Reducing Ionizing Radiation Associated with Atrial Fibrillation Ablation: An Ultrasound-Guided Approach.

Radiation exposure with cardiac interventional procedures is an emerging concern. Patients receiving radiofrequency ablation for atrial fibrillation (AF) still routinely undergo pre-ablation computed tomography (CT) scans for definition of left atrial and pulmonary vein anatomy, as well as creation of a surrogate geometry. In an effort to decrease ionizing radiation associated with AF ablation, an ultrasound-guided surrogate geometry approach is proposed as an alternative to routine CT imaging. Ten patients underwent AF ablation using intracardiac ultrasound for the creation of a surrogate left atrial geometry (CartoSound, Biosense Webster, CA); and ten control-cases who had conventional CT-guided imaging (CartoMerge, Biosense Webster, CA) were matched for age, gender, and type of catheter ablation. Sources of radiation included 1) intraprocedural fluoroscopy (CartoSound: 151 ± 43 mGray*cm^2, CartoMerge: 174 ± 130 mGray*cm^2; p=0.6) and 2) CT ionizing radiation (CartoSound: 0 mSv, CartoMerge 9.4 ± 2.3 mSv/CT scan.) When comparing clinical success rates after a trial of previously ineffective anti-arrhythmic drugs, ultrasound-guided AF ablation was non-inferior to a CT-guided approach. This potentially obviates the need for CT-guided imaging, therefore reducing doses of ionizing radiation by nearly 10 mSv per AF catheter ablation.

Typical atrial flutter as a risk factor for the development of atrial fibrillation in patients without otherwise demonstrable atrial tachyarrhythmias.

OBJECTIVE: To investigate the incidence of atrial fibrillation after successful radiofrequency ablation for typical atrial flutter (AFL) and to compare its incidence with that of a reference population from the Framingham Heart Study to determine whether atrial flutter is an independent predictor for development of atrial fibrillation. PATIENTS AND METHODS: Medical records of 234 patients who underwent radiofrequency ablation for AFL between January 1, 2002, and June 30, 2006, were reviewed. Patients were excluded if they had a history of atrial fibrillation or sustained atrial arrhythmia other than AFL or if they had atrial tachyarrhythmias other than AFL that could be induced during electrophysiology study (133 total patients excluded). The remaining 101 patients who underwent successful radiofrequency ablation for AFL were monitored for new-onset atrial fibrillation. RESULTS: During the mean+/-SD follow-up period of 574+/-315 days, atrial fibrillation developed in 13 (12.9%) of 101 patients. Atrial fibrillation developed in 12 of these patients within 6 months of ablation. The cumulative event-free rates (95% confidence intervals) were 97% (94%-100%) at 1 month, 91% (87%-97%) at 3 months, and 86% (81%-94%) at 6 months. Compared with the general population, patients aged 50 to 79 years who had ablation had a significantly higher incidence of atrial fibrillation (50-59 years, P=.01; 60-69 years, P=.001; 70-79 years, P=.007). CONCLUSION: Our finding of atrial fibrillation in 12.9% of patients whose atrial flutter was successfully eradicated suggests that patients with atrial flutter are at increased risk of developing atrial fibrillation, especially within the first 6 months after ablation.

Ventricular tachycardia in the absence of structural heart disease.

In up to 10% of patients who present with ventricular tachycardia (VT), obvious structural heart disease is not identified. In such patients, causes of ventricular arrhythmia include right ventricular outflow tract (RVOT) VT, extrasystoles, idiopathic left ventricular tachycardia (ILVT), idiopathic propranolol-sensitive VT (IPVT), catecholaminergic polymorphic VT (CPVT), Brugada syndrome, and long QT syndrome (LQTS). RVOT VT, ILVT, and IPVT are referred to as idiopathic VT and generally do not have a familial basis. RVOT VT and ILVT are monomorphic, whereas IPVT may be monomorphic or polymorphic. The idiopathic VTs are classified by the ventricle of origin, the response to pharmacologic agents, catecholamine dependence, and the specific morphologic features of the arrhythmia. CPVT, Brugada syndrome, and LQTS are inherited ion channelopathies. CPVT may present as bidirectional VT, polymorphic VT, or catecholaminergic ventricular fibrillation. Syncope and sudden death in Brugada syndrome are usually due to polymorphic VT. The characteristic arrhythmia of LQTS is torsades de pointes. Overall, patients with idiopathic VT have a better prognosis than do patients with ventricular arrhythmias and structural heart disease. Initial treatment approach is pharmacologic and radiofrequency ablation is curative in most patients. However, radiofrequency ablation is not useful in the management of inherited ion channelopathies. Prognosis for patients with VT secondary to ion channelopathies is variable. High-risk patients (recurrent syncope and sudden cardiac death survivors) with inherited ion channelopathies benefit from implantable cardioverter-defibrillator placement. This paper reviews the mechanism, clinical presentation, and management of VT in the absence of structural heart disease.