Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.     

Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination

BACKGROUND: Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear. METHODS AND RESULTS: The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit. CONCLUSIONS: Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.     

Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.     

Effects of azimilide dihydrochloride on circus movement atrial flutter in the canine sterile pericarditis model

INTRODUCTION: The effects of a Class III agent, azimilide dihydrochloride, on atrial flutter circuits were studies in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. METHODS AND RESULTS: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg i.v. azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. Effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 +/- 20.1 msec, mean +/- SD) compared with the normal zone (23.3 +/- 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. CONCLUSIONS: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.     

Unusual resetting patterns in response to single atrial extrastimuli during AV junctional reentrant tachycardia

INTRODUCTION: Two unusual resetting patterns were observed in two patients with slow-fast AV junctional reentrant tachycardia (AVJRT) submitted to an electrophysiologic study. METHODS AND RESULTS: After AVJRT induction, resetting was evaluated by introducing single extrastimuli at progressively shorter coupling intervals from the high right atrium (HRA) and the proximal coronary sinus (CS). An alteration in the return cycle length duration allowed demonstration of resetting. In the first patient, during and AVJRT with a large excitable gap, properly timed extrastimuli delivered both from the HRA and CS simultaneously reset the tachycardia and advanced the H electrogram of the preceding tachycardia beat. In the second patient, both HRA and CS stimulation apparently failed to reset AVJRT (return cycle length unchanged), but, at critical coupling intervals, the cycle length duration of the tachycardia beat following the return cycle was consistently shortened. CONCLUSION: During slow-fast AVJRT, single atrial stimulation from sites remote to the reentrant circuit may result in unusual resetting patterns. Further studies are required to evidence the full spectrum of resetting in AVJRT.     

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.     

Detection of BK polyomavirus genotypes in healthy and HIV-positive children

BACKGROUND: Atrial flutter is a common arrhythmia which frequently recurs after cardioversion and is relatively difficult to control with antiarrhythmic agents. AIMS: To evaluate the success rate, recurrence rate and safety of radiofrequency, (RF) ablation for atrial flutter in a consecutive series of patients with drug refractory chronic or paroxysmal forms of the arrhythmia. METHODS: Electrophysiologic evaluation of atrial flutter included activation mapping with a 20 electrode halo catheter placed around the tricuspid annulus and entrainment mapping from within the low right atrial isthmus. After confirmation of the arrhythmia mechanism with these techniques, an anatomic approach was used to create a linear lesion between the inferior tricuspid annulus and the eustachian ridge at the anterior margin of the inferior vena cava. In order to demonstrate successful ablation, mapping techniques were employed to show that bi-directional conduction block was present in the low right atrial isthmus. RESULTS: Successful ablation was achieved in 26/27 patients (96%). In one patient with a grossly enlarged right atrium, isthmus block could not be achieved. Of the 26 patients with successful ablation, there has been one recurrence of typical flutter (4%) during a mean follow-up period of 5.5 +/- 2.7 months. This patient underwent a successful repeat ablation procedure. Of eight patients with documented clinical atrial fibrillation (in addition to atrial flutter) prior to the procedure, five continued to have atrial fibrillation following the ablation. There were no procedural complications and all patients had normal AV conduction at the completion of the ablation. CONCLUSIONS: RF ablation is a highly effective and safe procedure for cure of atrial flutter. In patients with chronic or recurrent forms of atrial flutter RF ablation should be considered as a first line therapeutic option.     

An Italian experience of radiofrequency transcatheter ablation in type-I atrial flutter: the results and follow-up

