Catheter ablation of ventricular tachycardia in patients with structural heart disease.

Radiofrequency catheter ablation has revolutionized therapy of most forms of supraventricular tachycardia and ventricular tachycardia in the absence of structural heart disease by providing arrhythmia cure in almost 90% of patients. However, this treatment has not been nearly as successful in patients with ventricular tachycardia in the setting of structural heart disease, because of a number of factors. Some of these limitations are technical (imprecise mapping tools, multiple regions requiring ablation) although others are patient-related (hemodynamic instability during arrhythmia, progression of disease process). Because of these and other factors, the majority of patients in this group are treated with implantable defibrillators. Ablative therapy has an adjunctive role in their management, mainly to decrease the frequency of device therapy (particularly shocks). This review will discuss mapping and ablation techniques as well as patient selection and evaluation for this procedure.

Unusual features of intermediate septal bypass tracts.

INTRODUCTION: Intermediate septal (IS) AV bypass tracts, located along the tricuspid annulus between the His bundle and coronary sinus os, lie in close proximity to the AV node. Surgical or catheter ablation of IS bypass tracts incurs increased risk for development of complete heart block. We report additional unusual features of some IS bypass tracts that distinguish them from typical bypass tracts in other anatomic regions. METHODS AND RESULTS: We analyzed a consecutive series of 150 patients with a history of Wolff-Parkinson-White syndrome and supraventricular tachycardia who underwent ablation of bypass tracts. We studied the incidence and characteristics of AV conduction of IS bypass tracts compared with bypass tracts in other locations. Of the 150 patients in the study, 21 had an IS bypass tract (all had anterograde AV conduction). Ten (48%) of these 21 IS bypass tracts demonstrated anterograde decremental properties with atrial pacing versus 3 (2%) of 129 non-IS bypass tracts (P < 0.001). During ablation, a change in delta wave morphology before total loss of conduction in the IS bypass tract also occurred in 3 (14%) of 21 IS bypass tracts versus 0 of 129 non-IS bypass tracts (P = 0.0004). During ablation, a change in P wave to delta wave interval occurred in 4 (19%) of 21 IS bypass tracts versus 0 of 129 non-IS bypass tracts (P < 0.0001). One IS patient exhibited retrograde Wenckebach block in the bypass tract, and two IS patients showed loss of retrograde bypass tract conduction after ablation attempts that first changed the delta wave morphology. No non-IS patient had these features (P < 0.0001 for each comparison). CONCLUSION: Some IS bypass tracts have unusual properties that distinguish them from bypass tracts in other locations, perhaps due to the presence of multiple ventricular insertions of the bypass tract. It is possible that some cases represent true "nodoventricular" pathways.

Role of the Na(+)/H(+) exchanger in short-term atrial electrophysiological remodeling.

BACKGROUND: The pathophysiology underlying electrophysiological remodeling (ER) from rapid atrial rates is unknown. We tested the hypothesis that activation of the Na(+)/H(+) exchanger (NHE) by ischemia contributes to ER. METHODS AND RESULTS: Twenty-eight dogs were studied under autonomic blockade. In 15 closed-chest dogs, atrial fibrillation was simulated by right atrial pacing at 600 bpm over 5 hours. Of these, 9 (pace/NHEI) received HOE642, a selective inhibitor of the NHE, and 6 (pace/control) received saline. In pace/controls, atrial effective refractory period (AERP) at a drive cycle length (DCL) of 400 ms shortened from 143+/-7 to 118+/-5 ms (1 hour) and to 122+/-17 ms (5 hours). Shortening of AERP was prevented in the pace/NHEI group (P=0.02 compared with pace/controls). At baseline in all 15 dogs, pacing at shorter DCL resulted in shortening of AERP (physiological rate adaptation), which was lost at 5 hours in pace/controls. In pace/NHEI animals, rate adaptation was maintained despite 5 hours of pacing (P=0.02). In 13 other open-chest dogs, right atrial ERP was determined before and after occlusion of the right coronary artery. Five received HOE642 (ischemia/NHEI), 5 saline (ischemia/control), and 3 intravenous glibenclamide. In ischemia/controls, AERP(400) decreased (156+/-30 to 130+/-32 ms). Shortening of AERP was not prevented by glibenclamide (180+/-20 to 153+/-33 ms) but was prevented in ischemia/NHEI dogs (169+/-12 to 184+/-19 ms, P=0.001 compared with ischemia/controls and ischemia/glibenclamide). Rate adaptation was lost in ischemia/controls and preserved in ischemia/NHEI dogs (P=0. 02). CONCLUSIONS: Activation of the NHE is one mechanism underlying short-term ER.

