Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia.

We describe a case of post-incisional atrial tachycardia resembling typical atrial flutter on the surface ECG. Typical atrial flutter reentry was ruled out by the results of activation and entrainment mapping. Nevertheless, overdrive pacing from the lateral edge of the cavo-tricuspid isthmus produced tachycardia entrainment with concealed fusion associated with post-pacing and stimulus-to-P wave onset intervals exactly matching the tachycardia cycle length duration and the electrogram-to-P wave onset interval, respectively. Therefore, that site was firstly severed by sequential radiofrequency pulses. However, a transformation of the tachycardia P wave morphology and endocardial activation sequence, not associated with tachycardia termination or cycle length modification occurred. After additional mapping manoeuvres, a relatively small reentrant circuit was identified in the low and mid aspect of the lateral right atrium with the critical isthmus located between the lower border of a cannulation atriotomy and the crista terminalis, close to the inferior vena cava orifice. A single radiofrequency pulse at that site terminated the tachycardia. Both the electrocardiographic pattern and the endocardial mapping data obtained in our case might be explained by a split of the reentrant wavefront into a secondary wavelet which freely propagated through the cavo-tricuspid isthmus without completing the peritricuspid loop. In conclusion, bystander cavo-tricuspid isthmus activation during atrial tachycardia may simulate a typical atrial flutter pattern on the surface ECG. Further studies should evaluate the prevalence of this propagation pattern in post-incisional atrial reentry and atypical atrial flutters, and identify its implications for ablation strategy.

Iterative atrial tachycardia originating from the coronary sinus musculature.

A case of iterative atrial tachycardia leading to dilated cardiomyopathy is reported. During electrophysiologic study, the tachycardia showed a markedly irregular cycle length associated with changes in atrial activation breakthrough as demonstrated by coronary sinus (CS) recordings and frequently degenerated into self-terminating atrial fibrillation. Left atrial transseptal mapping demonstrated the earliest endocardial atrial activation close to the posterolateral mitral annulus, but this was invariably later than that recorded within the CS, where low-energy radiofrequency applications eliminated the tachycardia. No acute vessel damage was observed at postablation CS angiography. In accordance with previously published experimental data, we hypothesized that the muscular sleeves surrounding the CS might be involved in the genesis of this tachycardia. During 6-month follow-up, the patient remained asymptomatic without tachycardia recurrences and with complete recovery of left ventricular function, confirming the reversible nature of the tachycardia-induced cardiomyopathy.

Presence and significance of the left atrionodal connection during atrioventricular nodal reentrant tachycardia.

It has been suggested that the anatomic substrates of dual atrioventricular nodal pathways are likely to be the atrionodal connections. During atrioventricular nodal re-entrant tachycardia (AVNRT) or ventricular pacing (VP), an earliest retrograde atrial activation in the coronary sinus (CS) distal to the ostium (CS breakthrough) would suggest the presence of an exit from a left atrionodal connection. The aim of the study was to evaluate the incidence of such an atrial retrograde activation in the CS during AVNRT and VP. The retrograde atrial activation was recorded during typical AVNRT (38 patients, 27 women, mean age 44 +/- 18 years) by a multipolar catheter in the CS, a decapolar catheter in the His bundle position, and a deflectable quadripolar catheter along the tricuspid annulus anterior to the CS ostium. In 31 patients the retrograde atrial activation was recorded also during VP at a similar cycle length. A CS breakthrough was found in 18 patients during AVNRT (47%) and in 13 patients during VP (42%). Presence or absence of CS breakthrough was concordant between AVNRT and VP in 90% of the patients. A CS breakthrough, suggesting a left-sided atrionodal connection, is frequently recorded both during AVNRT and VP. In patients with a CS breakthrough pattern, the absence of correlation between the His bundle to the earliest CS retrograde atrial electrogram interval and AVNRT cycle length, or any other atrial activation times recorded in the posterior and anterior region of the Koch's triangle, would suggest that the left-sided atrionodal connection is a bystander during typical AVNRT.

