the amino acid chain of the I(Kr)-channel subunit. This casuistic contribution exemplifies some classical aspects of LQTS (typical adrenergic trigger mechanism, classical false diagnosis "epilepsy") and demonstrates the possibility of a genotypic classification guided by phenotypic ECG characteristics. It represents an unusual case of a LQTS with a high degree of malignancy, which requires aggressive therapeutic interventions for the family survivors.

Blocking effects of the antiarrhythmic drug propafenone on the HERG potassium channel.

Propafenone has been shown to affect the delayed-rectifier potassium currents in cardiomyocytes of different animal models. In this study we investigated effects and mechanisms of action of propafenone on HERG potassium channels in oocytes of Xenopus laevis with the two-electrode voltage-clamp technique. Propafenone decreased the currents during voltage steps and the tail currents. The block was voltage-dependent and increased with positive going potentials (from 18% block of tail current amplitude at -40 mV to 69% at +40 mV with 100 micromol/l propafenone). The voltage dependence of block could be fitted with the sum of a monoexponential and a linear function. The fractional electrical distance was estimated to be delta=0.20. The block of current during the voltage step increased with time starting from a level of 83% of the control current. Propafenone accelerated the increase of current during the voltage step as well as the decay of tail currents (time constants of monoexponential fits decreased by 65% for the currents during the voltage step and by 37% for the tail currents with 100 micromol/l propafenone). The threshold concentration of propafenone effect was around 1 micromol/l and the concentration of half-maximal block (IC50) ranged between 13 micromol/l and 15 micromol/l for both current components. With high extracellular potassium concentrations, the IC50 value rose to 80 degrees mol/l. Acidification of the extracellular solution to pH 6.0 increased the IC50 value to 123 micromol/l, alkalization to pH 8.0 reduced it to 10 micromol/l and coexpression of the beta-subunit minK had no statistically significant effect on the concentration dependence. In conclusion, propafenone has been found to block HERG potassium channels. The data suggest that propafenone affects the channels in the open state and give some hints for an intracellular site of action.

Clinical value of electrocardiographic parameters in genotyped individuals with familial long QT syndrome.

Rate corrected QT interval (QTc) and QT dispersion (QTd) have been suggested as markers of an increased propensity to arrhythmic events and efficacy of therapy in patients with long QT syndrome (LQTS). To evaluate whether QTc and QTd correlate to genetic status and clinical symptoms in LQTS patients and their relatives, ECGs of 116 genotyped individuals were analyzed. JTc and QTc were longest in symptomatic patients (n = 28). Both QTd and JTd were significantly higher in symptomatic patients than in asymptomatic (n = 29) or unaffected family members (n = 59). The product of QTd/JTd and QTc/JTc was significantly different among all three groups. Both dispersion and product put additional and independent power on identification of mutation carriers when adjusted for sex and age in a logistic regression analysis. Thus, symptomatic patients with LQTS show marked inhomogenity of repolarization in the surface ECG. QT dispersion and QT product might be helpful in finding LQTS mutation carriers and might serve as additional ECG tools to identify asymptomatic LQTS patients.

Effects of antiarrhythmic drugs on cloned cardiac voltage-gated potassium channels expressed in Xenopus oocytes.

The effects of 17 commonly used antiarrhythmic drugs on the rapidly activating cardiac voltage-gated potassium channels (Kv1.1, Kv1.2, Kv1.4, Kv1.5, Kv2.1 and Kv4.2) were studied in the expression system of the Xenopus oocyte. A systematic overview on basic properties was obtained using a simple and restricted experimental protocol (command potentials 10 mV and 50 mV positive to the threshold potential; concentration of 100 micromol/l each). The study revealed that 8 of 17 drugs yielded significant effects (changes >10% of control) on at least one type of potassium channel in the oocyte expression system. These drugs were ajmaline, diltiazem, flecainide, phenytoin, propafenone, propranolol, quinidine and verapamil, whereas the effects of adenosine, amiodarone, bretylium, disopyramide, lidocaine, mexiletine, procainamide, sotalol and tocainide were negligible. The drug effects were characterized by reductions of the potassium currents (except for quinidine and ajmaline). A voltage-dependence of drug effect was found for quinidine, verapamil and diltiazem. The different effect of the drugs was not related to the fast or slow current inactivation of the potassium channels (except for verapamil). Profiles of the individual drug effects at the different potassium channel types were identical for propafenone and flecainide and differed for all other substances. The study demonstrates marked differences in sensitivity to antiarrhythmic drugs within the group of voltage-operated cardiac potassium channel types. Taking the restrictions of the oocyte system into consideration, the findings suggest that several antiarrhythmic drugs exert significant effects at rapidly activating cardiac potassium channels.

