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conduction block in the ivc - tricuspid isthmus schwartzman et al j am coll cardiol 1996; 28:1519 shah et al j am coll

Organized Atrial Tachycardias

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conduction block in the ivc - tricuspid isthmus schwartzman et al j am coll cardiol 1996; 28:1519 shah et al j am coll

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    1. Hello, this is Bill Stevenson and in this presentation we will review catheter ablation for atrial flutter.Hello, this is Bill Stevenson and in this presentation we will review catheter ablation for atrial flutter.

    3. A classification of organized atrial tachycardias is shown on this slide. There are focal ectopic atrial tachycardias that originate from a point source activation spreads out from that source. Typical isthmus dependent atrial flutter is dependent on conduction through the isthmus formed by the tricuspid valve annulus and the inferior vena cava. This includes common clockwise flutter as the circuit is viewed from the right ventricle and looking up at the tricuspid valve annulus. The wavefront circulates down the septum, through the isthmus, up the lateral wall, and across the roof of the right atrium. Counter-clockwise flutter has a circuit revolving in the opposite direction. Lower loop re-entry involves propagation across the posterior wall of the right atrium, across the crista terminalis, and then through the common flutter isthmus. There is a large group of macro re-entrant non-isthmus dependent atrial flutters, most commonly these involve re-entry in the lateral wall of the right atrium. They can occur anywhere including in the left atrium. They are often associated with areas of scar, such as from prior repair of congenital heart disease or the mitral valve.A classification of organized atrial tachycardias is shown on this slide. There are focal ectopic atrial tachycardias that originate from a point source activation spreads out from that source. Typical isthmus dependent atrial flutter is dependent on conduction through the isthmus formed by the tricuspid valve annulus and the inferior vena cava. This includes common clockwise flutter as the circuit is viewed from the right ventricle and looking up at the tricuspid valve annulus. The wavefront circulates down the septum, through the isthmus, up the lateral wall, and across the roof of the right atrium. Counter-clockwise flutter has a circuit revolving in the opposite direction. Lower loop re-entry involves propagation across the posterior wall of the right atrium, across the crista terminalis, and then through the common flutter isthmus. There is a large group of macro re-entrant non-isthmus dependent atrial flutters, most commonly these involve re-entry in the lateral wall of the right atrium. They can occur anywhere including in the left atrium. They are often associated with areas of scar, such as from prior repair of congenital heart disease or the mitral valve.

    4. The re-entry circuit for common isthmus dependent flutter is shown here. The circulating flutter wave fronts are indicated by the yellow arrows. Propagation occurs up the septum, across the roof, and down the lateral wall of the right atrium forms a counter-clockwise circuit. Conduction is also occurring from the septum posteriorly around behind the inferior vena cava. It is likely that conduction is slow in the direction perpendicular to the Crista terminalis. In fact, conduction may be blocked here. This prevents short-circuiting of the re-entry circuit. The mechanism has been well defined. There is patient to patient variability in the course of the path, which is outside of the common isthmus. It may involve the lateral wall or come around posterior in a lower loop fashion. Some patients have a figure-eight circuit with both of these loops involved in the circuit. There can be areas of block along the Crista terminalis or there may be conduction through portion of the Crista terminalis. Some patients have small areas of conduction block present in the common flutter isthmus indicated by the presence of double potentials. There is also a great deal of variability in the anatomy of the common flutter isthmus. There can be thick pectinate muscles, which make ablation difficult or deep recesses, which can be difficult to get to access so that a catheter positioned for ablation may have problems. There may be areas of cooling from blood flow so with low power only small lesions are created.The re-entry circuit for common isthmus dependent flutter is shown here. The circulating flutter wave fronts are indicated by the yellow arrows. Propagation occurs up the septum, across the roof, and down the lateral wall of the right atrium forms a counter-clockwise circuit. Conduction is also occurring from the septum posteriorly around behind the inferior vena cava. It is likely that conduction is slow in the direction perpendicular to the Crista terminalis. In fact, conduction may be blocked here. This prevents short-circuiting of the re-entry circuit. The mechanism has been well defined. There is patient to patient variability in the course of the path, which is outside of the common isthmus. It may involve the lateral wall or come around posterior in a lower loop fashion. Some patients have a figure-eight circuit with both of these loops involved in the circuit. There can be areas of block along the Crista terminalis or there may be conduction through portion of the Crista terminalis. Some patients have small areas of conduction block present in the common flutter isthmus indicated by the presence of double potentials. There is also a great deal of variability in the anatomy of the common flutter isthmus. There can be thick pectinate muscles, which make ablation difficult or deep recesses, which can be difficult to get to access so that a catheter positioned for ablation may have problems. There may be areas of cooling from blood flow so with low power only small lesions are created.

