Plasma levels of NT-pro-BNP in patients with atrial fibrillation before and after electrical cardioversion.

OBJECTIVE: Plasma levels of brain natriuretic peptide (BNP) have been examined in studies on patients with persistent atrial fibrillation, both before and after electrical cardioversion. Studied patients often showed a comorbidity with congestive heart failure, which complicates interpretation of measured BNP values as a natriuretic peptide. The aim of this study was to examine plasma levels of N-terminal fragment pro-brain natriuretic peptide (NT-pro-BNP), which is the more stable but inactive cleavage product of pro-BNP in patients with atrial fibrillation, but normal left ventricular ejection fraction, before and after electrical cardioversion. PATIENTS AND METHODS: NT-pro-BNP plasma levels of 34 consecutive patients were measured before, shortly after and 11 days after electrical cardioversion. All patients showed a normal ejection fraction after echocardiographic or laevocardiographic criteria. RESULTS: At baseline, all patients showed elevated NT-pro-BNP compared to a healthy control group (1086 vs. 66.9 pg/ml, p<0.001). After a mean follow-up time of 11 days in patients with persistent restored sinusrhythm, NT-pro-BNP decreased from 1071 pg/ml at baseline to 300 pg/ml (p<0.001). In contrast, patients with recurrence of atrial fibrillation showed increased levels from 1570.5 pg/ml at baseline to 1991 pg/ml (p=0.13; n.s.). Recurrence of atrial fibrillation was independent from height of NT-pro-BNP levels at baseline (p=0.23). CONCLUSIONS: Atrial fibrillation in patients with a normal left ventricular ejection fraction is associated with elevated NT-pro-BNP plasma levels, which decrease when a persistent sinus-rhythm can be restored by electrical cardioversion. On the other hand, NT-pro-BNP seems to increase (n.s.) when recurrence of atrial fibrillation occurs. Finally, NT-pro-BNP is no valid predictor for long-term success of sinus-rhythm restoration by electrical cardioversion.

[Curative therapy in symptomatic atrial ectopy]. / Kurative Therapie bei symptomatischer atrialer Extrasystolie.

A female patient without underlying heart disease was highly symptomatic from short runs of atrial ectopy. Sustained atrial tachycardia or atrial fibrillation never occurred. Due to ineffective pharmacological therapy, catheter ablation combined with electroanatomic mapping (CARTO) was performed effectively. Characteristics of ectopic atrial tachycardia and the electrophysiological techniques are described.

Identification and ablation of atypical atrial flutter. Entrainment pacing combined with electroanatomic mapping.

Differentiation between typical and atypical atrial flutter solely based upon surface ECG pattern may be limited. However, successful ablation of atrial flutter depends on the exact identification of the responsible re-entrant circuit and its critical isthmus. Between August 2001 and June 2003, we performed conventional entrainment pacing within the cavotricuspid isthmus in 71 patients with sustained atrial flutter. In patients with positive entrainment we considered the arrhythmia as typical flutter and treated them with conventional ablation of the cavotricuspid isthmus. As a consequence of negative entrainment we performed 3D-electroanatomic activation mapping (CARTO trade mark ). Conventional ablation of the right atrial isthmus was successful in all patients (n = 54) with positive entrainment. We performed electroanatomic mapping in the remaining 17 patients (14 male; age 60.9 +/- 16 years) resulting in the identification of 6 cases with typical and 11 cases with atypical flutter. Therefore, entrainment pacing was able to predict the true presence of typical atrial flutter in 91.5%. Atypical flutter was right sided in 4 patients and left sided in 7 cases. Electrically silent ("low voltage") areas probably demonstrating atrial myopathy were identified in all cases with left sided and in 2 patients with right sided flutter. In these patients targets for ablation lines were located between silent areas and anatomic barriers (inferior pulmonary veins, mitral respectively tricuspid annulus, or vena cava inferior). In 1 patient, the investigation was stopped due to variable ECG pattern and atrial cycle lengths. In the remaining cases, ablation was acutely successful. One patient, after surgical closure of a ventricular septal defect, demonstrated a dual-loop intra-atrial reentry tachycardia dependent on two different isthmuses. This arrhythmia required ablation of those distinct isthmuses to be interrupted. After a mean follow-up of 8.8 +/- 3.4 months, there was one patient with a recurrence of left-sided atrial flutter. Another patient developed permanent atrial fibrillation shortly after the procedure. Mean duration time of the procedure was 235.6 +/- 56.4 min (right atrium: 196 +/- 17.3 min; left atrium: 267.2 +/- 59.5 min), and average fluoroscopy time was 21.8 +/- 11.7 min (right atrium: 9.5 +/- 6 min; left atrium: 28.9 +/- 7 min). There was no incidence of serious complications associated with these procedures. In conclusion, conventional pacing in the cavotricuspid isthmus combined with electroanatomic mapping was an effective method to differentiate between typical and atypical atrial flutter. Electroanatomic mapping was a powerful tool both for identification of different atrial re-entrant circuits including their critical isthmuses as well as for effective application of individual ablation line strategies.

