Catheter-induced mechanical trauma to accessory pathways during radiofrequency ablation: incidence, predictors and clinical implications

AbstractOBJECTIVESTo evaluate the incidence, predictors and clinical implications of nonintentionally catheter-induced mechanical trauma to accessory pathways during radiofrequency ablation procedures.BACKGROUNDData on the incidence and significance of catheter-induced trauma to accessory pathways are scarce.METHODSConsecutive patients (n = 381) undergoing radiofrequency ablation of accessory pathways at two different institutions were closely monitored for appearance of mechanical block of accessory pathways during catheter manipulation.RESULTSMechanical trauma to accessory pathways was observed in 37 (9.7%) patients. According to a multivariate analysis, the only independent variable associated with this phenomenon was the anatomical pathway location (p = 0.0001). The incidence of trauma of either right anteroseptal (38.5%) or right atriofascicular pathways (33.3%) was significantly greater than that of pathways (≤10%) at all remaining locations (p < 0.0001). The duration of conduction block observed ranged from ≤1 min to >30 min in 19% and 35% of patients, respectively. “Immediate” application of radiofrequency pulses at sites of mechanical block (<1 min after occurrence) was associated with a 78% long-term success rate at follow-up. This contrasted with a 25% long-term success rate in patients in whom pulses were delivered 30 min after occurrence of block (“delayed pulses”). Finally, in 24% of patients persistent trauma-induced conduction block led to discontinuation of the ablation procedure.CONCLUSIONSTrauma to accessory pathways is more common than previously recognized and frequently results in prolongation or discontinuation of the ablation procedure and in lower success rates. The only independent predictor of catheter-trauma to accessory pathways is the pathway location

Mode of onset of torsade de pointes in congenital long QT syndrome

Objectives.We sought to describe the mode of onset of spontaneous torsade de pointes in the congenital long QT syndrome.Background.Contemporary classifications of the long QT syndrome (LQTS) refer to the congenital LQTS as “adrenergic dependent” and to the acquired LQTS as “pause dependent.” Overlap between these two categories has been recognized, and a subgroup of patients with “idiopathic pause-dependent torsade” has been described. However, it is not known how commonly torsade is preceded by pauses in the congenital LQTS.Methods.We reviewed the electrocardiograms (ECGs) of all our patients with congenital LQTS evaluated for syncope or sudden death (30 patients). Documentation of the onset of torsade de pointes was available for 15 patients. All these patients had “definitive LQTS” by accepted clinical and ECG criteria.Results.Pause-dependent torsade de pointes was clearly documented in 14 of the 15 patients (95% confidence interval 68% to 100%). The cycle length of the pause leading to torsade was 1.3 ± 0.2 times longer than the basic cycle length, and most pauses leading to torsade were unequivocally longer than the preceding basic cycle length (80% of pauses were >80 ms longer than the preceding cycle length).Conclusions.The “long-short” sequence, which has been recognized as a hallmark of torsade de pointes in the acquired LQTS, plays a major role in the genesis of torsade in the congenital LQTS as well. Our findings have important therapeutic implications regarding the use of pacemakers for prevention of torsade in the congenital LQTS

From whole exome sequencing to patient-specific therapy: another example of how basic research pays off in patient care

I n the past 20 years, molecular genetics has successfullyentered the arrhythmia field.1,2 The identification of the genetic basis of many of the arrhythmia syndromes provided us the tools for better understanding of the pathophysiolog-ical basis of these syndromes,2 for presymptomatic testing (potentially also prenatally with the possibility of extrauterine fertilization and selection of embryos without the identified mutation) and for timely treatment of family members of a more clearly affected proband,3,4 for gene-specific therapy2 and, occasionally, also for new, mechanism-driven therapy.2 For example, gene-specific treatment has become very common in the long QT syndrome.2 Examples of truly new therapeutic modalities, envisioned only after unraveling the molecular genetic basis and the associated pathophysiolog-ical mechanism, however, are relatively scarce. A good example is the identification of flecainide as a highly effectiv