    5. The approach to common counter-clockwise atrial flutter, which is shown on this slide. We typically use a deflectable 20-pole electrode catheter and place this so that the proximal electrodes are in the high right atrium and the catheter then swings down along the lateral wall of the right atrium, through the common flutter isthmus, and the tip electrodes are in the coronary sinus. This facilitates rapid recognition of the typical counter-clockwise atrial flutter activation sequence as shown. Occasionally, we will use more detailed activation sequence maps, as shown on the right where the activation sequence is displayed in a color-coded inner red beam earliest and then progressing to yellow, green, blue, and purple. Of course, since re-entry is a complete circle there is not a truly earliest or latest region and in the lower right-hand portion of this figure the earliest activation meets latest activation that is typical for re-entry. The additional colors in between the purple and the orange are interpolated by the mapping system in this case. Now when you have this activation sequence, the odds are very high that the rhythm you are dealing with is atrial flutter. However, left atrial arrhythmias and even focal atrial tachycardias can mimic this activation sequence on occasion. With left atrial tachycardias, there may be activation over Bachmann’s bundle conducting across the roof of the right atrium and then down the lateral wall. So, a limited mapping sequence will appear to be similar to that of counter-clockwise flutter so we need to do a bit more to sort this out and what our approach is, is to use entrainment mapping in this regard. The approach to common counter-clockwise atrial flutter, which is shown on this slide. We typically use a deflectable 20-pole electrode catheter and place this so that the proximal electrodes are in the high right atrium and the catheter then swings down along the lateral wall of the right atrium, through the common flutter isthmus, and the tip electrodes are in the coronary sinus. This facilitates rapid recognition of the typical counter-clockwise atrial flutter activation sequence as shown. Occasionally, we will use more detailed activation sequence maps, as shown on the right where the activation sequence is displayed in a color-coded inner red beam earliest and then progressing to yellow, green, blue, and purple. Of course, since re-entry is a complete circle there is not a truly earliest or latest region and in the lower right-hand portion of this figure the earliest activation meets latest activation that is typical for re-entry. The additional colors in between the purple and the orange are interpolated by the mapping system in this case. Now when you have this activation sequence, the odds are very high that the rhythm you are dealing with is atrial flutter. However, left atrial arrhythmias and even focal atrial tachycardias can mimic this activation sequence on occasion. With left atrial tachycardias, there may be activation over Bachmann’s bundle conducting across the roof of the right atrium and then down the lateral wall. So, a limited mapping sequence will appear to be similar to that of counter-clockwise flutter so we need to do a bit more to sort this out and what our approach is, is to use entrainment mapping in this regard.

    6. This slide shows pacing from the lateral right atrium electrodes 15 and 16 on a 20-pole mapping catheter. You can see that the cycle length of the tachycardia is 260 milliseconds. We paced slightly faster than that to accelerate all of the electrograms to the paced cycle length. The post-pacing interval has been measured from the last stimulus. This entrains the tachycardia to the next activation at the pacing site. This is 270 milliseconds, only 10 milliseconds longer than the tachycardia cycle length. So we now know that the lateral right atrium is in this flutter circuit. The next thing that we do is pace from another site typically down in the flutter isthmus or at the medial side of isthmus and also confirm that that site is in the flutter circuit. If those two regions are both in the tachycardia circuit, then you can be very confident that this arrhythmia is indeed isthmus dependent flutter. If only the lateral right atrium is in the circuit, you may be dealing with one of those macro re-entrant flutters, which are not isthmus dependent. If the lateral right atrium is remote from the circuit with a long post-pacing interval relative to the tachycardia cycle length, you could even be dealing with a left atrial flutter. This takes just a moment to do and then you have got your re-entry circuit location confirmed. This slide shows pacing from the lateral right atrium electrodes 15 and 16 on a 20-pole mapping catheter. You can see that the cycle length of the tachycardia is 260 milliseconds. We paced slightly faster than that to accelerate all of the electrograms to the paced cycle length. The post-pacing interval has been measured from the last stimulus. This entrains the tachycardia to the next activation at the pacing site. This is 270 milliseconds, only 10 milliseconds longer than the tachycardia cycle length. So we now know that the lateral right atrium is in this flutter circuit. The next thing that we do is pace from another site typically down in the flutter isthmus or at the medial side of isthmus and also confirm that that site is in the flutter circuit. If those two regions are both in the tachycardia circuit, then you can be very confident that this arrhythmia is indeed isthmus dependent flutter. If only the lateral right atrium is in the circuit, you may be dealing with one of those macro re-entrant flutters, which are not isthmus dependent. If the lateral right atrium is remote from the circuit with a long post-pacing interval relative to the tachycardia cycle length, you could even be dealing with a left atrial flutter. This takes just a moment to do and then you have got your re-entry circuit location confirmed.