BACKGROUND: Type I atrial flutter (AF) is a supraventricular tachycardia that is notoriously disabling and resistant to antiarrhythmic drugs. The introduction of an effective non-pharmacologic technique, such as radiofrequency catheter ablation (RF), opened new therapeutic prospects for the management of this arrhythmia. The aim of our study was to evaluate the long-term efficacy of atrial flutter RF using a successful procedure marker of bi-directional conduction block in the isthmus. METHODS: In the last consecutive 50 patients (pts) who underwent RF procedure for AF at our Center (46 pts during spontaneous or induced AF and 4 in sinus rhythm) after the successful interruption of AF we performed the usual reinduction attempts and well atrial pacing from 2 sites in the right atrium (in 18 pts before and after RF and in 32 only after RF). The sites of pacing were site 1: low lateral right atrium (LRA); site 2: proximal coronary sinus (PCS). The 50 pts consisted of 13 females, 37 males with a mean age of 62.5 +/- 9.7 years (35-83). The end-point for the procedure was: 1) abrupt interruption of AF; 2) inability to reinduce AF; 3) recognition of atrial activation sequence during pacing in LRA and in PCS compatible with conduction block in the isthmus. RESULTS: The RF was successful in terminating AF in all pts after 11 +/- 7 applications of energy. After ablation, sustained AF was no longer inducible by atrial pacing. After RF, during pacing in sinus rhythm from LRA, the lower septum and PCS presented a delayed activation after the His region. Similarly, during pacing from PCS after ablation, the atrial activation sequence was modified: the low lateral right atrium was now activated by a single front after the high lateral atrium. No acute complications were noted in any pts during or after procedure. AF recurred in 9 pts. Four pts now present chronic atrial fibrillation. The mean follow-up period is 14.8 +/- 8 months. All the patients were discharged without antiarrhythmic therapy. CONCLUSIONS: The mechanism of successful ablation is the bi-directional conduction block in the isthmus with the evidence of the changes in the right atrial activation sequence during atrial pacing in sinus rhythm in LRA and in PCS before and after RF.     

Spinal inputs from lateral columns to reticulospinal neurons in lampreys

The excitable gap of a reentrant circuit has both temporal (time during the cycle length that the circuit is excitable) and spatial (length of the circuit that is excitable at a given time) properties. We determined the temporal and spatial properties of the excitable gap in reentrant circuits caused by nonuniform anisotropy. Myocardial infarction was produced in canine hearts by ligation of the left anterior descending coronary artery. Four days later, reentrant circuits were mapped in the epicardial border zone of the infarcts with a multielectrode array during sustained ventricular tachycardia induced by programmed stimulation. During tachycardia, premature impulses were initiated by stimulation at sites around and in the reentrant circuits, and their conduction characteristics in the circuit were mapped. All circuits had a temporal excitable gap in at least part of the circuit, which allowed premature impulses to enter the circuit. Completely and partially excitable segments of the temporal gap were identified by measuring conduction velocity of the premature impulses; conduction was equal to the native reentrant wave front in completely excitable regions and slower than the reentrant wave front in partially excitable regions. In some circuits, a temporal gap existed throughout the circuit, permitting the entire circuit to be reset over a range of premature coupling intervals, although the size of the gap varied at different sites. In other circuits, the gap became so small at local sites that even though premature impulses could enter the circuit, the circuit could not be reset. Premature impulses could terminate reentry in circuits that could be reset or not. We also found a significant spatial gap, which was identified by determining the distance between the head of the circulating wave front, which could be located on the activation map, and its tail, which was the site most distal from the head as located by the site of entry of the premature wave front into the circuit. The spatial gap could also vary in different parts of the circuit. Therefore, nonuniform anisotropic reentrant circuits have both a temporal and spatial excitable gap with fully and partially excitable components that change in different parts of the circuit.     

Isolated paralysis of the ramus marginalis mandibulae nervi facialis: clinical aspects, etiology, diagnosis and therapy. An overview]

INTRODUCTION: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. METHODS AND RESULTS: The study population consisted of 144 patients (mean age 56 +/- 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 +/- 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. CONCLUSION: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.     

