[Show abstract][Hide abstract] ABSTRACT: Reducing sympathetic output to the heart from the neuraxis can protect against ventricular arrhythmias. The purpose of this study was to assess the value of thoracic epidural anesthesia (TEA) and left cardiac sympathetic denervation (LCSD) in the management of ventricular arrhythmias in patients with structural heart disease.
Clinical data of 14 patients (25 to 75 years old, mean+/-SD of 54.2+/-16.6 years; 13 men) who underwent TEA, LCSD, or both to control ventricular tachycardia (VT) refractory to medical therapy and catheter ablation were reviewed. Twelve patients were in VT storm, and 2 experienced recurrent VT despite maximal medical therapy and catheter ablation procedures. The total number of therapies per patient before either procedure ranged from 5 to 202 (median of 24; 25th and 75th percentile, 5 and 56). Eight patients underwent TEA, and 9 underwent LCSD (3 patients had both procedures). No major procedural complications occurred. After initiation of TEA, 6 patients had a large (> or =80%) decrease in VT burden. After LCSD, 3 patients had no further VT, 2 had recurrent VT that either resolved within 24 hours or responded to catheter ablation, and 4 continued to have recurrent VT. Nine of 14 patients survived to hospital discharge (2 TEA alone, 3 TEA/LCSD combined, and 4 LCSD alone), 1 of the TEA alone patients underwent an urgent cardiac transplantation.
Initiation of TEA and LCSD in patients with refractory VT was associated with a subsequent decrease in arrhythmia burden in 6 (75%) of 8 patients (68% confidence interval 51% to 91%) and 5 (56%) of 9 patients (68% confidence interval 34% to 75%), respectively. These data suggest that TEA and LCSD may be effective additions to the management of refractory ventricular arrhythmias in structural heart disease when other treatment modalities have failed or may serve as a bridge to more definitive therapy.
[Show abstract][Hide abstract] ABSTRACT: Long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT) are two of the most common, potentially lethal, cardiac channelopathies. Treatment strategies for the primary and secondary prevention of life-threatening polymorphic ventricular tachycardia/fibrillation include pharmacotherapy with beta-blockers, implantable cardioverter defibrillators, and left cardiac sympathetic denervation (LCSD).
This study sought to report our institutional experience with LCSD using video-assisted thoracic surgery (VATS).
From November 2005 through November 2008, 20 patients (8 female, average age at surgery 9.1 +/- 9.7 years, range 2 months to 42 years) underwent LCSD via either a traditional approach (N = 2) or VATS (N = 18). A total of 12 patients had genotype-positive LQTS (7 LQT1, 2 LQT2, 1 LQT3, 2 LQT1/LQT2), 2 had JLNS, 4 had genotype-negative LQTS, and 2 had CPVT1. Electronic medical records were reviewed for patient selection, perioperative complications, and short-term outcomes.
LCSD was performed as a secondary prevention strategy in 11 patients (8 LQTS patients, average QTc 549 ms) and as primary prevention in 9 patients (average QTc 480 ms). There were no perioperative complications, including no intraoperative ectopy, no uncontrolled hemorrhage, and no VATS cases requiring conversion to a traditional approach. The average length of available follow-up was 16.6 +/- 9.5 months (range 4 to 40 months). Among the 18 patients who underwent VATS-LCSD, the average time from operation to dismissal was 2.6 days (range 1 day to 15 days), the majority being next-day dismissals. Among those receiving LCSD as secondary prevention, there has been a marked reduction in cardiac events.
We present a series of 20 patients with LQTS and CPVT who underwent LCSD, 18 using VATS. The minimally invasive VATS surgical approach was associated with minimal perioperative complications, including no intraoperative ectopy and excellent immediate and short-term outcomes. Videoscopic denervation surgery, in addition to traditional LCSD, offers a safe and effective treatment option for the personalized medicine required for patients with LQTS/CPVT.
Heart rhythm: the official journal of the Heart Rhythm Society 07/2009; 6(6):752-9. DOI:10.1016/j.hrthm.2009.03.024 · 5.08 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Drug-induced long QT syndrome is a serious adverse drug reaction. Methadone prolongs the QT interval in vitro in a dose-dependent manner. In the inpatient setting, the frequency of QT interval prolongation with methadone treatment, its dose dependence, and the importance of cofactors such as drug-drug interactions remain unknown.
We performed a systematic, retrospective study comparing active or former intravenous drug users receiving methadone and those not receiving methadone among all patients hospitalized over a 5-year period in a tertiary care hospital. A total of 167 patients receiving methadone fulfilled the inclusion criteria and were compared with a control group of 80 injection drug users not receiving methadone. In addition to methadone dose, 15 demographic, biological, and pharmacological variables were considered as potential risk factors for QT prolongation.
Among 167 methadone maintenance patients, the prevalence of QTc prolongation to 0.50 second((1/2)) or longer was 16.2% compared with 0% in 80 control subjects. Six patients (3.6%) in the methadone group presented torsades de pointes. QTc length was weakly but significantly associated with methadone daily dose (Spearman rank correlation coefficient, 0.20; P<.01). Multivariate regression analysis allowed attribution of 31.8% of QTc variability to methadone dose, cytochrome P-450 3A4 drug-drug interactions, hypokalemia, and altered liver function.
QT interval prolongation in methadone maintenance patients hospitalized in a tertiary care center is a frequent finding. Methadone dose, presence of cytochrome P-450 3A4 inhibitors, potassium level, and liver function contribute to QT prolongation. Long QT syndrome can occur with low doses of methadone.
Archives of Internal Medicine 07/2006; 166(12):1280-7. · 17.33 Impact Factor
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