Limitation of the long-lived 121Te contaminant in production of 123I through the 124Xe(p,x) route.

The 13.2 h half-life radioisotope (123)I is widely used in clinical nuclear medicine diagnosis. At present it is mostly produced in nca form by proton irradiation of highly enriched (124)Xe in dedicated gas target set-ups and relying on the decay chain (123)Cs-(123)Xe-(123)I. Depending on the irradiation conditions contamination with long-lived (121)Te, a daughter product of the co-produced rather short lived (121)I, occurs and can limit the useful shelf life of the (123)I solution. Excitation function of the (124)Xe(p,α)(121)I, (124)Xe(p,2n)(123)Cs and (124)Xe(p,2p)(123)Xe reactions are measured up to 35 MeV using the stacked gas cell technique and high-resolution γ-ray spectrometry. The experimental data were compared with the earlier literature values, with new results of the ALICE-IPPE and EMPIRE-II codes and with the data taken from the TENDL-2009 database. Existing discrepancies in cross-section data are largely solved and new recommended values are proposed. From fits to the new excitation curves integral (123)I batch yields and (121)Te contaminations for realistic production conditions are derived. Optimization of irradiation and cooling times and energy degradation in the target can strongly influence the contamination level.

C reactive protein concentration and recurrence of atrial fibrillation after electrical cardioversion.

BACKGROUND: To test the hypothesis that a high C reactive protein (CRP) concentration would predict recurrence of atrial fibrillation (AF) after cardioversion in patients taking antiarrhythmic drugs. METHODS: 111 patients who underwent direct current cardioversion for symptomatic AF were enrolled. Blood was drawn for CRP determination before cardioversion on the same day. All patients were taking antiarrhythmic drugs before and after electrical cardioversion. RESULTS: After a mean follow up of 76 days, 75 patients had recurrence of AF. In univariate analysis, the median CRP concentration was significantly higher in patients with AF recurrence (3.95 mg/l v 1.81 mg/l, p = 0.002). Among the 55 patients with CRP in the upper 50th centile, 44 (80%) experienced recurrence of AF over a total follow up of 8.98 patient years, whereas among the 56 patients with CRP in the lower 50th centile, 31 (55%) experienced recurrence of AF over a total follow up of 14.3 patient years (p < 0.001). The adjusted hazard ratio comparing the upper 50th centile of CRP with the lower 50th centile of CRP was 2.0 (95% confidence interval 1.2 to 3.2, p = 0.007). CONCLUSIONS: CRP is independently associated with recurrence of AF after electrical cardioversion among patients taking antiarrhythmic drugs. These results suggest that inflammation may have a role in the pathogenesis of AF resistant to antiarrhythmic drugs.

Usefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope: a randomized control study.

INTRODUCTION: The efficacy of midodrine for the management of patients with neurocardiogenic syncope was assessed prospectively in a randomized control study. METHODS AND RESULTS: Patients who had at least monthly occurrences of syncope and a positive tilt-table test were included in the study. A total of 61 patients were randomly allocated to treatment either with midodrine or with fluid, salt tablets, and counseling. Midodrine was given at a starting dose of 5 mg three times a day and increased up to a dose of 15 mg three times a day when required. Midodrine was given during the daytime every 6 hours. Thirty-one patients were assigned to treatment with midodrine; the other 30 patients were advised to increase their fluid intake and were instructed to recognize their prodromes and abort the progression to syncope. Patients were followed-up for at least 6 months. A quality-of-life questionnaire was administered at the time of randomization and 6 months after. At the 6-month follow-up, 25 (81%) of 31 midodrine-treated patients and 4 (13%) of the 30 fluid-therapy patients had remained asymptomatic (P < 0.001). One patient had to discontinue taking midodrine due to severe side effects and another six patients experienced minor side effects that did not require drug discontinuation. CONCLUSION: Midodrine appeared to provide a significant benefit in patients with neurocardiogenic syncope. To prevent recurrence of symptoms, dose adjustments were required in about one third of patients.

Ventricular tachycardias arising from the aortic sinus of valsalva: an under-recognized variant of left outflow tract ventricular tachycardia.