Infarct related artery patency: relation to serial electropharmacological studies and outcome in patients with previous myocardial infarction and ventricular tachyarrhythmias.

Evidence suggests that infarct related artery (IRA) patency may improve survival after acute myocardial infarction, which is thought to be partially due to a lower incidence of malignant ventricular tachyarrhythmias. However, little is known about the effect of IRA patency on antiarrhythmic drug response and long-term outcome in patients with previous infarction who already experienced sustained ventricular tachyarrhythmias. A total of 152 patients with remote myocardial infarction and documented ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent coronary angiography and programmed ventricular stimulation before and after oral administration of d,l-sotalol (240-640 mg/day). D,l-sotalol suppressed inducibility of VT/VF in 37 (25.2%) patients. The IRA was patent in 38.1% of all patients. There was no significant difference in the frequency of drug response between patients with patent or occluded IRAs (26.8% vs 24.2%, P = 0.87). In patients with a patent IRA, d,l-sotalol tended to be more effective in the absence of a left ventricular aneurysm, although this difference did not reach statistical significance (P = 0.38). Ejection fraction and collateral blood flow had no effect on drug response in the presence or absence of IRA patency. During follow-up (13.0 +/- 19.9 months) of 29 patients discharged on oral d,l-sotalol, 3 patients experienced symptomatic VT and 4 sudden death. Arrhythmia recurrence and death of all cause (n = 6) and cardiac death (n = 4) were independent of IRA patency status. IRA patency had no effect on short-term drug response to d,l-sotalol in patients with remote myocardial infarction and documented VT/VF. Long-term outcome of patients with sustained ventricular tachyarrhythmias is independent of IRA patency status. In contrast to a previous report, outcome of electropharmacological testing was not predicted by the patency of the IRA.

Fetoscopic transesophageal electrocardiography and stimulation in fetal sheep: a minimally invasive approach aimed at diagnosis and termination of therapy-refractory supraventricular tachycardias in human fetuses.

BACKGROUND: Therapy-refractory supraventricular tachycardia commonly results in hydrops and death in human fetuses. The purpose of this study in fetal sheep was to assess the feasibility of a minimally invasive fetoscopic approach for fetal transesophageal electrocardiography and stimulation aimed at diagnosis and termination of these tachycardias. METHODS AND RESULTS: We studied a total of 10 fetal sheep (87 to 103 days of gestation; term=145 days). We entered the amniotic cavity using a percutaneous fetoscopic approach and placed various electrophysiology catheters into the fetal esophagus. We recorded the number of animals in which fetoscopic transesophageal electrocardiography and stimulation were successful and assessed pacing success and thresholds for different catheters. In addition, we monitored for potential adverse effects from stimulation and for other complications of the operation. Recording of transesophageal electrocardiograms was successful in all fetal sheep. Capture during stimulation was successfully documented by additional fetal bipolar surface electrocardiograms in 7 fetuses. In fetuses in which fetal surface electrocardiograms were not recorded, pacing stimulus artifacts interfered with documentation of capture. Although stimulation thresholds were high, the maternal rhythm was not affected by fetal stimulation. CONCLUSIONS: Fetoscopic fetal transesophageal electrocardiography and stimulation are feasible in fetal sheep. This minimally invasive approach might have the potential to improve diagnosis and management of therapy-refractory supraventricular tachycardias in human fetuses.

Autosomal recessive long-QT syndrome (Jervell Lange-Nielsen syndrome) is genetically heterogeneous.

Jervell Lange-Nielsen syndrome (JLNS) is a recessive disorder with congenital deafness and long-QT syndrome (LQTS 1). Mutations in the potassium-channel gene KVLQT1 (LQTS 1) have been identified in JLNS and in autosomal-dominant LQTS as well. We performed haplotype analysis with microsatellite markers in a Lebanese family with JLNS, but failed to detect linkage at LQTS 1. Moreover, using this approach, we excluded two other ion-channel genes involved in autosomal-dominant LQTS, HERG (LQTS 2) and SCN5A (LQTS 3). Our findings indicate that JLNS is genetically heterogeneous and that, in this family, an unknown LQTS gene causes the disease.