Trans-septal catheterization for radiofrequency catheter ablation of cardiac arrhythmias. Results and safety of a simplified method.

AIM: This study reports on the results and safety of a simplified method of trans-septal catheterization for radiofrequency catheter ablation of cardiac arrhythmias. METHODS AND RESULTS: Over 5 years, 411 patients underwent trans-septal catheterization for radiofrequency catheter ablation: 388 patients had a left-sided accessory pathway, 19 a left-sided focal atrial tachycardia, two atrial fibrillation and two post-infarction ventricular tachycardia. All but one patient with ventricular tachycardia underwent elective trans-septal catheterization. In the absence of a patent foramen ovale, puncture of the atrial septum was performed by using an 8F Mullins sheath and a Brockenbrough needle, according to the simplified method described in this paper. Trans-septal catheterization was accomplished in 383/388 patients (98.7%); in 41 patients a second trans-septal catheterization and radiofrequency catheter ablation was performed for initial failure or recurrence. Radiofrequency catheter ablation was successful in 96% of accessory pathway patients, 90% of atrial tachycardia patients, in both patients with atrial fibrillation and in both patients with ventricular tachycardia. No complication related to trans-septal catheterization was observed. CONCLUSION: In experienced hands and according to the method described in this paper, the elective use of transseptal catheterization for radiofrequency catheter ablation in a large cohort of patients with cardiac arrhythmias is feasible, safe and allows successful ablation in the vast majority of the patients.

Insulin induces tyrosine dephosphorylation of a 92 kDA protein in suspended monocytes.

Monocytes bear insulin receptors similar to those expressed in other tissues, but insulin action in these cells remains unclear. There is evidence that adhesion, by generating a complex array of irreversible transformations, may modify the response of cells to other stimuli, such as hormones. The present study aimed to characterise the pattern of insulin induced tyrosine phosphorylation of monocytes in suspension. Monocytes in suspension were obtained by sequential gradient centrifugation and the tyrosine phosphoproteins were analyzed by immunoblot with antiphosphotyrosine antibodies. The major result of the study is that in suspended monocytes insulin induced a dose and time dependent dephosphorylation of a protein with a molecular mass of about 92 kDa without stimulating the tyrosine phosphorylation of the Insulin Receptor Substrat-1 (IRS-1). In conclusion, we showed that in monocytes in suspension insulin seems to activate a tyrosine phosphatase, which, in turn, dephosphorylates a protein with an apparent molecular weight of 92 kDa.

Origin of junctional rhythm during radiofrequency ablation of atrioventricular nodal reentrant tachycardia in patients without structural heart disease.

Junctional rhythm is commonly observed during radiofrequency catheter ablation of the fast or slow pathways of atrioventricular nodal reentrant tachycardia (AVNRT). However, the origin of these beats remains unclear. We analyzed the retrograde atrial activation sequence of 16 patients (mean +/- SD: 41.2 +/- 18.9 years old) undergoing catheter ablation for typical AVNRT with detailed catheter mapping of the triangle of Koch. The earliest atrial activations were concordant during tachycardia and junctional rhythm in only 5 of 16 patients. The findings suggest that junctional rhythm is unlikely to represent direct stimulation of the atrioventricular (AV) node via a discrete slow pathway but rather results from enhanced automaticity from > or =1 sites in the AV nodal transitional zone. The ensuing atrial activation pattern results from anisotropic spread from these sites. In addition, these data imply that the original concept of the AV node comprising 2 anatomically defined pathways may not be valid, and that a functionally defined pathway model may be a more accurate representation.

The variable contribution of functional and anatomic barriers in human ventricular tachycardia: an analysis with resetting from two sites.