    7. Once we know we are dealing with atrial flutter, then we select a place to make an ablation line. This slide shows the electroanatomic map of the flutter circuit. If we tilt it up, we see tricuspid annulus at the top, inferior vena cava at the bottom, and activation proceeding from lateral to medial. That is simply a matter of placing a continuous series of ablation lines through the isthmus to result in conduction block. Once we know we are dealing with atrial flutter, then we select a place to make an ablation line. This slide shows the electroanatomic map of the flutter circuit. If we tilt it up, we see tricuspid annulus at the top, inferior vena cava at the bottom, and activation proceeding from lateral to medial. That is simply a matter of placing a continuous series of ablation lines through the isthmus to result in conduction block.

    8. This is recorded during RF application. There is termination of the atrial flutter. You see that immediately prior to block there is a bit of slowing of conduction in the isthmus. Electrograms between poles 5, 6, and 3, 4, which is the septal side of the isthmus in this case show gradually prolongation of the conduction interval between these sites. Then block occurs after de-polarization at electrode 3, 4. So we are making our ablation lesion on the septal side of that. This is recorded during RF application. There is termination of the atrial flutter. You see that immediately prior to block there is a bit of slowing of conduction in the isthmus. Electrograms between poles 5, 6, and 3, 4, which is the septal side of the isthmus in this case show gradually prolongation of the conduction interval between these sites. Then block occurs after de-polarization at electrode 3, 4. So we are making our ablation lesion on the septal side of that.

    9. Conduction block in the IVC - Tricuspid IsthmusSchwartzman et al J Am Coll Cardiol 1996; 28:1519Shah et al J Am Coll Cardiol 2000; 35: 1478 After RF terminates atrial flutter conduction through the isthmus often persists Conduction slowing often occurs before isthmus block conduction slowing can be rate dependent Recovery of conduction after initial isthmus block is common Now once we have terminated atrial flutter, we are not necessarily finished because conduction commonly persists through the isthmus after termination of the flutter. Pacing on either side of the isthmus may easily show this. Conduction slowing in the isthmus often occurs prior to block. If you stop at this point with the resolution of edema from the additional ablation lesions, there will be some recovery and a high risk of recurrence of atrial flutter.Now once we have terminated atrial flutter, we are not necessarily finished because conduction commonly persists through the isthmus after termination of the flutter. Pacing on either side of the isthmus may easily show this. Conduction slowing in the isthmus often occurs prior to block. If you stop at this point with the resolution of edema from the additional ablation lesions, there will be some recovery and a high risk of recurrence of atrial flutter.

    10. So, you need to do a bit more and at this point. What we typically do is to begin pacing from either the coronary sinus electrodes or the lateral right atrium to assess conduction through the isthmus. This schematic shows what happens with pacing from the coronary sinus. As you will see, you have conduction up and around the lateral wall as well as through the isthmus with fusion in the lateral wall and no block. On the right hand side of the figure after block is achieved, activation comes down the lateral wall with no evidence of fusion. Double potentials will be recorded along the line of block.So, you need to do a bit more and at this point. What we typically do is to begin pacing from either the coronary sinus electrodes or the lateral right atrium to assess conduction through the isthmus. This schematic shows what happens with pacing from the coronary sinus. As you will see, you have conduction up and around the lateral wall as well as through the isthmus with fusion in the lateral wall and no block. On the right hand side of the figure after block is achieved, activation comes down the lateral wall with no evidence of fusion. Double potentials will be recorded along the line of block.