Molecular analysis at the Harvey Ras-1 gene in patients with long QT syndrome.

Patients with long QT syndrome (LQTS; MIM 1921500) frequently suffer from syncope and are threatened by sudden cardiac death due to ventricular arrhythmias, typically of the torsade de pointes type. Initial progress in revealing the molecular basis of the disease was made by the observation of genetic linkage of the disease locus to the Harvey Ras-1 gene (HRAS 1) on chromosome 11p15.5. More recently loci on chromosomes 3, 4, and 7 have also been found to be linked to LQTS, thus demonstrating heterogeneity in the causes for this disease. The present study performed sequence analysis on the HRAS 1 gene in patients with congenital and acquired LQTS to determine the frequency of HRAS 1 mutations in patients with this disease. In neither group were no mutations identified in the coding regions or in the splice donor and acceptor sites. Alleles characterized by a T to C transition in exon 1 and an insertion/deletion polymorphism upstream of exon 1 showed no significant difference in their frequencies between LQTS patients and normal controls. No quantitative influence of the such characterized genotypes on the QT duration was observed. These results demonstrate that structural mutations in the HRAS 1 gene are not a frequent cause of LQTS. Also, since there was no association of different alleles at the HRAS 1 locus with changes in QT duration, it appears unlikely that this gene is a major contributor to this disease.

Idiopathic left ventricular tachycardia: new insights into electrophysiological characteristics and radiofrequency catheter ablation.

OBJECTIVES: This study was performed to investigate the electrophysiological characteristics of idiopathic left ventricular tachycardia and to determine the feasibility of radiofrequency catheter ablation for nonpharmacological cure. BACKGROUND: The underlying electrophysiological mechanism of idiopathic left ventricular tachycardia with right bundle branch block morphology and left-axis deviation is presently not known. Additionally, only limited data describing the results of radiofrequency catheter ablation for treatment of idiopathic left ventricular tachycardia so far exist. METHODS: Electrophysiological studies and radiofrequency catheter ablation were performed in 5 patients (3 male and 2 female, mean age 31 +/- 10 years) with idiopathic left ventricular tachycardia (cycle length 376 +/- 72 msec). The patients had a history of recurrent palpitations of 4 +/- 1 years and had been treated unsuccessfully with 2 +/- 1 antiarrhythmic drugs. Sustained ventricular tachycardia with right bundle branch block morphology and left- or right-axis deviation was documented in all patients. RESULTS: Inducibility with critically timed ventricular extrastimuli, inverse relationships of the coupling interval of the initiating extrastimulus and the interval to the first beat of the tachycardia, continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia, and fragmented late potentials during sinus rhythm suggested reentrant activation as the underlying mechanism in three patients. On the other hand, induction dependent on isoproterenol infusion and rapid ventricular pacing and exercise inducibility indicated different electrophysiological characteristics in the remaining two patients. During electrophysiological study, intravenous verapamil terminated ventricular tachycardia in all patients, whereas ventricular tachycardia did not respond to intravenous adenosine, autonomic maneuvers, or intravenous beta-blocking agent esmolol. Catheter mapping revealed earliest endocardial activation during ventricular tachycardia in different areas of the left ventricular septum being distributed from the base to the mid-apical portion of the septum in all patients. In 4 of 5 patients, radiofrequency catheter ablation (median number of pulses 4, range 1-9) resulted in complete abolition of idiopathic left ventricular tachycardia during a follow-up of 4-43 months (median 10) without antiarrhythmic drugs. Successful target sites for catheter ablation included continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia and late potentials during sinus rhythm (2 patients), polyphasic fragmented presystolic potentials during ventricular tachycardia (1 patient), and pace mapping with identical QRS morphology compared to the ventricular tachycardia and "earliest" detectable activity during tachycardia (1 patient). No procedure related complications occurred. CONCLUSIONS: Two different patterns of electrophysiological properties of idiopathic left ventricular tachycardia were observed, indicating that this arrhythmia entity does not represent a homogeneous group. The "origin" of the tachycardias as identified by successful radiofrequency catheter ablation was located in different areas of the left ventricular septum and was distributed from the base to the mid-apical region. Radiofrequency catheter ablation was an effective and safe treatment modality in most of these patients. Distinct target site characteristics for successful catheter ablation including polyphasic diastolic activity during tachycardia and fragmented late potentials during sinus rhythm could be identified.