OBJECTIVES: To describe a normal heart left bundle branch block, inferior axis ventricular tachycardia (VT), that could not be ablated from the right or left ventricular outflow tracts. BACKGROUND: Whether these VTs are epicardial and can be identified by a specific electrocardiographic pattern is unclear. METHODS: Twelve patients with normal heart left bundle branch block, inferior axis VT and previously failed ablation were included in this study. Together with mapping in the right and left ventricular outflow tracts, we obtained percutaneous epicardial mapping in the first five patients and performed aortic sinus of Valsalva mapping in all patients. RESULTS: No adequate pace mapping was observed in the right and left ventricular outflow tracts. Earliest ventricular activation was noted in the epicardium and the aortic cusps. All patients were successfully ablated from the aortic sinuses of Valsalva (95% CI 0% to 18%). The electrocardiographic pattern associated with this VT was left bundle branch block, inferior axis and early precordial transition with Rs or R in V2 or V3. Ventricular tachycardia from the left sinus had rS pattern in lead I, and VT from the noncoronary sinus had a notched R wave in lead I. None of the patients had complications and all remained arrhythmia-free at a mean follow-up of 8 +/- 2.6 months. CONCLUSIONS: Normal heart VT with left bundle branch block, inferior axis and early precordial transition can be ablated in the majority of patients from either the left or the noncoronary aortic sinus of Valsalva.

A simple method of mapping atrial premature depolarizations triggering atrial fibrillation.

Atrial premature depolarizations (APDs) originating from focal sites, particularly the pulmonary veins (PV), may become triggers of atrial fibrillation (AF). Accurate mapping of APDs with conventional methods may be time consuming and expose the patient to unnecessary instrumentation of the left atrium. We hypothesized that the atrial activation sequence recorded using a simple system that includes an esophageal catheter and a custom-made 16-electrode catheter with two sets of floating electrodes eight in the coronary sinus and eight in the high right atrium) could be sufficient to localize the APDs. The study included 29 patients with frequent APDs and AF refractory to antiarrhythmic medications. The APD site of origin was confirmed with single-point sequential mapping techniques using the CARTO system ten patients) or by placement of multielectrode catheters in the right and left PV (19 patients). Of the 29 patients, 20 patients had a single APD focus; 8 patients had two different APD morphologies; and 1 patient had three APD foci. Mapping for ablation of the APD foci showed earliest activation in the left superior PV in 12 patients, right superior PV in 15 patients, right middle PV in 4 patients, right inferior PV in 1 patient, the lingular branch of the left superior PV in 2 patients, left inferior PV in 2 patients, and right atrium along the crista terminalis in 3 patients. The activation sequence and relative timing of the recordings obtained with our catheter configuration was highly predictive of right and left atrial origin and, more importantly, of right and left PV foci.

Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a three-dimensional nonfluoroscopic mapping system: long-term follow-up.

The purpose of this study was to assess the feasibility and long-term results of empirical isolation of both superior pulmonary veins in patients with chronic AF. Although localizing and ablating the focal triggers of AF has been proven an effective approach, this strategy is time consuming, often requires multiple procedures, and carries the risk of pulmonary vein stenosis. Whether ostial electrical isolation of the superior pulmonary veins, without initial detailed mapping, is a more efficient approach is not known. The study included 71 consecutive patients who had chronic AF. Using a nonfluoroscopic electroanatomic mapping system, the left and right superior pulmonary veins were ablated circumferentially at the venoatrial junction, with the aim of achieving electrical isolation of the veins. Following ablation, if frequent atrial ectopies were present, mapping and ablation were considered. The patients were periodically followed with 48-hour Holter and loop recorder monitoring. After the ablation of the right and left superior pulmonary veins 59 (83%) of 71 patients maintained sinus rhythm without premature atrial beats. The remaining 12 patients underwent further mapping and ablation including 5 patients who required isolation of the left inferior pulmonary veins. True electrical isolation could be achieved only in 45 (31%) of the 147 targeted veins. At the latest follow-up (mean 29 +/- 8 months), 80% of the patients with upper vein isolation remained in sinus rhythm off medications, 62% of the patients maintained sinus rhythm on previously ineffective medications, and 17% continued to be in AF. Fourteen (20%) patients developed intermittent episodes of left atrial flutter, and mapping in these patients revealed large electrically silent areas in the left atrium. Empirical isolation of pulmonary veins appeared to be an effective approach to help maintain sinus rhythm in patients with chronic AF. True electrical isolation of the pulmonary veins was associated with a higher likelihood of long-term success. Left atrial flutter was seen in a significant number of patients at long-term follow-up.

Radiofrequency ablation of a right atrial appendage-ventricular accessory pathway by transcutaneous epicardial instrumentation.

Epicardial location of accessory AV pathways may be responsible for the failure of conventional endocardial radiofrequency catheter ablation. Transcutaneous epicardial instrumentation provides access to the normal pericardium with no need for invasive thoracotomy or thoracoscopy. We report the case of successful epicardial mapping and ablation of a right atrial appendage-ventricular connection using a percutaneous epicardial approach, after repeated failure of endocardial ablation attempts.