OBJECTIVES: This study sought to investigate the influence of stimulation site on the properties of the circuit in ventricular tachycardia. BACKGROUND: A fully excitable gap can be demonstrated in most human ventricular tachycardias. This requires the presence of an arc of block so that the entire circuit can recover from refractoriness within the period of the cycle length. Resetting characterizes the conduction properties of the tissue within the ventricular tachycardia circuit. Previous studies have not investigated the possibility of site-dependent differences in the resetting response. METHODS: Resetting was performed from the right ventricular apex and outflow tract in 23 patients. Two characteristics of the resetting response were analyzed: 1) the total duration of the flat portion, and 2) the slope of the increasing portion. RESULTS: A flat portion of the resetting response was observed in 18 tachycardias; in 8 of the 18, there was a significant site-dependent difference (> or = 40 ms) in the duration of the flat portion. A significant site-dependent difference in the slope of the increasing portion of the resetting curve was seen in 6 of 22 tachycardias. In all, a stimulation site-dependent change in at least one characteristic of the resetting response was seen in 12 (52%) of the 23 tachycardias. CONCLUSIONS: A stimulation site-dependent change in the flat portion of the resetting response is compatible with an arc of block that is at least partially functional in nature. A change in the slope of the increasing portion is compatible with either partially functional circuit barriers or variation in properties of conduction and refractoriness at different locations within the circuit, or both. These observations suggest that a spectrum of circuit properties may exist in humans, with a variable contribution of anatomic and functional characteristics.

Heterogeneity of retrograde fast-pathway conduction pattern in patients with atrioventricular nodal reentry tachycardia: observations by simultaneous multisite catheter mapping of Koch's triangle.

BACKGROUND: Selective ablation of either the fast of the slow pathway resulting in cure of AV nodal reentry tachycardia (AVNRT) has led to the concept that these pathways are discrete, anatomically defined structures. We hypothesized that if a discrete retrograde fast pathway exists, it should be possible to record a single focus of early atrial activation near the apex of Koch's triangle, with sequential spread of depolarization to the rest of the atria. METHODS AND RESULTS: We evaluated 46 patients (33 women, 13 men; mean age, 45 +/- 17 years) undergoing electrophysiology study and catheter ablation for typical AVNRT. Retrograde atrial activation during AVNRT (337 +/- 43 ms) and ventricular pacing at a similar cycle length (352 +/- 51 ms) was recorded in the region of Koch's triangle with a decapolar catheter in the His bundle position, a multipolar catheter in the coronary sinus, and a deflectable quadripolar catheter along the tricuspid annulus anterior to the coronary sinus ostium. Earliest atrial activation was recorded at the apex of the triangle of Koch in 38 patients during ventricular pacing and in 43 patients during AVNRT. A broad wave front of atrial activation was recorded in 17 patients during ventricular pacing and in 26 patients during AVNRT. During AVNRT, only 2 patients had a single early site with focal and sequential activation along the tendon of Todaro. There was concordance in the pattern of atrial activation between ventricular pacing and AVNRT in only 21 of 46 patients. CONCLUSIONS: Retrograde atrial activation over the fast pathway is heterogeneous within Koch's triangle and the coronary sinus, both for the entire population and for individual patients during different modes of activation. These data do not support the concept of an anatomically discrete retrograde fast pathway.

Anatomic substrate for idiopathic left ventricular tachycardia.