Recurrence and late block of accessory pathway conduction following radiofrequency catheter ablation.

INTRODUCTION: Many issues regarding the recurrence of accessory pathway conduction and the long-term outcome of late block of accessory pathway conduction are still unknown or controversial. METHODS AND RESULTS: Data from 217 patients who underwent an initially successful radiofrequency ablation of accessory pathways and 7 patients with late block of accessory pathway conduction following an initially unsuccessful ablation were analyzed. During a mean follow-up of 19 +/- 11 months, accessory pathway conduction resumed in 21 (10%) of 217 patients following an initially successful ablation and in 6 (86%) of 7 patients with late block of accessory pathway conduction (P < 0.01). After initially successful ablations, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. A late electrophysiologic study at 6 months uncovered recurrence in only 1 of 124 asymptomatic patients, but failed to detect the late recurrence in 2 patients in whom the accessory pathway conduction resumed after more than 6 months. Multivariate analysis revealed that independent predictors for recurrence of accessory pathway conduction were concealed accessory pathway, presence of transient effect of radiofrequency pulse, and more than 5 pulses required for initial cure. Accessory pathway location, length of the tip electrode of the ablation catheter, and repeat radiofrequency pulses ("safety pulses") after effective pulses did not predict resumption of accessory pathway conduction. CONCLUSIONS: After initially successful ablation, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. Late electrophysiologic testing had little prognostic value in asymptomatic patients following successful ablation. Application of "safety pulses" did not prevent recurrence. Late block of accessory pathway conduction did not predict long-term efficacy.

[High frequency catheter ablation of left-sided manifest accessory conduction pathways during sinus rhythm and in continuous atrial fibrillation]. / Hochfrequenz-Katheterablation linksseitiger manifester akzessorischer Leitungsbahnen während Sinusrhythmus und bei anhaltendem Vorhofflimmern.

Atrial fibrillation is frequently initiated during radiofrequency catheter ablation of accessory pathways. It has been generally believed that initiation of atrial fibrillation may complicate the localization of accessory pathway. Therefore, most centers currently perform cardioversion in order to continue the ablation session. The purpose of the present study was to assess the feasibility and the electrophysiologic criteria for successful radiofrequency catheter ablation of left sided accessory pathways during atrial fibrillation in patients with WPW-syndrome. Radiofrequency ablation was performed in 87 patients with left-sided manifest accessory pathways during atrial fibrillation (n = 16) or during sinus rhythm (n = 71). The criteria for localization of accessory pathways were recording of stable accessory pathway potentials, local ventricular activation preceding the onset of the intrinsic flection of the unipolar electrogram and a QS pattern of the unipolar electrogram. Overall, the accessory pathways were successfully interrupted in 85/87 patients (98%). During the first ablation procedure, abolishing of accessory pathways was achieved in 15 of 16 patients (94%) during atrial fibrillation compared to 64 of 71 patients (90%) during sinus rhythm (n.s.). The total procedure time and fluoro time was significantly shorter during atrial fibrillation than during sinus rhythm (161 +/- 91 min vs. 216 +/- 128 min, p < 0.05, and 31 +/- 24 vs. 41 +/- 26 min. p < 0.05, respectively). Thus, it is feasible and very effective to perform radiofrequency ablation of left-sided manifest accessory pathways during atrial fibrillation. Precise localization of accessory pathway during atrial fibrillation seems even easier than during sinus rhythm as indicated by shorter procedure and fluoro times in the atrial fibrillation group.

Radiofrequency catheter ablation of ventricular tachycardia following implantation of an automatic cardioverter defibrillator.