First human experience with pulmonary vein isolation using a through-the-balloon circumferential ultrasound ablation system for recurrent atrial fibrillation.

BACKGROUND: Standard mapping and ablation of focal sources of atrial fibrillation are associated with very long procedure times and low efficacy. An anatomic approach to complete pulmonary vein isolation could overcome these limitations. METHODS AND RESULTS: Fifteen patients with atrial fibrillation refractory to medication underwent circumferential isolation of the pulmonary veins by using a novel catheter, with an ultrasound transducer (8-MHz) mounted near the tip, in a saline-filled balloon. Twelve atrial foci and/or atrial fibrillation triggers were identified in 9 patients (pulmonary vein locations: left upper, 3; right upper, 6; right middle, 1; right lower, 1; and left inferior, 1). In 5 patients, lesions were placed in the absence of any mapped triggers. Irrespective of trigger mapping, circumferential isolation of both upper pulmonary veins was attempted in all patients. The lower pulmonary veins were ablated when sinus rhythm activation mapping revealed evidence of a sleeve of atrial muscle in the vein. The median number of lesions per patient required to isolate 1 pulmonary vein was 4 (range, 1 to 29). After ablation, no evidence of narrowing was seen with repeat venography or follow-up computed tomography scan. After a mean follow-up of 35+/-6 weeks, 5 patients had recurrence of atrial fibrillation. Three responded to drugs that were previously ineffective, and 2 remained in atrial fibrillation. CONCLUSIONS: This novel ultrasound ablation system can successfully isolate multiple pulmonary veins. At early follow-up, this approach seems to be effective in preventing recurrent atrial fibrillation in a significant number of patients.

Association of exercise-induced ventricular ectopic activity with thallium myocardial perfusion and angiographic coronary artery disease in stable, low-risk populations.

This study sought to determine the association of exercise-induced ventricular ectopic activity with thallium perfusion defects and severity of angiographic coronary artery disease (CAD). Two cohorts consisting of adults without heart failure or known severe ventricular ectopic activity at rest were studied. The first cohort consisted of adults (n = 2,743) who underwent maximum exercise thallium stress testing. The second cohort consisted of adults (n = 423) who underwent coronary angiography within 90 days of treadmill testing. Significant exercise-induced ventricular ectopic activity was defined as frequent ventricular premature complexes or nonsustained ventricular tachycardia. Severe CAD was defined as left main CAD (> or = 50% stenosis), 3-vessel CAD (> or = 70% stenosis), or 2-vessel CAD with > or = 70% stenosis of the proximal left anterior descending artery. In the thallium cohort, exercise-induced ventricular ectopic activity was associated with a greater frequency of thallium defects (35.2% vs 18.7%, odds ratio [OR] 2.35, 95% confidence intervals [CI] 1.62 to 3.42, p <0.001); after adjusting for possible confounders, this association persisted (for any defect adjusted OR 1.66, 95% CI 1.09 to 2.53, p = 0.02; for septal defect adjusted OR 2.77, 95% CI 1.51 to 5.07, p <0.001). There was no association between exercise-induced ventricular ectopic activity and mortality during 2 years of follow-up. In the angiographic cohort, there was no association of exercise-induced ventricular ectopy with severe CAD (19% vs 20%, OR 0.93, 95% CI 0.41 to 2.09, p = NS). Exercise-induced ventricular ectopic activity was associated with a greater likelihood of thallium perfusion defects, but was not associated with angiographic severity of coronary disease or with short-term mortality.

Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications.

OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.

Exercise testing and training in patients with malignant arrhythmias.

Patients with malignant arrhythmias are a challenge when they present to the laboratory for exercise testing and training. The complex metabolic and electrophysiological changes that occur during and after exercise may suppress or potentiate arrhythmias and alter the efficacy and safety of antiarrhythmic agents. The presence of an ICD adds a level of complexity to the study; however, a general understanding of how ICDs function and a review of the programmed parameters before the study will result in a lesser likelihood of complication and more efficient and appropriate action, should a complication occur. Exercise testing and training are valuable methods for the evaluation and treatment of patients with malignant ventricular arrhythmias. Exercise testing is a useful adjunctive technique in the exposure of arrhythmia and the evaluation of the efficacy and proarrhythmic potential of antiarrhythmic agents. These patients are excellent candidates for rehabilitation and exercise training programs, which may result in increased functional capacity and improved quality of life. With this knowledge and adherence to the appropriate guidelines for patient selection and testing, exercise testing and training of patients with malignant arrhythmias can be prescribed and conducted in a safe, controlled manner in an atmosphere of confidence and professionalism.