Clinical study on 6 cases of urosepsis associated with septic shock

A linear lesion created at the right atrial isthmus by radiofrequency current application can successfully eliminate common atrial flutter (AF). The mechanism of unsuccessful cases has not yet been well delineated. This study sought to investigate the cause of unsuccessful cases of radiofrequency catheter ablation of AF. Sixty-six patients with refractory common AF were referred for radiofrequency catheter ablation. Radiofrequency current was applied to the right atrial isthmus between the inferior vena cava and tricuspid annulus or between the coronary sinus orifice and tricuspid annulus. In 5 (8%) of the 66 patients, a morphological change of the flutter wave was observed in the 12-lead ECG concomitant with the change of the atrial excitation sequence during the delivery of radiofrequency energy without the termination of atrial flutter. In 8 (12%) patients, the morphology of the new AF wave, which was provoked electrically after the termination of the original AF, was different, and the average flutter cycle length also differed in 3 cases (2%). The results of radiofrequency application could be misinterpreted as unsuccessful when the occurrence of another, different type of AF has been overlooked following the elimination of the original AF during the radiofrequency catheter ablation procedure. It is possible that the flutter circuit can take an alternative pathway despite the complete conduction block at the right atrial isthmus.     

Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter

BACKGROUND: The electrophysiological mechanisms for successful catheter ablation of atrial flutter (AFI) targeting the inferior vena cava-tricuspid annulus (IVC-TA) isthmus have not been determined. METHODS AND RESULTS: Twenty patients with common AFI were studied. All had inducible common AFI, and 8 of them had both common and reverse AFI. Right atrial (RA) activation sequences were investigated during pacing from sites proximal (low lateral RA) and distal (proximal coronary sinus) to the IVC-TA isthmus both during entrainment of common or reverse AFI and during pacing in sinus rhythm. This was repeated after ablation. During pacing in sinus rhythm from the low lateral RA, the septum was activated by caudocranial and craniocaudal wave fronts. Similarly, during pacing from the proximal coronary sinus, the lateral RA was activated by two wave fronts. Catheter ablation of the IVC-TA isthmus induced dramatic changes in mapping due to the loss of caudocranial wave front in all but 1 patient. The septum and the lateral RA were activated by a single craniocaudal front as during entrainment of reverse or common AFI, respectively. After a follow-up of 8 +/- 2 months, common or reverse AFI occurred in 4 patients. Two had no or only unidirectional changes in the isthmus conduction induced by ablation. The other 2 had a late recovery of conduction. CONCLUSIONS: The present study provides evidence that the mechanism of successful AFI ablation targeting the IVC-TA isthmus is local bidirectional conduction block. This change can be used as a new and complementary electrophysiological end point for the procedure. AFI recurrences are associated with failure to achieve a permanent block.     

Conduction properties of the crista terminalis in patients with typical atrial flutter: basis for a line of block in the reentrant circuit

INTRODUCTION: Previous mapping studies in patients with typical atrial flutter have demonstrated the crista terminalis to be a posterior barrier of the reentrant circuit forming a line of block. However, the functional role of the crista terminalis in patients with or without a history of atrial flutter is not well known. The aim of this study was to determine whether the conduction properties of the crista terminalis are different between patients with and those without a history of atrial flutter. METHODS AND RESULTS: The study population consisted of 12 patients with clinically documented atrial flutter (group 1) and 12 patients with paroxysmal supraventricular tachycardia as well as induced atrial flutter (group 2). A 7-French, 20-pole, deflectable Halo catheter was positioned around the tricuspid annulus. A 7-French, 20-pole Crista catheter was placed along the crista terminalis identified by the recording of double potentials with opposite activation sequences during typical atrial flutter. After sinus rhythm was restored, pacing from the low posterior right atrium near the crista terminalis was performed at multiple cycle length to 2:1 atrial capture. No double potentials were recorded along the crista terminalis during sinus rhythm in both groups. In group 1, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 638 +/- 119 msec. After infusion of propranolol, it was prolonged to 832 +/- 93 msec without change of the interdeflection intervals of double potentials. In group 2, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 214 +/- 23 msec. After infusion of procainamide, it was prolonged to 306 +/- 36 msec with increase of interdeflection interval of double potentials. CONCLUSION: The crista terminalis forms a line of transverse conduction block during typical atrial flutter. Poor transverse conduction property in the crista terminalis may be the requisite substrate for clinical occurrence of typical atrial flutter.     