Atrial fibrillation produced by prolonged rapid atrial pacing is associated with heterogeneous changes in atrial sympathetic innervation.

BACKGROUND: Structural and electrophysiological changes of the atria occur with prolonged rapid rates; however, the effects of sustained atrial fibrillation (AF) on autonomic innervation of the atria are unknown. We hypothesized that electrophysiological remodeling from rapid atrial rates is accompanied by altered atrial autonomic innervation. METHODS AND RESULTS: Six dogs (paced group) underwent atrial pacing at 600 bpm; 9 dogs (control animals) were not paced. All paced dogs developed sustained AF by week 4 of pacing. All 15 animals underwent positron emission tomography imaging of the atria with [C-11] hydroxyephedrine (HED) to label sympathetic nerve terminals. HED retention in the atria was significantly greater in paced dogs compared with control animals (P=0.03). Tissue samples from the atrial appendages had a greater concentration of norepinephrine in paced animals than in control animals (P=0.01). The coefficient of variation of HED retention was also greater in paced animals (P=0.05) and was greater in the right atrium than in the left atrium (P=0.004). Epicardial activation maps of AF were obtained in the paced animals at baseline and with autonomic manipulation. Mean AF cycle length was longer in the right atrium (109.2+/-5 ms) than in the left atrium (85.8+/-5.5 ms) at baseline (P=0.005). AF cycle length did not vary significantly from baseline (97.6+/-13.4 ms) with stellate stimulation (100.5+/-6 ms) but lengthened with propranolol (107.5+/-6.1 ms, P=0.03). CONCLUSIONS: Rapid rates of AF produce a heterogeneous increase in atrial sympathetic innervation. These changes parallel disparate effects of rapid pacing-induced AF on atrial electrophysiology.

Heterogeneous atrial denervation creates substrate for sustained atrial fibrillation.

BACKGROUND: Heterogeneous electrophysiological properties, which may be due in part to autonomic innervation, are important in the maintenance of atrial fibrillation (AF). We hypothesized that heterogeneous sympathetic denervation with phenol would create a milieu for sustained AF. METHODS AND RESULTS: After the determination of baseline inducibility, 15 dogs underwent atrial epicardial phenol application and 11 underwent a sham procedure. After 2 weeks of recovery, the animals had repeat attempts at inducing AF and effective refractory period (ERP) testing. Epicardial maps were obtained to determine local AF cycle lengths. ERPs were determined at baseline and during sympathetic, vagal, and simultaneous vagal/sympathetic stimulation. Dogs then underwent PET imaging with either a sympathetic ([11C]hydroxyephedrine, HED) or parasympathetic (5-[11C]methoxybenzovesamicol, MOBV) nerve label. None of the animals had sustained AF (>60 minutes) at baseline. None of the sham dogs and 14 of 15 phenol dogs had sustained AF at follow-up. Sites to which phenol was applied had a significantly shorter ERP (136+/-17.6 ms) than those same sites in the sham controls (156+/-19.1 ms) (P=0.01). Although there was no difference in the ERP change with either vagal or sympathetic stimulation alone between phenol and nonphenol sites, the percent decrease in ERP with simultaneous vagal/sympathetic stimulation was greater in the phenol sites (17+/-8%) than in the nonphenol sites (9+/-9%) (P=0.01). There was a significantly increased dispersion of refractoriness (21+/-6.4 ms in the sham versus 58+/-14 ms in the phenol dogs, P=0.01) as well as dispersion of AF cycle length (49+/-10 ms in the sham versus 105+/-12 ms in the phenol dogs, P=0.0001). PET images demonstrated defects of HED uptake in the areas of phenol application, with no defect of MOBV uptake. CONCLUSIONS: Heterogeneous sympathetic atrial denervation with phenol facilitates sustained AF.

Atrial macroreentry involving the myocardium of the coronary sinus: a unique mechanism for atypical flutter.

Atrial flutter involving either clockwise or counterclockwise rotation around the tricuspid annulus utilizing the subeustachian isthmus has been well described. However, macroreentrant atrial circuits in atypical atrial flutter in patients who have not undergone previous surgery or without atrial disease are not well defined. We describe a patient without structural heart disease who presented with an atrial macroreentrant rhythm. Entrainment mapping demonstrated a critical isthmus within the coronary sinus. Activation mapping demonstrated double potential throughout the length of the coronary sinus with disparate activation sequences. A circuit involving the myocardium of the coronary sinus, exiting in the lateral left atrium, down the interatrial septum, and reentering into the coronary sinus was identified. Successful ablation of the rhythm was accomplished by a circumferential radiofrequency application within the coronary sinus.