BACKGROUND: Idiopathic left ventricular tachycardia (ILVT) characterized by QRS complexes with right bundle-branch block (RBBB) morphology and left axis deviation is a distinct clinical syndrome that also demonstrates a characteristic response to verapamil and inducibility from the atrium in patients without structural heart disease. A false tendon has been described in the left ventricle in a patient with ILVT in whom surgical resection of the false tendon resulted in cure. We hypothesized that the false tendon is responsible for the genesis of similar ventricular tachycardia (VT) in others. METHODS AND RESULTS: We performed transthoracic (TTE) and/or transesophageal (TEE) two-dimensional echocardiograms in 15 patients undergoing catheter ablation for ILVT. There were 12 men and 3 women (mean age, 31 +/- 12 years, with average symptom duration of 11 +/- 9 years). The mean VT cycle length was 360 +/- 70 ms, and all had RBBB morphology with left axis deviation. Cardiac chamber sizes, left ventricular wall thickness, and wall motion were normal in all ILVT patients. TTE and/or TEE demonstrated a false tendon extending from the posteroinferior left ventricular free wall to the left ventricular septum in all ILVT patients. The false tendons were thick (> or = 2 mm maximal thickness) in 5 patients and thin (< 2 mm maximal thickness) in 10 patients. We compared ILVT patients with a control group of 671 consecutive patients referred for echocardiography for other reasons. The mean age for the control group was 42 years. A false tendon was seen in the left ventricle in 34 of 671 (5%). In the control group patients with a false tendon, 2 patients had a history of VT (left bundle-branch block morphology) and 1 had ventricular fibrillation. The false tendons in the control patients were also oriented transversely across the ventricular cavity but were somewhat thinner (< 2 mm maximal thickness in 32 of 34 patients). Catheter ablation with the use of radiofrequency and/or direct current applied to the posteroapical septum resulted in cure in 14 of 15 patients. CONCLUSIONS: A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum.

Catheter ablation of idiopathic left ventricular tachycardia.

Idiopathic left ventricular tachycardia (ILVT) characterized by right bundle branch block, left axis morphology, response to verapamil and inducibility from the atrium in patients without structural heart disease may represent a distinct clinical entity. We report our experience with catheter ablation of this uncommon arrhythmia using radiofrequency energy (RF) and/or direct current (DC) shocks. Six men and 2 women, aged 16-50 years (mean +/- SD, 32 +/- 13), had recurrent VT for 16 +/- 16 years with a mean frequency of 4 +/- 3 episodes/year. Three patients had syncope during VT. None had identifiable structural heart disease. Catheter ablation was guided by earliest endocardial activation, presence of a high frequency presystolic potential and/or pacemapping of the left ventricle. The left ventricle was accessed via a retrograde aortic approach in 6 patients, a transeptal approach in 1 patient, and a combined approach in the remaining patient. All patients had inducible right bundle branch block morphology, left axis VT with a mean cycle length (CL) of 361 +/- 61 ms. A presystolic potential preceding ventricular activation and the His potential during VT was identified in 4 patients. All ablation sites were identified in a relatively uniform location, in the inferoapical left ventricle. Noninducibility of VT was obtained with RF in 3 patients and with DC in 5 patients. In 1 patient, DC delivery after unsuccessful RF prevented further inducibility. Similarly, RF was successful in 1 patient in whom an initial DC attempt was ineffective. Mean total procedure time was 282 +/- 51 minutes and mean total fluoroscopy time was 40 +/- 15 minutes. There were no complications. One patient treated with DC shock had recurrence of VT during treadmill test the day after ablation and refused repeat ablation. During a mean follow-up of 17 +/- 13 months, no VT recurrences or other cardiovascular events occurred. In conclusion, catheter ablation in the inferoapical left ventricle is an effective treatment for this type of ILVT. RF energy can be safely complemented by low energy DC shocks when the former is ineffective.

Effect of shock timing on efficacy and safety of internal cardioversion for ventricular tachycardia.