Mechanism and location of atrial flutter in transplanted hearts: observations during transient entrainment from distant sites

OBJECTIVES: This study was designed to elucidate the location and mechanism of typical atrial flutter in the transplanted heart. BACKGROUND: Although the F wave morphology in atrial flutter is similar in nontransplanted and transplanted hearts, the surgical incision needed for the atrial anastomosis may create a distinct electrophysiologic substrate of atrial flutter. METHODS: Entrainment from the lateral wall of the right atrium and interatrial septum was used to determine the location of atrial flutter in five patients with a transplanted heart and six patients with a nontransplanted heart. The difference between the first postpacing interval (FPPI) and the flutter cycle length (FCL) was used as an index of proximity to the circuit. RESULTS: In the transplant group, the FPPI was equal to the FCL at sites located close to the tricuspid annulus (TA); the mean differences (+/-SD) were 1 +/- 5 and -1 +/- 2 ms at the lateral wall and interatrial septum, respectively. However, from sites close to the surgical incision at the lateral wall and at the interatrial septum, these differences were significantly longer (29 +/- 12 and 27 +/- 9 ms, respectively, p < 0.05). In the nontransplant group, the FPPI was similar to the FCL at points in the lateral wall and interatrial septum close to the TA (mean difference 7 +/- 6 and 6 +/- 11 ms, respectively) and at sites close to the crista terminalis (CT) in the lateral wall (mean difference 4 +/- 4 ms). However, in sites separated from the TA at the interatrial septum the difference was markedly longer (35 +/- 11 ms, p < 0.05). CONCLUSIONS: Atrial flutter in transplanted hearts may best be explained by macroreentry around the tricuspid ring. In non-transplanted hearts a different structure (perhaps the CT?) may be the basis for atrial flutter at the lateral wall.     

Atrial conduction abnormalities in patients with systemic progressive sclerosis

BACKGROUND: Atrial abnormalities in patients with progressive systemic sclerosis have not been evaluated in terms of intra-atrial conduction. We hypothesized that a delay in atrial conduction in these patients might produce diastolic abnormalities as well as atrial arrhythmias. OBJECTIVE: To evaluate the atrial function of patients with progressive systemic sclerosis by using echocardiography to measure the intra-atrial electromechanical activation coupling interval. METHODS: Twenty patients with progressive systemic sclerosis were assessed by Doppler echocardiography. Twenty age-matched healthy controls were also evaluated. Two-dimensional guided M-modes of ventricular long axes were recorded using simultaneous phono- and electrocardiograms of the apical four chamber view at the right lateral, septal and left lateral sites of the atrioventricular rings. Transmitral and tricuspid pulsed Doppler flow velocities were also recorded. Filtered P wave duration was measured on the signal averaged ECG to determine the duration of atrial electrical activation. RESULTS: There was a delay in P on the electrocardiogram (P) at the onset of atrial contraction on long axis M-modes at all three atrioventricular ring sites in patients with progressive systemic sclerosis as compared with controls (P-right; 56 +/- 13 vs 47 +/- 10 ms, P-septal; 74 +/- 14 vs 55 +/- 10 ms, and P-lateral; 93 +/- 16 vs 72 +/- 11 ms, P < 0.01). Inter-atrial conduction time [(P-lateral)-(P-right)] was delayed in patients with progressive systemic sclerosis, compared with healthy controls (37 +/- 15 vs 25 +/- 6 ms, P < 0.01). Mitral A waves acceleration and deceleration times were also decreased in the patients. The interval was prolonged between P to the onset and the peak of the A wave in transmitral flow. Duration of the filtered P wave was significantly prolonged in progressive systemic sclerosis as compared with controls (124 +/- 12 ms vs 106 +/- 8 ms, P < 0.01). PQ intervals, E waves and acceleration and deceleration times did not differ significantly in progressive systemic sclerosis vs, controls. The A wave acceleration rate on transmitral flow (peak A wave velocity/acceleration time) showed a significant correlation with inter-atrial conduction delay (r = 0.55, P < 0.01). CONCLUSIONS: Intra-atrial electromechanical coupling intervals were delayed in patients with progressive systemic sclerosis. Thus, the mechanical late diastolic filling time due to atrial contraction in the total diastolic phase was severely limited, and this resulted in a restricted mitral A wave. We should therefore evaluate patients with progressive systemic sclerosis for significant atrial abnormalities.     