    11. Nice examples of this are illustrated here in the publication from Tada and co-workers. In the left hand figure labeled incomplete block, you see the nice V-shaped activation of the lateral wall indicating fusion as the wave front comes down from E8,E7,E6 and up from the coronary sinus and E1, E2, and E3. On the right hand panel, after complete block is achieved, activation of the lateral wall is from high to low. The presence of double-potentials, there is also very instructive during pacing from either side of that region of block. In this case when there is incomplete block, you see that the two arrows under the ablation electrodes identify two potentials, which are separated by 94 milliseconds. Once block is achieved, these become more widely separated 132 milliseconds. This could be shown in the double-potentials separated by greater than 100 milliseconds is relatively specific for complete conduction block through the isthmus. The electrogram polarity of the signal recorded on the side opposite from the pacing site of the flutter line is also of interest. It can indicate conduction block. We see that when there is incomplete block the second potential labeled by the arrow at the ablation site is a QR kind of complex. After conduction block is achieved, the second potential develops more of an S-wave consistent with activation of by a wave front, which is traveling completely towards that site. Reversal of polarity of the potential on the side opposite the pacing site from the block is another marker of conduction block in the isthmus. Nice examples of this are illustrated here in the publication from Tada and co-workers. In the left hand figure labeled incomplete block, you see the nice V-shaped activation of the lateral wall indicating fusion as the wave front comes down from E8,E7,E6 and up from the coronary sinus and E1, E2, and E3. On the right hand panel, after complete block is achieved, activation of the lateral wall is from high to low. The presence of double-potentials, there is also very instructive during pacing from either side of that region of block. In this case when there is incomplete block, you see that the two arrows under the ablation electrodes identify two potentials, which are separated by 94 milliseconds. Once block is achieved, these become more widely separated 132 milliseconds. This could be shown in the double-potentials separated by greater than 100 milliseconds is relatively specific for complete conduction block through the isthmus. The electrogram polarity of the signal recorded on the side opposite from the pacing site of the flutter line is also of interest. It can indicate conduction block. We see that when there is incomplete block the second potential labeled by the arrow at the ablation site is a QR kind of complex. After conduction block is achieved, the second potential develops more of an S-wave consistent with activation of by a wave front, which is traveling completely towards that site. Reversal of polarity of the potential on the side opposite the pacing site from the block is another marker of conduction block in the isthmus.

    12. Markers of Conduction Block increase in trans-isthmus conduction time differential pacing double potentials 100 - 110 ms interval between potentials along entire ablation line differential pacing reversal of electrogram polarity on the opposite side of the ablation line from the pacing site change in p-wave morphology pacing lateral to the ablation line This slide summarizes potential markers of conduction block in the common flutter isthmus. First, an increase in trans-isthmus conduction time with differential pacing so that after block is achieved, pacing on one side results in a long conduction time to the opposite side. If you move the pacing site a little bit further from the line of block, you will see that the conduction time to the opposite side decreases when you have block. This increases when there still slow conduction through the flutter isthmus. Secondly, double-potentials, as we discussed, with a relatively long interval of more than 100 to 110 milliseconds between the two potentials. We like to see this present along the entire ablation line. If we move our pacing site a little bit further from the line of block, then the conduction time from the pacing site to the potential generated by the wave front activates the distal side of the line becomes shorter and that to the proximal side becomes a little bit longer and the opposite occurs if there is still conduction through the isthmus. Thirdly, reversal of the electrogram polarity on the opposite side of the line of block, when block is achieve, and finally one can also look for changes in P-wave morphology when pacing in the low lateral right atrium on the free wall side of the line of block and these are all reviewed nicely in the references listed at the bottom of this slide. On a daily basis, we find that interpreting the double-potentials and simply doing differential pacing is quite useful. There are times where the double-potentials are not easily detectible in the common isthmus, particularly if you have had to do a lot of RF and you have low amplitude signals everywhere through the isthmus. Then it is useful to have some of these other markers to help confirm when you have conduction block. This slide summarizes potential markers of conduction block in the common flutter isthmus. First, an increase in trans-isthmus conduction time with differential pacing so that after block is achieved, pacing on one side results in a long conduction time to the opposite side. If you move the pacing site a little bit further from the line of block, you will see that the conduction time to the opposite side decreases when you have block. This increases when there still slow conduction through the flutter isthmus. Secondly, double-potentials, as we discussed, with a relatively long interval of more than 100 to 110 milliseconds between the two potentials. We like to see this present along the entire ablation line. If we move our pacing site a little bit further from the line of block, then the conduction time from the pacing site to the potential generated by the wave front activates the distal side of the line becomes shorter and that to the proximal side becomes a little bit longer and the opposite occurs if there is still conduction through the isthmus. Thirdly, reversal of the electrogram polarity on the opposite side of the line of block, when block is achieve, and finally one can also look for changes in P-wave morphology when pacing in the low lateral right atrium on the free wall side of the line of block and these are all reviewed nicely in the references listed at the bottom of this slide. On a daily basis, we find that interpreting the double-potentials and simply doing differential pacing is quite useful. There are times where the double-potentials are not easily detectible in the common isthmus, particularly if you have had to do a lot of RF and you have low amplitude signals everywhere through the isthmus. Then it is useful to have some of these other markers to help confirm when you have conduction block.

