No abstract

During SR, excellent or good pace-maps at sites of isolated potentials within areas of scar identify areas of fixed block that are protected and part of the critical isthmus of post-infarction VT. Shared common pathways might explain why non-targeted VTs might become noninducible after ablation of other VTs.

Background-Because the genesis of atrial fibrillation (AF) is multifactorial and variable, an ablation strategy that involves pulmonary vein isolation and/or a particular set of ablation lines may not be equally effective or efficient in all patients with AF. A tailored strategy that targets initiators and drivers of AF is a possible alternative to a standardized lesion set. Methods and Results-Catheter ablation was performed in 153 consecutive patients (mean age, 56Ϯ11 years) with symptomatic paroxysmal AF with the use of an 8-mm tip radiofrequency ablation catheter. The esophagus was visualized with barium. The pulmonary veins and left atrium were mapped during spontaneous or induced AF. Arrhythmogenic pulmonary veins were isolated or encircled. If AF was still present or inducible, complex electrograms in the left atrium, coronary sinus, and superior vena cava were targeted for ablation. The end point of ablation was absence of frequent atrial ectopy and spontaneous AF during isoproterenol infusion and noninducibility of AF. Routine energy applications near the esophagus were avoided. During follow-up, left atrial flutter developed in 19% of patients and was still present in 10% at Ͼ12 weeks of follow-up. A repeat ablation procedure was performed in 18% of patients. During a mean follow-up of 11Ϯ4 months, 77% of patients were free from AF and/or atrial flutter without antiarrhythmic drug therapy. Pericardial tamponade or transient neurological events occurred in 2% of procedures. Conclusions-A tailored ablation strategy that only targets triggers and drivers of AF is feasible and eliminates paroxysmal

The Purkinje system may be part of the re-entry circuit in patients with post-infarction monomorphic VT, resulting in a type of VT with a relatively narrow QRS complex that mimics fascicular VT.

Prevention of sudden death in the young adult should focus on evaluation for causes known to be associated with SUD (e.g., primary arrhythmia) among persons <35 years of age, with an emphasis on atherosclerotic coronary disease in those ≥ 35 years of age.