title: Ablation of polymorphic ventricular tachycardias in patients with structural heart disease.
abstract: OBJECTIVE
  Monomorphic ventricular premature beats (VPB) originating from the Purkinje network can induce polymorphic ventricular tachycardia (PMVT) and ventricular fibrillation (VF) storm. We hereby report the results of targeted ablation to treat PMVT/VF storms initiated by monomorphic VPB in seven patients with structural heart disease and left ventricular (LV)-dysfunction (n=4 withcoronary artery disease (CAD), n=2 with chronic and remote myocarditis, n=1 after aortic valve replacement).
  
  
  RESULTS
  Pace-mapping and activation mapping was used to identify optimal ablation targets. Earliest activation during mapping was found midseptal of LV in three patients, midinferoseptal of LV in two patients. One patient with myocarditis showed earliest activation at free wall of right ventricle, the other one basal midseptal of LV. Local ventricular electrograms at the successful ablation sites were preceded by short, high frequency, low amplitude potentials by 22-90 ms (median 35 ms). The same local potentials were seen in sinus rhythm. Cycle lengths of VT ranged between 200 and 360 ms (median 245 ms). A median of nine radiofrequency (RF)-ablations (range 3-19) were necessary to abolish all local Purkinje potentials at the site of earliest activation. Two patients with CAD died due to refractory heart failure. The other five patients had no recurrence of PMVT and VF during follow up (median 10 months, range 1-27 months).
  
  
  CONCLUSIONS
  The distal Purkinje network plays an important role in triggering PMVT/VF in patients with structural heart disease. Ablation of the triggering VPB originating from the Purkinje arborization is feasible; prevents recurrence in a long-term follow up; and is potentially life saving in patients with severe LV-dysfunction after myocardial infarction, in patients after aortic valve replacement, or in patients with myocarditis particularly when medical treatment, including antiarrhythmic drugs, failed to suppress electrical storms.
authors.affiliation: Department of Electrophysiology, University of Leipzig, Heart Center, Leipzig, Germany. kerstin.bode@med.uni-leipzig.de
authors.forename: Kerstin
authors.initials: K
authors.lastname: Bode
authors.forename: Gerhard
authors.initials: G
authors.lastname: Hindricks
authors.forename: Christopher
authors.initials: C
authors.lastname: Piorkowski
authors.forename: Philipp
authors.initials: P
authors.lastname: Sommer
authors.forename: Jan
authors.initials: J
authors.lastname: Janousek
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Dagres
authors.forename: Arash
authors.initials: A
authors.lastname: Arya
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D005117:Cardiac Complexes, Premature / Q000209:etiology / Q000601:surgery*; D005260:Female; D006331:Heart Diseases / Q000150:complications / Q000601:surgery*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011690:Purkinje Fibers / Q000601:surgery*; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000601:surgery*; D016896:Treatment Outcome; D014693:Ventricular Fibrillation / Q000209:etiology / Q000601:surgery*