    13. This slide diagrams one of the more common misleading findings that mimics failure to achieve conduction block and this is a Crista shunt. Typically, what happens is pacing from the coronary sinus you have conduction posterior to the inferior vena cava breaking through the Crista terminalis and activating that low lateral aspect of the flutter isthmus earlier than you anticipate if there is complete block. One sees activation in the low lateral right atrium a bit earlier than activation at the electrodes just superior to that. You think that you don’t have block. There are two ways to sort this out. One is you can pace from the coronary sinus and do a detailed activation map. However, that is somewhat time consuming. Another method described by Anselme and co-workers is in the references listed. Pacing from the posterior wall of the right atrium you may see conduction through the Crista terminalis. Pacing posterior to the coronary sinus on the posterior wall shortens the conduction time to the lateral right atrium. It would lengthen it if there is still slow conduction through the common flutter isthmus. This slide diagrams one of the more common misleading findings that mimics failure to achieve conduction block and this is a Crista shunt. Typically, what happens is pacing from the coronary sinus you have conduction posterior to the inferior vena cava breaking through the Crista terminalis and activating that low lateral aspect of the flutter isthmus earlier than you anticipate if there is complete block. One sees activation in the low lateral right atrium a bit earlier than activation at the electrodes just superior to that. You think that you don’t have block. There are two ways to sort this out. One is you can pace from the coronary sinus and do a detailed activation map. However, that is somewhat time consuming. Another method described by Anselme and co-workers is in the references listed. Pacing from the posterior wall of the right atrium you may see conduction through the Crista terminalis. Pacing posterior to the coronary sinus on the posterior wall shortens the conduction time to the lateral right atrium. It would lengthen it if there is still slow conduction through the common flutter isthmus.

    14. This illustrates the importance of assessing conduction up and down across the flutter line. It is not unusual to have gaps in conduction. One may see widely split double-potentials at one end of the line and narrow double-potentials in these regions of gaps as illustrated. Additional RF applications may be required.This illustrates the importance of assessing conduction up and down across the flutter line. It is not unusual to have gaps in conduction. One may see widely split double-potentials at one end of the line and narrow double-potentials in these regions of gaps as illustrated. Additional RF applications may be required.

    15. There are a number of tools now available to try and create bigger lesions, which help facilitate achieving block in the common flutter isthmus. A saline irrigated ablation catheter cools the tip electrode allowing greater power delivery before maximal temperature is achieved. This catheter is approved for use in ventricular tachycardia. However, it has been studied for use in atrial flutter ablation. A catheter which is available in Europe, but investigational in the US, uses an external irrigation system with small holes in the end of the catheter. Saline flows out these holes. This has been used in atrial flutter. There is an improved 8 mm electrode catheter. This operates on the same principle as the irrigated catheters as in that large electrode tip is cooled by circulating blood. It allows for greater power delivery. These catheters can create conduction block in the common flutter isthmus with a smaller number of RF applications. They can facilitate the procedure.There are a number of tools now available to try and create bigger lesions, which help facilitate achieving block in the common flutter isthmus. A saline irrigated ablation catheter cools the tip electrode allowing greater power delivery before maximal temperature is achieved. This catheter is approved for use in ventricular tachycardia. However, it has been studied for use in atrial flutter ablation. A catheter which is available in Europe, but investigational in the US, uses an external irrigation system with small holes in the end of the catheter. Saline flows out these holes. This has been used in atrial flutter. There is an improved 8 mm electrode catheter. This operates on the same principle as the irrigated catheters as in that large electrode tip is cooled by circulating blood. It allows for greater power delivery. These catheters can create conduction block in the common flutter isthmus with a smaller number of RF applications. They can facilitate the procedure.