[Clinical experiences with cooled radiofrequency ablation of ectopic atrial tachycardia employing an electroanatomic mapping system]. / Klinische Erfahrungen mit der gekühlten Radiofrequenzablation ektoper atrialer Tachykardien unter Einsatz eines elektroanatomischen Mappingsystems.

Due to its variable origin success for ablation of ectopic atrial tachycardia (EAT) has been difficult to achieve using conventional mapping and ablation strategies. In contrast, no information in the literature is available about the use of a nonfluoroscopic, 3-dimensional electroanatomic mapping system (CARTO) combined with the cooled ablation technology creating deeper lesions in experimental studies compared to standard catheters. In 20 consecutive patients (15 female; age 52.5 +/- 15.4 years), a single focus responsible for clinical EAT has been mapped. Twelve EATs were located in the right atrium, whereas 8 foci were left sided including 3 origins within a pulmonary vein (PV). Due to the reported development of PV stenosis in the ablative treatment of focal atrial fibrillation, direct ablation applied inside the PV was avoided. Instead, PV-disconnection achieved by the use of a Lasso trade mark catheter in 1 case and by circumferential ablation around the PV in 2 other patients was preferred. In 2 patients, ablation was not attempted because of an origin located directly in the area of the atrioventricular node. In another case, CARTO mapping was stopped due to persistent mechanical termination of the tachycardia with no possibility of reinduction. In the latter, ablation was performed in sinus rhythm at the earliest mapped site before terminating. Three weeks later another episode of EAT was noted in this patient. In the remaining 17 cases, ablation was associated with acute success and no recurrences of sustained tachycardia in all patients. Mean duration time was 192 +/- 53.3 min (right atrium 161 +/- 37.9 min; left atrium 229.6 +/- 46.2 min), and average fluoroscopic time was 22.8 +/- 9.7 min (right atrium 17.1 +/- 6.2 min; left atrium 29.8 +/- 8.9 min). There was no incidence of serious complications associated with this procedure. In conclusions, electroanatomical mapping including cooled ablation was a safe and feasible strategy in treating EATs. The benefit of this technique may imply the combination of both precise localization of the focus and effective applications of radiofrequency pulses, thereby minimizing acute failures or reablation. Due to the time consuming point by point data acquisition, the ability to generate precise maps demonstrating the earliest activation at their exact anatomical location can be limited by transient or persistent termination of the tachycardia.

[Catheter ablation of ectopic atrial tachycardia by electrical pulmonary vein disconnection]. / Katheterablation einer ektopen atrialen Tachykardie mittels elektrischer Pulmonalvenendiskonnektion.

We report a 25-year-old female patient with a long history of symptomatic paroxysmal supraventricular tachycardia. Electroanatomic activation mapping demonstrated a focal tachycardia originating in the right upper pulmonary vein, 3 cm distal to the ostium. Due to the recent experiences in the management of focal atrial fibrillation with catheter ablation, direct ablation applied inside the pulmonary vein was avoided. Instead, an electrical disconnection of the pulmonary musculature from the left atrium guided by a circumferential 10-electrode mapping catheter was performed. The patient has since been asymptomatic during follow-up.

Nitric oxide inhibits APO-1/Fas-mediated cell death.

Activation of the cysteine protease caspases, which are homologous to the product of Caenorhabditis elegans cell-death gene ced 3, is required to mediate APO-1/Fas-induced apoptosis. We report here that nitric oxide (NO) released by exogenous NO donors, as well as NO endogenously derived by transfection with the inducible NO synthase, substantially suppresses APO-1/Fas-triggered cell death of Jurkat cells. The inhibitory NO effect was independent of cGMP, because 8-bromo-cGMP did not influence APO-1/Fas-mediated apoptosis. In contrast, NO interferes with the APO-1/Fas-induced stimulation of caspases. NO inhibits the proteolytic cleavage of caspase-3 (CPP32) into its active subunits, thereby suppressing caspase-3 activity. In addition, NO potently inhibits apoptosis induction by overexpresssion of the death domain protein FADD or the immediate downstream target caspase-8. These results suggest that NO modulates the proteolytic cascade upstream of caspase-3. Indeed, NO specifically S-nitrosylates caspase-8 and caspase-1 and thereby may prevent activation of the proteolytic cascade. The NO-mediated increase in the resistance toward induction of apoptosis may play a major role in mediating immune responses, as well as in the pathogenesis of autoimmune diseases.