Treatment of Resistant Port-Wine Stains with a Variable-Pulse Pulsed Dye Laser

BACKGROUND: The conventional pulsed dye laser (PDL), operating at a wavelength of 585 nm and a pulse duration of 0.45 ms, usually does not achieve complete clearance in the majority of port-wine stains (PWSs). OBJECTIVE: In this study, we demonstrate the efficacy of a variable-pulse pulsed dye laser (VPPDL) equipped with cryogen spray cooling (CSC) in the treatment of PWS that have become resistant to PDL treatment. METHODS: Forty Asian patients with Fitzpatrick skin types III to IV were enrolled in this study. All patients had previously been treated by the PDL at least eight times (mean, 12.8+/-5.9) and had reached a treatment plateau. A VPPDL with a wavelength of 595 nm and a spot size of 7 mm was used. The patients were treated with fluences between 9 and 15 J/cm(2) and pulse durations of 1.5 to 10 ms. Four treatments were administered at 8-week intervals for each lesion. Three months after the last treatment, all patients were evaluated for the degree of improvement by two independent clinicians. RESULTS: Eight patients had excellent improvement, 9 had good improvement, 11 had fair improvement, and 12 had poor improvement. No complications were observed during the course of laser treatment. Vessels larger than 30 microm were not seen in the biopsy specimens obtained after the final treatment. CONCLUSION: The VPPDL is more effective than the PDL and the VPPDL should be used for treating PDL-resistant PWSs. Nonetheless, vessels less than 30 mum in diameter are resistant to both PDL and VPPDL treatment.     

Idiopathic Focal Ventricular Arrhythmias Originating from the Anterior Papillary Muscle in the Left Ventricle

Introduction: Focal ventricular arrhythmias (VAs) have been reported to arise from the posterior papillary muscle in the left ventricle (LV). We report a distinct subgroup of idiopathic VAs arising from the anterior papillary muscle (APM) in the LV.
Methods and Results: We studied 432 consecutive patients undergoing catheter ablation for VAs based on a focal mechanism. Six patients were identified with ventricular tachycardia (VT, n = 1) or premature ventricular contractions (PVCs, n = 5) with the earliest site of ventricular activation localized to the base (n = 3) or middle portion (n = 3) of the LV APM. No Purkinje potentials were recorded at the ablation site during sinus rhythm or the VAs. All patients had a normal baseline electrocardiogram and normal LV systolic function. The VAs exhibited a right bundle branch block (RBBB) and right inferior axis (RIA) QRS morphology in all patients. Oral verapamil and/or Na⁺ channel blockers failed to control the VAs in 4 patients. VT was not inducible by programmed electrical stimulation in any of the patients. In 4 patients, radiofrequency current with an irrigated or conventional 8-mm-tip ablation catheter was required to achieve a lasting success. Two patients had recurrent PVCs after a conventional radiofrequency ablation with a 4-mm-tip ablation catheter had initially suppressed the arrhythmia.
Conclusions: VAs may arise from the base or middle portion of the APM and are characterized by an RBBB and RIA QRS morphology and focal mechanism. Catheter ablation of APM VAs is typically challenging, and creation of a deep radiofrequency lesion may be necessary for long-term success.     

Idiopathic Left Ventricular Arrhythmias Originating Adjacent to the Left Aortic Sinus of Valsalva: Electrophysiological Rationale for the Surface Electrocardiogram

IVT Arising Adjacent to the Left Sinus of Valsalva. Background: Idiopathic ventricular arrhythmias (VAs) may be amenable to catheter ablation within or adjacent to the left sinus of Valsalva (LSOV). However, features that discriminate these sites have not been defined. The purpose of this study was to determine the electrocardiographic and electrophysiological features of VAs originating within or adjacent to the LSOV. Methods and Results: We studied 48 consecutive patients undergoing successful catheter ablation of idiopathic VAs originating from the left coronary cusp (LCC, n = 29), aortomitral continuity (AMC, n = 10) and great cardiac vein or anterior interventricular cardiac vein (Epi, n = 9). A small r wave, or rarely an R wave, was typically observed in lead I during the VAs and pacing in these regions. An S wave in lead V5 or V6 occurred significantly more often during both the VAs and pacing from the AMC than during that from the LCC and Epi (p < 0.05 to 0.0001). For discriminating whether VA origins can be ablated endocardially or epicardially, the maximum deflection index (MDI = the shortest time to the maximum deflection in any precordial lead/QRS duration) was reliable for VAs arising from the AMC (100%), but was less reliable for LCC (73%) and Epi (67%) VAs. In 3 (33%) of the Epi VAs, the site of an excellent pace map was located transmurally opposite to the successful ablation site (LCC = 1 and AMC = 2). Conclusions: The MDI has limited value for discriminating endocardial from epicardial VA origins in sites adjacent to the LSOV probably due to preferential conduction, intramural VA origins or myocardium in contact with the LCC. (J Cardiovasc Electrophysiol, Vol. 21, pp. 170‐176, February 2010)