    16. I would sound a note of caution. When ablating on the septal side of the isthmus, there is some risk of injuring AV conduction. The reason for this is not completely clear. It may be damage to the AV nodule artery or a catheter malposition, but it has been reported. Secondly, if you are in the orifice of the coronary sinus with one of these cool tip or large tip electrode catheters, there is some possibility of damage to the right coronary artery in that location. Therefore, when using a large tip catheter be very careful to apply our lesions outside of the coronary sinus. We prefer to be on the more lateral side of the flutter isthmus although that is a little bit wider region and may requires additional RF applications. In general, however, the efficacy is similar - ablating on either the septal side isthmus or the lateral side of the isthmus. The site is really selected by ease of catheter manipulation and avoiding any very high voltage areas that may indicate big thick pectinate muscles. I would sound a note of caution. When ablating on the septal side of the isthmus, there is some risk of injuring AV conduction. The reason for this is not completely clear. It may be damage to the AV nodule artery or a catheter malposition, but it has been reported. Secondly, if you are in the orifice of the coronary sinus with one of these cool tip or large tip electrode catheters, there is some possibility of damage to the right coronary artery in that location. Therefore, when using a large tip catheter be very careful to apply our lesions outside of the coronary sinus. We prefer to be on the more lateral side of the flutter isthmus although that is a little bit wider region and may requires additional RF applications. In general, however, the efficacy is similar - ablating on either the septal side isthmus or the lateral side of the isthmus. The site is really selected by ease of catheter manipulation and avoiding any very high voltage areas that may indicate big thick pectinate muscles.

    17. These data from a nice study by Natale and co-workers really makes the point that catheter ablation should be first-line therapy for recurrent atrial flutter. They randomized treatment in sixty-one patients who had had recurrent atrial flutter and who had not failed prior antiarrhytmic drug therapy. Randomized treatments were antiarrhytmic drugs shown versus catheter ablation. During an average follow-up of twenty-two months, atrial flutter recurred in over ninety percent of the drug treated patients and almost two-thirds of them had atrial fibrillation. In contrast, atrial flutter recurred in only six percent of those treated with catheter ablation and fewer than a third had atrial fibrillation during follow-up. Eighty percent were in sinus rhythm at last follow-up. Complications of atrial flutter ablation are quite infrequent. They are often no more than minor groin hematomas. Many of our flutter ablations are performed as out-patient procedures. However, it is important to manage anticoagulation in a fashion similar to that which you would use for a cardioversion. If the patient is in atrial flutter at the time of the procedure, follow guidelines developed for anticoagulation of atrial fibrillation. These data from a nice study by Natale and co-workers really makes the point that catheter ablation should be first-line therapy for recurrent atrial flutter. They randomized treatment in sixty-one patients who had had recurrent atrial flutter and who had not failed prior antiarrhytmic drug therapy. Randomized treatments were antiarrhytmic drugs shown versus catheter ablation. During an average follow-up of twenty-two months, atrial flutter recurred in over ninety percent of the drug treated patients and almost two-thirds of them had atrial fibrillation. In contrast, atrial flutter recurred in only six percent of those treated with catheter ablation and fewer than a third had atrial fibrillation during follow-up. Eighty percent were in sinus rhythm at last follow-up. Complications of atrial flutter ablation are quite infrequent. They are often no more than minor groin hematomas. Many of our flutter ablations are performed as out-patient procedures. However, it is important to manage anticoagulation in a fashion similar to that which you would use for a cardioversion. If the patient is in atrial flutter at the time of the procedure, follow guidelines developed for anticoagulation of atrial fibrillation.

    18. These data from Hsieh et al demonstrates that atrial fibrillation is the biggest problem following flutter ablation. Patients who have had prior atrial fibrillation have a substantial risk of arrhythmia recurrence over the next couple of years, of fibrillation typically and not flutter. Patients who have not had fibrillation prior to ablation have a lower risk. However, with long follow-up, it is likely we are going to see more than twenty percent back with episodes of atrial fibrillation. In their study, recurrence of atrial flutter occurred in nine percent of patients during long-term follow-up.These data from Hsieh et al demonstrates that atrial fibrillation is the biggest problem following flutter ablation. Patients who have had prior atrial fibrillation have a substantial risk of arrhythmia recurrence over the next couple of years, of fibrillation typically and not flutter. Patients who have not had fibrillation prior to ablation have a lower risk. However, with long follow-up, it is likely we are going to see more than twenty percent back with episodes of atrial fibrillation. In their study, recurrence of atrial flutter occurred in nine percent of patients during long-term follow-up.

