Background-The summit of the left ventricle (LV) is the most superior portion of the epicardial LV bounded by an arc from the left anterior descending coronary artery, superior to the first septal perforating branch to the left circumflex coronary artery. Ventricular arrhythmias (VAs) originating from this region may present challenges for catheter ablation. Methods and Results-We studied 27 consecutive patients with VAs originating from the LV summit. The great cardiac vein (GCV) divides this region between an inferior area accessible to ablation and a superior, inaccessible area. Successful ablation was achieved within the GCV in 14 patients and on the epicardial surface in 4. Ventricular prepotentials were recorded at the successful ablation site in 80% of these patients. In 5 patients, ablation was abandoned because of inaccessibility of the catheter to the myocardium or high impedance with radiofrequency application within the GCV. In the remaining 4 patients, epicardial mapping suggested VA origins in a region of low voltage that was located superior to the GCV (inaccessible area), and ablation was abandoned because of close proximity to the coronary arteries or high impedance. A right bundle-branch block, transition zone, R-wave amplitude ratio in leads III to II, Q-wave amplitude ratio in leads aVL to aVR, and S waves in lead V 6 accurately predicted the site of origin. Conclusions-LV summit VAs may be ablated within the GCV or inferior to the GCV on the epicardial surface, though sites superior to the GCV are usually inaccessible to ablation. (Circ Arrhythm Electrophysiol. 2010;3:616-623.)
There are differences in the electrocardiographic and electrophysiological features among VAs originating from these regions that are helpful for their diagnosis and effective catheter ablation.
The occurrence of ventricular premature depolarizations in survivors of myocardial infarction is a risk factor for subsequent sudden death, but whether antiarrhythmic therapy reduces the risk is not known. The Cardiac Arrhythmia Suppression Trial (CAST) is evaluating the effect of antiarrhythmic therapy (encainide, flecainide, or moricizine) in patients with asymptomatic or mildly symptomatic ventricular arrhythmia (six or more ventricular premature beats per hour) after myocardial infarction. As of March 30, 1989, 2309 patients had been recruited for the initial drug-titration phase of the study: 1727 (75 percent) had initial suppression of their arrhythmia (as assessed by Holter recording) through the use of one of the three study drugs and had been randomly assigned to receive active drug or placebo. During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5). They also accounted for the higher total mortality (56 of 730 [7.7 percent] and 22 of 725 [3.0 percent], respectively; relative risk, 2.5; 95 percent confidence interval, 1.6 to 4.5). Because of these results, the part of the trial involving encainide and flecainide has been discontinued. We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.
Background-Atrial fibrillation (AF) may recur after pulmonary vein isolation (PVI) as the result of either recurrent PV conduction or non-PV foci. This study characterized the electrophysiological findings of patients with recurrent AF after initially successful PVI and the clinical outcome after a repeat procedure. Methods and Results-Among 185 patients undergoing PVI, 52 reported no significant improvement in their clinical course. We analyzed PV conduction in 51 PVs (15 patients) at repeat PVI. All PVs were isolated with either RF (30 W, 50°C, 60 seconds) or cryoablation (Ϫ80°C for 5 minutes). At repeat study, 42 of the previously isolated 51 PVs had return of conduction. All patients had recurrent conduction in Ն2 PVs, with only 1 non-PV focus identified. The mean number of RF applications required to re-isolate the PVs was fewer at the repeat compared with the initial procedure (10Ϯ6 versus 4Ϯ2, PϽ0.005). Over a period of 15Ϯ6 months, all but 1 patient was clinically improved by the second procedure. Conclusions-In patients with recurrent AF after PVI, return of PV conduction can be expected. Repeat PVI provides significant clinical benefit for these patients. These results suggest that if permanent PV isolation is the ablation strategy, different techniques may be required to improve long-term efficacy.
Background-Several distinct forms of focal ventricular tachycardia (VT) from the left ventricle (LV) have been described. We report a new syndrome of VT arising from the base of the posterior papillary muscle in the LV. Methods and Results-Among 290 consecutive patients who underwent ablation for VT or symptomatic premature ventricular complexes (PVCs) based on a focal mechanism, 7 patients were found to have an ablation site at the base of the posterior papillary muscle in the LV. All patients had normal LV systolic function and a normal baseline electrocardiogram. The electrocardiogram during VT or PVCs demonstrated a right bundle-branch block and superior-axis QRS morphology in all patients. VT was not inducible by programmed atrial or ventricular stimulation. In 2 patients with sustained VT, overdrive pacing neither terminated VT nor demonstrated any criterion for transient entrainment. Activation mapping localized the earliest site of activation to the base of the posterior papillary muscle in all patients. When Purkinje potentials were recorded at the site of successful ablation, these potentials preceded local ventricular muscle potentials during sinus rhythm. During VT or PVCs, however, the ventricular muscle potential always preceded the Purkinje potentials. After recurrence of VT or PVCs with standard radiofrequency ablation, irrigated ablation was successful in eliminating the arrhythmia in all patients. Over a mean follow-up period of 9 months, all patients have been free of PVCs and VT. Conclusion-We present a distinct syndrome of VT arising from the base of the posterior papillary muscle in the LV by a nonreentrant mechanism. Ablation can be challenging, and irrigated ablation may be necessary for long-term success.
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