OBJECTIVES: The present study reports on the complementary role of two nonpharmacological options of antiarrhythmic therapy. BACKGROUND: Catheter ablation, antitachycardia surgery, and the implantable cardioverter defibrillator (ICD) have become important tools in the management of ventricular tachyarrhythmias. However, the emergence of ventricular tachyarrhythmias after implantation of an ICD is possible because the arrhythmogenic substrate is not affected. PATIENTS AND METHODS: Six of 180 patients developed frequent episodes of monomorphic ventricular tachycardia (n = 2) or incessant ventricular tachycardia (n = 4) following implantation of an ICD and underwent radiofrequency (RF) catheter ablation. Catheter ablation was performed using a RF generator HAT 200. Energy was delivered between a 4-mm tip electrode of the ablation catheter and a patch electrode. RESULTS: Catheter ablation was done 6.8 +/- 5 months following ICD implantation; 6 +/- 2.2 RF impulses were delivered at the site of origin of ventricular tachycardia characterized by early endocardial activation during ventricular tachycardia, identical pace mapping and long latency between stimulus, and QRS-complex in five patients. New bundle branch reentry was the underlying mechanism of ventricular tachycardia in one patient. RF catheter ablation resulted in termination of incessant ventricular tachycardia. Immediately postablation, the documented ventricular tachycardia was rendered noninducible in all patients. No ICD malfunctions have been observed. One patient died due to heart failure 24 hours after successful ablation of the incessant ventricular tachycardia. During a follow-up of 5-19 months, episodes of ventricular tachycardia recurred in four patients. All episodes could be controlled by the ICD without frequent cardioversions. CONCLUSION: RF catheter ablation is a complementary therapeutic option in case of frequent or incessant ventricular tachycardia after ICD implantation.

[Percutaneous high frequency current catheter ablation in permanent ventricular tachycardia of the "bundle-branch reentry" type after implantation of an automatic cardioverter-defibrillator]. / Perkutane Hochfrequenzstrom-Katheterablation bei permanenter ventrikulärer Tachykardie vom "bundle branch reentry"-Typ nach Implantation eines automatischen Kardioverter-Defibrillators.

A 65-year-old female patient with a history of recurrent sustained ventricular tachycardia presented with an incessant ventricular tachycardia (cycle length 360-400 ms) following implantation of a cardioverter-defibrillator (ICD). The tachycardia could not be terminated by antiarrhythmic drug treatment, antitachycardia pacing or internal defibrillation via the ICD. An invasive electrophysiologic study revealed that the mechanism of this newly occurring tachycardia was bundle branch reentry. The patient underwent emergency catheter ablation using radiofrequency (RF) current. Endocardial mapping of the right bundle branch and of the distal His bundle was performed and a bundle branch reentry tachycardia was diagnosed. After delivery of the fifth RF-impulse, the tachycardia terminated and complete AV block was induced. No malfunction of the ICD was observed following RF-ablation. The patient was hemodynamically stable with a junctional escape rhythm and antibradycardia pacing back-up of the ICD (VVI-mode). This case report demonstrates the feasibility of RF catheter ablation in the treatment of incessant bundle branch reentry tachycardia as a complementary option after implantation of an ICD.

Catheter ablation of ventricular tachycardia using radiofrequency current.

Catheter ablation techniques have evolved as an alternative to map-guided surgery and proven effective in a variety of supraventricular tachyarrhythmias. Direct current catheter ablation has been shown to be effective in about 50 to 70% of cases. Approximately, 60% of patients with structural heart disease and monomorphic ventricular tachycardia were successfully treated using direct current ablation techniques. This overall success rate and possible risks associated with the use of direct current have stimulated the search for other energy sources appropriate for catheter ablation. Presently, only a few preliminary reports on the clinical efficacy of radiofrequency energy for the treatment of ventricular tachyarrhythmias in man exist. 23 patients with identifiable heart disease at a mean age of 52 +/- 17 years underwent radiofrequency catheter ablation. 16 patients had coronary artery disease, one patient dilative cardiomyopathy and six patients had arrhythmogenic right ventricular disease. All patients presented with chronic current sustained ventricular tachycardia. After detailed endocardial catheter mapping radiofrequency energy was applied at the site of earliest ventricular activation during ventricular tachycardia which could be entrained during fixed rate ventricular pacing at the site of origin of ventricular tachycardia. At all ablation sites a long latency between the stimulus and QRS complex was noted. Of 23 patients 18 were treated with radiofrequency alone whereas in five patients a second ablation procedure using direct current was performed. Following the ablation procedures, 14 patients (61%) remained free of ventricular tachycardia. One patient died due to congestive heart failure 21 months following ablation.(ABSTRACT TRUNCATED AT 250 WORDS)