    19. Now, as catheter ablation is becoming the first line treatment for atrial flutter, we are increasingly asked whether an arrhythmia that has a somewhat atypical appearance on the surface electrocardiogram is atrial flutter. In some cases, the only way to know is to do the electrophysiology study. So in this electrocardiogram is it flutter? Well, the P-waves are very small amplitude and are difficult to see. Certainly, the ventricular rate is organized and the activation sequence map of this arrhythmia on the insert panel shows an activation sequence consistent with clockwise flutter. Entrainment confirmed that indeed this was the case.Now, as catheter ablation is becoming the first line treatment for atrial flutter, we are increasingly asked whether an arrhythmia that has a somewhat atypical appearance on the surface electrocardiogram is atrial flutter. In some cases, the only way to know is to do the electrophysiology study. So in this electrocardiogram is it flutter? Well, the P-waves are very small amplitude and are difficult to see. Certainly, the ventricular rate is organized and the activation sequence map of this arrhythmia on the insert panel shows an activation sequence consistent with clockwise flutter. Entrainment confirmed that indeed this was the case.

    20. Atypical electrocardiographic patterns are often seen when the atria are very diseased. Although the P-wave morphology may not be typical of an isthmus dependent flutter in someone who has had prior repair congenital heart disease or prior valve surgery, in fact isthmus dependent flutter is still the most common macro reentrant atrial arrhythmia that you will encounter in those patients. It is often worth a look at electrophysiologic study. It is important to keep an open mind in the approach to these patients. Some of the arrhythmias will be macro reentrant and non-isthmus dependent. They can still be ablated. Occasionally, one encounters a focal atrial tachycardia that mimics an activation sequence of common atrial flutter. Atypical electrocardiographic patterns are often seen when the atria are very diseased. Although the P-wave morphology may not be typical of an isthmus dependent flutter in someone who has had prior repair congenital heart disease or prior valve surgery, in fact isthmus dependent flutter is still the most common macro reentrant atrial arrhythmia that you will encounter in those patients. It is often worth a look at electrophysiologic study. It is important to keep an open mind in the approach to these patients. Some of the arrhythmias will be macro reentrant and non-isthmus dependent. They can still be ablated. Occasionally, one encounters a focal atrial tachycardia that mimics an activation sequence of common atrial flutter.

    21. This slide shows an electrocardiogram from a patient with prior ASD repair. The P-wave amplitude is very low, but you can see positive P-waves in II, III, and F. The rate is relatively slow. One might be suspicious on a focal atrial tachycardia.This slide shows an electrocardiogram from a patient with prior ASD repair. The P-wave amplitude is very low, but you can see positive P-waves in II, III, and F. The rate is relatively slow. One might be suspicious on a focal atrial tachycardia.

    22. Intracardiac tracings confirm that indeed there is an atrial tachycardia. The activation sequence revealed a double-loop reentry circuit, as shown. The right atrium is seen from a right posterior oblique position here with wave-front circulating around to regions of scar. This is the most common location for scar related macro reentry - non-isthmus dependent following cardiac surgery. Intracardiac tracings confirm that indeed there is an atrial tachycardia. The activation sequence revealed a double-loop reentry circuit, as shown. The right atrium is seen from a right posterior oblique position here with wave-front circulating around to regions of scar. This is the most common location for scar related macro reentry - non-isthmus dependent following cardiac surgery.

    23. Our experience with these arrhythmias is summarized from our publication a few years ago by Etienne Delacretaz. In twenty patients with prior cardiac surgery for congenital heart disease, he identified forty-seven reentry circuits. The most common were isthmus dependent common flutters seen in eighteen and lateral wall circuits seen in nineteen cases. Septal reentry circuits were relatively infrequent. Left atrial circuits were also infrequent. Our experience with these arrhythmias is summarized from our publication a few years ago by Etienne Delacretaz. In twenty patients with prior cardiac surgery for congenital heart disease, he identified forty-seven reentry circuits. The most common were isthmus dependent common flutters seen in eighteen and lateral wall circuits seen in nineteen cases. Septal reentry circuits were relatively infrequent. Left atrial circuits were also infrequent.

    24. Markowitz and colleagues showed a nice series of atrial flutters occurring after mitral valve surgery. Their study demonstrated that left atrial macro reentry, focal ectopic atrial tachycardias, and right atrial macro reentry all occur in this situation as well. Markowitz and colleagues showed a nice series of atrial flutters occurring after mitral valve surgery. Their study demonstrated that left atrial macro reentry, focal ectopic atrial tachycardias, and right atrial macro reentry all occur in this situation as well.