Successful irrigated-tip catheter ablation of atrial flutter resistant to conventional radiofrequency ablation

BACKGROUND: Catheter ablation of typical right atrial flutter is now widely performed. The best end point has been demonstrated to be bidirectional isthmus block. We investigated the use of irrigated-tip catheters in a small subset of patients who failed isthmus ablation with conventional radiofrequency (RF) ablation. METHODS AND RESULTS: Of 170 patients referred for ablation of common atrial flutter, conventional ablation of the cavotricuspid isthmus with >21 applications failed to create a bidirectional block in 13 (7.6%). An irrigated-tip catheter ablation was performed on identified gaps in the ablation line according to a protocol found to be safe in animals: a moderate flow rate of 17 mL/min and temperature-controlled (target, 50 degrees C) RF delivery with a power limit of 50 W. Bidirectional isthmus block was achieved in 12 patients by use of a mean delivered power of 40+/-6 W with a single application in 6 patients and 2 to 6 applications in the other 6. No side effects occurred during or after the procedure. CONCLUSIONS: Irrigated-tip catheter ablation is safe and effective for achieving cavotricuspid isthmus block when conventional RF energy has failed.     

Atrial macroreentry involving the myocardium of the coronary sinus: a unique mechanism for atypical flutter

Atrial flutter involving either clockwise or counterclockwise rotation around the tricuspid annulus utilizing the subeustachian isthmus has been well described. However, macroreentrant atrial circuits in atypical atrial flutter in patients who have not undergone previous surgery or without atrial disease are not well defined. We describe a patient without structural heart disease who presented with an atrial macroreentrant rhythm. Entrainment mapping demonstrated a critical isthmus within the coronary sinus. Activation mapping demonstrated double potential throughout the length of the coronary sinus with disparate activation sequences. A circuit involving the myocardium of the coronary sinus, exiting in the lateral left atrium, down the interatrial septum, and reentering into the coronary sinus was identified. Successful ablation of the rhythm was accomplished by a circumferential radiofrequency application within the coronary sinus.     

Radiofrequency catheter ablation in patients with common atrial flutter

BACKGROUND: Type 1 atrial flutter is produced by a reentry circuit located in the right atrium that can be interrupted applying radiofrequency in the inferior cava-tricuspid valve isthmus. AIM: To report our experience in the treatment of atrial flutter with radiofrequency ablation. PATIENTS AND METHODS: Nine patients (eight male) whose ages ranged from 6 to 72 years old were studied. Two patients had an operated congenital cardiopathy, two had high blood pressure, one was subjected previously to radiofrequency ablation due to a left paraspecific pathway, one developed a cardiac failure secondary to tachycardia and three did not have evidences of cardiopathy. RESULTS: In two patients, atrial flutter was not interrupted. In the other seven patients, radiofrequency ablation was successful. There were three relapses in the first month after the procedure, of these, two patients were successfully treated again. After a mean follow up of 4.5 months, these patients are asymptomatic and without antiarrhythmic drugs. Analysis of obtained signals, showed that radiofrequency that interrupted atrial flutter always occurred in zones of double potentials. CONCLUSIONS: Radiofrequency ablation is an effective treatment for atrial flutter and the zone of successful ablation is associated to the presence of double atrial potentials.     

Radiofrequency catheter ablation in type I atrial flutter: preliminary experience of 10 cases