OBJECTIVES: We examined the effect of shock timing within the QRS complex on cardioversion efficacy in a randomized crossover test of shocks delivered at two timing intervals relative to QRS onset. BACKGROUND: The local ventricular electrogram is used in implantable cardioverter-defibrillators to synchronize cardioversion shocks to terminate ventricular tachycardia. However, the timing of the local electrogram relative to global ventricular depolarization is variable, depending on the site of ventricular tachycardia origin. METHODS: Transvenous defibrillation leads were positioned in the right ventricular apex (cathode), coronary sinus and superior vena cava (anodes) of patients with sustained monomorphic ventricular tachycardia. After repeat ventricular tachycardia induction, sequential shocks with energy settings of 0.5 to 22 J were delivered simultaneously with QRS onset (QRS + 0 shock) or 100 ms after QRS onset (QRS + 100 shock). QRS onset was determined from the surface electrocardiogram. Cardioversion threshold, defined as the lowest shock energy for successful ventricular tachycardia termination, was measured for these two timings. RESULTS: Fifteen patients (13 men, 2 women; mean [+/- SD] age 60.5 +/- 7.7 years) completed testing. Cardioversion threshold was significantly lower with QRS + 100 shocks than QRS + 0 shocks (3.1 +/- 3.5 vs. 10.5 +/- 7.4 J, p < 0.01). Thirteen patients (87%) experienced ventricular tachycardia acceleration with QRS + 0 shocks, but only three patients (20%) had ventricular tachycardia acceleration using QRS + 100 shocks (p < 0.01). Of the 32 failed QRS + 0 shocks, 25 (78%) caused ventricular tachycardia acceleration, whereas only 5 (36%) of the 14 failed QRS + 100 shocks caused ventricular tachycardia acceleration (p < 0.05). Cardioversion threshold was not correlated with ventricular tachycardia cycle length, QRS duration, left ventricular ejection fraction or left ventricular diastolic volume (p = NS). CONCLUSIONS: Internal cardioversion shocks delivered late in the QRS complex during ventricular tachycardia are more effective and have a lower risk of ventricular tachycardia acceleration than those delivered near QRS onset.

Effect of adenosine or adenosine triphosphate on antidromic tachycardia.

OBJECTIVES: This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia. BACKGROUND: Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. METHODS: We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [+/- SD] 32 +/- 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia. RESULTS: Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five patients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP. CONCLUSIONS: 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.

Mechanism of 'inappropriate' sinus tachycardia. Role of sympathovagal balance.

BACKGROUND: "Inappropriate" sinus tachycardia (IST) is an uncommon and poorly defined atrial tachycardia characterized by inappropriate tachycardia and exaggerated acceleration of heart rate with "normal" P wave. The mechanism of this tachycardia is unknown. The purpose of the present study was to determine the role of autonomic balance in the genesis of IST. METHODS AND RESULTS: Six female patients aged 23 to 38 years with IST and 10 age- and sex-matched control subjects were assessed with the following autonomic function tests: (1) sympathovagal balance to the sinus node assessed by calculating the LF/HF (low frequency/high frequency) ratio using power spectral analysis both in the supine position and after 10 minutes of head-up tilt to 60 degrees, (2) cardiovagal reflex assessed by cold face test (CFT), (3) beta-adrenergic sensitivity as determined by calculating isoproterenol dose-response curves and isoproterenol chronotropic dose 25 (CD25), and (4) intrinsic heart rate (IHR) assessed after autonomic blockade with atropine 0.04 mg/kg and propranolol 0.2 mg/kg administered as an intravenous bolus. No significant differences in the LF/HF ratio both in the supine position (2.8 +/- 0.3 versus 2.6 +/- 0.4) and during upright tilt (8.7 +/- 1.3 versus 8.5 +/- 0.5) were observed between control subjects and IST patients. Cardiovagal response to CFT was markedly depressed in all patients (6.3% IST patients versus 24.2% control subjects, P < .001). beta-Adrenergic hypersensitivity to isoproterenol was noted in all patients (mean CD25, 0.29 +/- 0.10 microgram IST patients versus 1.27 +/- 0.4 microgram control subjects; P < .001), and high IHR was noted in all cases. The patients were treated with high doses of beta-blockers with adequate short-term control. Radiofrequency catheter ablation of the sinus node area was performed in one drug-refractory patient. CONCLUSIONS: These findings suggest that the mechanism leading to IST is related to a primary sinus node abnormality characterized by a high IHR, depressed efferent cardiovagal reflex, and beta-adrenergic hypersensitivity.

[Atrioventricular reciprocating tachycardia with QRS type left branch block in patients undergoing radiofrequency catheter ablation: analysis of the substrate and mechanism of tachycardia]. / Tachicardia reciprocante atrioventricolare con QRS tipo blocco di branca sinistra in soggetti da sottoporre ad ablazione transcatetere mediante radiofrequenza: analisi del substrato e del meccanismo della tachicardia.