    25. Left Atrial Flutter: Jais et al Circulation 2000- positive p – wave in V1- atypical for common flutter in II, III, AVF Finally, atypical electrocardiographic appearances can also be left atrial flutter. Left atrial flutter is more difficult to ablate. The risk of approaching this arrhythmia are, of course, greater requiring left atrial access and more rigorous attention to anticoagulation. One can suspect you are dealing with a left atrial circuit when you find long post-pacing intervals (not at the tachycardia cycle length) in the right atrium. There are some P-wave clues as wel. These are summarized here in this nice article by Jais and colleagues in Circulation from 2000. A completely positive P-wave in V1 with atypical morphology for isthmus dependent flutter in the limb leads is often a clue that you are dealing with a left atrial flutter.Finally, atypical electrocardiographic appearances can also be left atrial flutter. Left atrial flutter is more difficult to ablate. The risk of approaching this arrhythmia are, of course, greater requiring left atrial access and more rigorous attention to anticoagulation. One can suspect you are dealing with a left atrial circuit when you find long post-pacing intervals (not at the tachycardia cycle length) in the right atrium. There are some P-wave clues as wel. These are summarized here in this nice article by Jais and colleagues in Circulation from 2000. A completely positive P-wave in V1 with atypical morphology for isthmus dependent flutter in the limb leads is often a clue that you are dealing with a left atrial flutter.

    26. Scar – related (Incisional) Macroreentrant Atrial Tachycardias Non-isthmus dependent atrial tachycardia can not be reliably predicted from the ECG Ablation is often more difficult multiple circuits are common difficult to define critical isthmus difficult to achieve block across an isthmus Mapping is facilitated by an advanced mapping system Successful ablation: 50 – 88% Akar, et al.2001,Chan, et al.2000,Delacretaz, et al.2001, Nakagawa, et al.2001,Triedman, et al.1997 Jais, et al.2000,Saoudi, et al.2001,Tai, et al.2001,Thomas, et al.2000 In summary, you cannot reliably distinguish scar related or incisional macro reentry atrial tachycardias that are not isthmus dependent from those that are isthmus dependent based only on the electrocardiogram in many patients. Ablation of these arrhythmias is more difficult. They often are associated with multiple potential reentry circuits. It can be difficult to define a critical isthmus and to achieve block and an advanced mapping system is useful for guiding ablation in these patients. Employing these technologies success rates are improving in probably in the range of up to eighty percent or so, recurrences are more common than with isthmus dependent atrial flutters. In summary, you cannot reliably distinguish scar related or incisional macro reentry atrial tachycardias that are not isthmus dependent from those that are isthmus dependent based only on the electrocardiogram in many patients. Ablation of these arrhythmias is more difficult. They often are associated with multiple potential reentry circuits. It can be difficult to define a critical isthmus and to achieve block and an advanced mapping system is useful for guiding ablation in these patients. Employing these technologies success rates are improving in probably in the range of up to eighty percent or so, recurrences are more common than with isthmus dependent atrial flutters.

    27. Catheter Ablation of Atrial Flutter First line therapy for recurrent, typical flutter Excellent efficacy, low risk Subsequent atrial fibrillation occurs in >20-30% of patients Non-isthmus dependent flutter is occasionally encountered, particularly in patients with prior atrial surgery efficacy is less predictable In summary, catheter ablation in atrial flutter is an excellent first-line therapy for patients with recurrent isthmus dependent atrial flutter. It has excellent long-term efficacy and low risk. Atrial fibrillation occurs in twenty to thirty percent of patients during long-term follow-up, but this is usually somewhat easier to manage than the initial atrial flutter. Non-isthmus dependent flutter is occasionally encountered particularly in patients with prior atrial surgery and occasionally in patients with atrial scarring of unclear etiology and ablation of these is a bit more difficult.In summary, catheter ablation in atrial flutter is an excellent first-line therapy for patients with recurrent isthmus dependent atrial flutter. It has excellent long-term efficacy and low risk. Atrial fibrillation occurs in twenty to thirty percent of patients during long-term follow-up, but this is usually somewhat easier to manage than the initial atrial flutter. Non-isthmus dependent flutter is occasionally encountered particularly in patients with prior atrial surgery and occasionally in patients with atrial scarring of unclear etiology and ablation of these is a bit more difficult.

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