Common atrial flutter results from macroreentry in the right atrium. Catheter ablation of slow conduction, between tricuspid annulus and inferior vena cava (TA-IVC) or tricuspid annulus and coronary sinus ostium (TA-CS os) has been reported to terminate and prevent recurrence of this arrhythmia. We reported 10 consecutive patients, 7 men and 3 women, who underwent radiofrequency catheter ablation of common atrial flutter. The mean age was 59.4 +/- 11.2 years (range 42-82 years). During the paroxysmal atrial flutter, all patients had palpitation, 4 had dyspnea on exertion, 3 patients had syncope and 1 patient had presyncope. The mean duration of symptoms was 5.7 +/- 4.9 years (range 0.5-13 years). Two patients had dilated cardiomyopathy, 1 Ebstein's anomaly and 1 chronic obstructive pulmonary disease. Four patients (40%) had history of atrial fibrillation (AF) before ablation. The mean cycle length of atrial rhythm was 257.2 +/- 36.6 ms. Ablation was done by anatomical approach and could terminate arrhythmia in 9 patients (90%), 7 from TA-IVC, 2 from TA-CS os without major complication. The mean number of applications was 20.4 +/- 16.9 and turned atrial flutter to normal sinus rhythm in 13.5 +/- 10.7 seconds. Fluoroscopic and procedure times were 38.4 +/- 31.4 and 157.2 +/- 68.8 minutes, respectively. During the follow-up period of 24.0 +/- 28.7 weeks, 2 patients had recurrent atrial arrhythmia, 1 atrial fibrillation and 1 atrial flutter type I, giving the final success rate of 70 per cent. All patients who had recurrence or failure had a history of paroxysmal AF before ablation. In conclusion, radiofrequency catheter ablation in atrial flutter type I, using anatomical approach, is an effective treatment to terminate and prevent this arrhythmia in short term follow-up. It may be considered as an alternative treatment in patients with atrial flutter who were refractory to antiarrhythmic agents.     

Alveolar ridge reconstruction and/or preservation using root form bioglass cones

OBJECTIVE: Since the 1990's radiofrequency ablation radiofrequency ablation of atrial flutter has evolved in its methods and results. We have reviewed the long term outcome in 62 patients with typical (common) or reversed (clockwise) flutter undergoing radiofrequency ablation between 1990 and 1997. PATIENTS AND METHODS: Fifty men and 12 women, aged 22-78 years (57 +/- 12) with flutter recurring after cardioversion and antiarrhythmic drugs make this series. Flutter was typical in 59 cases and reversed in 3. There was no heart disease in 14, bronchopulmonary disease in 10, coronary disease in 9, cardiomyopathies in 6 and other processes in the remainder. In 5 cases with previous surgery for atrial or ventricular septal defect, Ebstein's anomaly or myxoma, we treated also a macro-reentry tachycardia around the atriotomy in the right atrium. Radiofrequency ablation was directed to the inferior vena cava-tricuspid isthmus in typical and reversed flutter, and to the isthmus between the inferior end of the atriotomy and the inferior vena cava, in the lateral right atrium, in the atriotomy tachycardias. We subdivided our patients in Group 1 (24 patients), treated until the end of 1994, and Group 2 (38 patients) treated since 1995 using specially designed catheters and trying to produce isthmus block as the endpoint of the procedure. RESULTS: Radiofrequency ablation interrupted flutter in 61 of 62 cases (98.4%), and the atriotomy tachycardia in all 5. The number of application in Group 1 was 18.6 +/- 10.1 vs 12 +/- 10 in Group 2 (p < 0.05). Follow-up was 40 +/- 24 months in Group 1 vs 16 +/- 9.5 in Group 2. Flutter recurred in 58% of Group 1 and 13% of Group 2 patients (p < 0.001), usually 1-3 months after radiofrequency ablation and they were successfully treated by new radiofrequency ablation with a small number of applications. There was no recurrence of atriotomy tachycardia. Atrial fibrillation occurred in 14 patients (23%) (11 paroxysmal, 3 persistent), with equal incidence in both groups. At the end of follow-up 85% of the patients were in sinus rhythm, although 6 needed pacemakers for sinus node dysfunction (3) or AV ablation (3). Antiarrhythmic drugs were used by 46% of patients in Group 1 and 26% in Group 2 (p = NS) for atrial arrhythmias or recurrent flutter. CONCLUSIONS: Radiofrequency ablation is an effective treatment for flutter and macro-reentry atriotomy tachycardia. Progress in methods have improved results significantly. Atrial fibrillation can still be a problem in 20-25% of the patients after flutter control.