John G. Kall

Atrial Fibrillation After Radiofrequency Ablation of Type I Atrial Flutter Time to Onset, Determinants, and Clinical Course

BACKGROUND The occurrence of atrial fibrillation after ablation of type I atrial flutter remains an important clinical problem. To gain further insight into the pathogenesis and significance of postablation atrial fibrillation, we examined the time to onset, determinants, and clinical course of atrial fibrillation after ablation of type I flutter in a large patient cohort. METHODS AND RESULTS Of 110 consecutive patients with ablation of type I atrial flutter, atrial fibrillation was documented in 28 (25%) during a mean follow-up of 20.1+/-9.2 months (cumulative probability of 12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17 clinical and procedural variables, only a history of spontaneous atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8, P=0.001) and left ventricular ejection fraction <50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5, P=0.001) were significant and independent predictors of subsequent atrial fibrillation. The presence of both these characteristics identified a high-risk group with a 74% occurrence of atrial fibrillation. Patients with only 1 of these characteristics were at intermediate risk (20%), and those with neither characteristic were at lowest risk (10%). The determinants and clinical course of atrial fibrillation did not differ between an early (< or = 1 month) compared with a later onset. Atrial fibrillation was persistent and recurrent, requiring long-term therapy in 18 patients, including 12 of 19 (63%) with prior atrial fibrillation and left ventricular dysfunction. CONCLUSIONS Atrial fibrillation after type I flutter ablation is primarily determined by the presence of a preexisting structural and electrophysiological substrate. These data should be considered in planning postablation management. The persistent risk of atrial fibrillation in this population also suggests a potentially important role for atrial fibrillation as a trigger rather than a consequence of type I atrial flutter.

Atypical Atrial Flutter Originating in the Right Atrial Free Wall

BACKGROUND Data from experimental models of atrial flutter indicate that macro-reentrant circuits may be confined by anatomic and functional barriers remote from the tricuspid annulus-eustachian ridge atrial isthmus. Data characterizing the various forms of atypical atrial flutter in humans are limited. METHODS AND RESULTS In 6 of 160 consecutive patients referred for ablation of counterclockwise and/or clockwise typical atrial flutter, an additional atypical atrial flutter was mapped to the right atrial free wall. Five patients had no prior cardiac surgery. Incisional atrial tachycardia was excluded in the remaining patient. High-density electroanatomic maps of the reentrant circuit were obtained in 3 patients. Radiofrequency energy application from a discrete midlateral right atrial central line of conduction block to the inferior vena cava terminated and prevented the reinduction of atypical atrial flutter in each patient. Atrial flutter has not recurred in any patient (follow-up, 18+/-17 months; range, 3 to 40 months). CONCLUSIONS Atrial flutter can arise in the right atrial free wall. This form of atypical atrial flutter could account for spontaneous or inducible atrial flutter observed in patients referred for ablation and is eliminated with linear ablation directed at the inferolateral right atrium.

Conduction Properties of the Inferior Vena Cava‐Tricuspid Annular Isthmus in Patients with Typical Atrial Flutter

Conduction Properties of the Annular Isthmus. Introduction: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter.

What Can We Expect from Prophylactic Implantable Defibrillators

Death due to ventricular tachyarrhythmia (VT) remains an important public health problem; patients with prior myocardial infarction (MI) constitute the largest identifiable population for prophylactic interventions. Targeting of progressively higher-risk subgroups of post-MI survivors carries inevitable tradeoffs with respect to the global impact of interventions on overall mortality. Therapy with aspirin, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors comprise the benchmark against which all additional interventions, including implantable defibrillators, must be measured. Initial enthusiasm for empiric amiodarone therapy has been tempered by the limited benefit demonstrated in recent randomized trials. Trials of other class III antiarrhythmic drugs, including both d,l-sotalol and d-sotalol, have also failed to demonstrate survival benefit. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated significantly improved survival associated with defibrillators in a small subgroup of post-MI survivors with a high short-term risk of death. The ultimate number and optimal criteria for selection of patients who may benefit from prophylactic defibrillator therapy after MI will undergo continued evolution as new data from current and ongoing trials become available.

Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR intervals

Three patients with typical atrioventricular nodal reentrant tachycardia (AVNRT) and markedly prolonged PR intervals (>300 ms) without dual pathway physiology at baseline or during isoproterenol infusion underwent successful fast pathway ablation and remained asymptomatic without recurrent AVNRT, atrioventricular block, or symptomatic bradycardia for a mean of 19 months. In patients with recurrent AVNRT and markedly prolonged PR intervals, selective ablation of the retrograde fast pathway can eliminate AVNRT without further impairment of anterograde atrioventricular nodal function.

Frozen Shoulder Syndrome Associated with Subpectoral Defibrillator Implantation

Pectoral implantation of transvenous non-thoracotomy internal cardioverter defibrillators (ICD) has resulted in very few complications whether placed subpectorally or subcutaneously. We report the case of a 68 year old man with a subpectorally implanted MINI-plus (Cardiac Pacemakers, Incorporated, St. Paul, Mn.) transvenous ICD who developed nearly instantaneous severe ipsilateral shoulder pain and immobilization. The symptoms progressed despite aggressive physical therapy.We elected to remove the device from the pectoral site and place it in a traditional abdominal position due to the severity, duration and refractoriness of his symptoms. This procedure utilized the chronic Endotak DSP (Model 0125, Cardiac Pacemakers, Incorporated) transvenous lead, a compatible Endotak DSP lead extender (Model 6952, Cardiac Pacemakers, Incorporated) and the above described ICD. Immediate relief of symptoms was accomplished by relocation of the device to an abdominal site.This intervention should be reserved for patients with severely debilitating symptoms. Prospective comparison of subpectoral and subcutaneous surgical approaches with respect to patient comfort and acceptance and complications may be warranted.

Adenosine‐Sensitive Bundle Branch Reentry

Adenosine‐Sensitive Bundle Branch Reentry. Introduction: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so‐called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown.

Electroanatomic imaging using magnetic catheter tracking in the diagnosis and treatment of atrial arrhythmias

Recent data emphasize the importance of structural factors in the pathophysiology of atrial arrhythmias. As a consequence, catheter ablation increasingly has become an anatomically oriented procedure. A recently developed magnetic catheter tracking system provides spatially precise and realistic three-dimensional reconstructions of endocardial geometry. A variety of electrophysiologic data can be superimposed on these reconstructions, including activation sequence, electrogram amplitude and morphologic features, response to pacing maneuvers, and sites of planned or delivered radiofrequency energy ablation. These features enhance the ability to analyze and visualize arrhythmia mechanisms, plan and execute appropriate ablation strategies, and provide new opportunities for physiologic research.