BACKGROUND: Among patients (pts) with atrioventricular accessory pathway (AP), some cases show wide complex arrhythmias with different QRS morphology. In a subset of these pts, an atrioventricular reentrant tachycardia with left bundle branch block morphology (LBBBM-AVRT) is observed. The aim of this study is: 1) to identify the substrate and the reentrant mechanism underlying the LBBBM-AVRT in pts undergoing radiofrequency catheter ablation (RFCA) of AP; 2) to report the results achieved by RFCA of the identified substrate. METHODS: From May 1991 to April 1993, among the 168 pts who underwent RFCA for arrhythmias related to an AP, 12 (7.1%) (8M, 4F, mean age 35 +/- 21 yrs, range 8-65) showed LBBBM-AVRT, alone or associated with other arrhythmias. Pts, in whom LBBBM was rate-related during orthodromic AVRT, were excluded from this study. During sinus rhythm, QRS complex was normal in 1 pt, while ventricular preexcitation due to a right-sided Kent bundle (KB) was present in 4 pts; among the other pts without preexcitation, 3 showed left bundle branch block (LBBB) and 4 right bundle branch block. In 2 pts, an Ebstein disease was present, while dilated cardiomyopathy was observed in another. The LBBBM-AVRT was iterative in 3 pts and in 6 pts it was the only arrhythmia observed; the mean tachycardia cycle length was 341 +/- 49 msec (range 250-428). In 1 pt, the LBBBM-AVRT was induced only after successful RFCA of a right-sided AP, responsible for orthodromic AVRT. All pts underwent diagnostic electrophysiologic study and RFCA during the same session. RESULTS: In 6/12 pts one or more KBs were observed, while in the remaining 6 an atrioventricular or atriofascicular "Mahaim like" bundle (MB) was present; the patient population was divided into 4 groups on the basis of the substrate and the reentrant mechanism responsible for LBBBM-AVRT. In Group 1, 3 pts were included: the LBBBM-AVRT was an orthodromic AVRT involving the nodal conduction antegradely (showing LBBB also during sinus rhythm) and a left-sided unidirectional KB, retrogradely. In all the 3 pts, the LBBBM-AVRT was iterative and not controlled by antiarrhythmic agents and RFCA of the KB abolished the arrhythmia. Two further pts were included in Group 2: in these pts with multiple bilateral KBs, the LBBBM-AVRT involved a right-sided KB antegradely and a left-sided one, retrogradely. In these 2 pts both KBs were successfully ablated. In 1 pt, considered in Group 3, the LBBBM-AVRT was sustained by an antidromic circuit involving a right-sided KB antegradely and the nodal conduction retrogradely; in this pt the KB was completely interrupted after two RFCA procedures. The remaining 6 pts with MB were included in Group 4: at least one associated electrophysiologic abnormality was present in all (dual A-V nodal pathway in 4/6 and a right-sided KB in 4/6); Ebstein disease was also observed in 2 of them. In 4/6 pts the LBBBM-AVRT was an antidromic tachycardia involving the nodal conduction retrogradely and the MB antegradely; in 3/4 pts the MB was ablated (along with a nodal reentrant tachycardia in 1 pt), while in the remaining pt in whom the non-sustained LBBBM-AVRT, inducible only after RFCA of a right-sided KB, had not been clinically observed, no further ablation was mandatory. In the remaining 2 pts in Group 4, the LBBBM-AVRT was due to the involvement of MB in other arrhythmias such as an AVRT due to a right-sided KB and a "slow-slow" nodal reentrant tachycardia, respectively; the LBBBM-AVRT were abolished by RFCA of these two underlying arrhythmias. All pts are asymptomatic during a 7.9 +/- 6.9 months follow-up. CONCLUSIONS: The LBBBM-AVRT is observed in a minority (7.1%) of the cases referred for RFCA of AP. (ABSTRACT TRUNCATED)