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Circulation. 1996;94:244-246

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(Circulation. 1996;94:244-246.)
© 1996 American Heart Association, Inc.

Articles

The Atrial Flutter Reentrant Circuit

Additional Pieces of the Puzzle

George F. Van Hare, MD; Albert L. Waldo, MD

the Divisions of Cardiology, Departments of Medicine and Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Correspondence to Albert L. Waldo, MD, Division of Cardiology, University Hospitals of Cleveland, 11100 Euclid Ave, Cleveland, OH 44106.


Key Words: atrial flutter • reentry • electrophysiology • arrhythmia • catheter ablation • Editorials


*    Introduction
up arrowTop
 *Introduction
down arrowReferences
 
For a time, there was a substantial school of thought that held that atrial flutter was due to a single focus firing rapidly.1 It has more recently been established that atrial flutter is due to reentry.1 Over the years, and largely on the basis of animal studies, the nature of the atrial flutter reentrant circuit has been thought or demonstrated to include reentry around anatomic obstacles such as the great veins or the pulmonary veins, reentry around atrial lesions, and reentry around functional obstacles.2 Reentry around the tricuspid annulus was demonstrated in the presence of critical right atrial lesions,3 and many years ago, Sir Thomas Lewis could only explain a limited sequential site atrial flutter map in a canine model by postulating reentry around the mitral annulus.4 However, it is now accepted that classic (type I) atrial flutter in patients is due to macroreentry involving the right atrium.1 Initial activation mapping studies of the typical form of atrial flutter in patients showed a "counterclockwise" reentrant activation in the right atrium,5 6 7 but the elements of the right atrium that supported reentry and were critical to the maintenance of the atrial flutter reentrant circuit were not yet appreciated.

From studies using concealed entrainment techniques8 as well as techniques for precise placement of ablative lesions, it is now well established that one critical element of the atrial flutter reentrant circuit is the isthmus between the inferior vena cava and the tricuspid valve annulus.9 In this issue of Circulation, two carefully performed studies provide additional important details concerning the critical elements of the reentrant circuit.10 11 Both studies rely on the concept of concealed entrainment to support conclusions involving whether certain atrial sites are part of the atrial flutter reentrant circuit. This mapping technique is an excellent example of how the concept of transient entrainment, initially used clinically to establish a reentrant mechanism for a particular tachyarrhythmia,12 is now used as a method of differentiating sites that are "in the reentrant circuit" from those that are "out" in tachyarrhythmias that are known or presumed to be reentrant.13 The method, which relies on showing equivalence between the atrial flutter cycle length and the postpacing interval at the candidate site, allows one to map the atria completely in lieu of obtaining multiple simultaneous electrogram recordings.

The use of the term "concealed entrainment" has been used variably by several authors. As originally defined, concealed entrainment denotes the inability to demonstrate the criteria for entrainment (for example, constant fusion, progressive fusion) by pacing during tachycardia despite the fact that the reentrant nature of the rhythm is certain.14 Concealed entrainment may occur for several reasons. As originally described, pacing downstream from the site of exit from a zone of slow conduction may cause one to be unable to demonstrate the criteria for entrainment, as there may not be enough antidromic spread of activation to produce fusion on the ECG. Concealed entrainment also may result if one paces in a zone of slow conduction. In such a case, the antidromic wave front is confined to the protected zone of slow conduction and so does not produce fusion on the ECG. In this type of concealed entrainment, there will be significantly greater latency between the stimulus and the onset of the P wave or QRS complex (depending on the heart chamber being paced) than with entrainment in which there is fusion, due to antegrade conduction in a protected zone of slow conduction. Such a zone either may be part of the reentrant circuit and critical to the arrhythmia or may be part of a bystander site, not critical to maintenance of tachycardia.15

Differentiation between concealed entrainment at critical sites versus bystander sites can be established in two ways, both of which are used in the studies by Kalman et al10 and Nakagawa et al.11 First, one may note the latency during pacing from the site (stimulus-to-P wave) and compare it with the conduction time during tachycardia (electrogram-to-P wave). For sites in the circuit, these should be equivalent, whereas for bystander sites, latency will be longer than conduction time. Second, one may assess the postpacing interval at the candidate site, comparing it with the cycle length of the tachycardia. For sites in the circuit, the postpacing interval should equal the tachycardia cycle length. However, for bystander sites, the postpacing interval will be significantly longer than the tachycardia cycle length, as the time taken for the wave of activation to return to the pacing site will equal the tachycardia cycle length plus the time necessary for conduction to and from the circuit. The latter method is applicable to the situation of concealed entrainment as well as to entrainment when there is fusion on the ECG. Both methods are potentially limited by the possibility of decremental conduction in the circuit or by oscillations in tachycardia cycle length. The first method relies on the ability to assess the P waves, both during tachycardia as well as during pacing for entrainment, although this task may be difficult because of several issues. If there is relatively rapid atrioventricular conduction, generally 2:1 or greater, P waves fall on T waves and are difficult to assess. If the P waves are of low voltage and difficult to see, consistent determination of the stimulus-to-P wave interval becomes quite difficult, if not impossible. This is seen commonly in patients after surgery for congenital heart disease, such as the Mustard or Senning procedure. Finally, even in the absence of these factors, subtle changes in flutter wave morphology may be difficult to recognize because of the lack of high frequency components in the signal. For these reasons, the second method, involving assessment of postpacing intervals, is in practice much more powerful for the careful mapping of atrial flutter because it does not rely on the assessment of P waves.

Kalman et al10 studied 13 patients with typical atrial flutter, performing careful entrainment maps of the region of the right atrium adjacent to the tricuspid valve annulus as well as the region of the foramen ovale, the right atrial appendage, and the distal coronary sinus. Sites were determined to be "in the circuit" or "out of the circuit" on the basis of the results of analysis of postpacing intervals. Their conclusion that the tricuspid annulus constitutes the "anterior barrier" in typical flutter is based on showing that sites around the tricuspid annulus are activated sequentially and in a counterclockwise fashion and that these sites all lie within the atrial flutter circuit. That the tricuspid annulus is a barrier is obvious-it is where the right atrial tissue ends. Their concept has more to do with the relationship between the tricuspid annulus and the crista terminalis, which their group has shown previously to be a site of posterior block in the atrial flutter circuit.16 Their current study successfully rejects the unstated alternative hypothesis that other structures in the right atrium between the crista terminalis and the tricuspid annulus are important in constraining atrial activation. Their concept of a "funnel" of conducting tissue in the right atrium is attractive, the "funnel" being formed by the tricuspid annulus anteriorly and the crista terminalis posteriorly (with its extension as the eustachian valve/ridge). This funnel forces atrial activation to the narrow isthmus between the tricuspid annulus and the inferior vena cava, where, because of the short distance, the reentrant circuit is most amenable to successful ablation.

In the study by Nakagawa et al,11 the region of the coronary sinus ostium is explored in detail in 30 patients with typical atrial flutter using similar techniques of entrainment pacing and assessment of postpacing intervals. Their work is an excellent example of how precisely placed radiofrequency lesions, used to eliminate small areas of myocardium, can help to understand the details of reentrant circuits. As Mines17 admonished us many decades ago, activation sequence mapping alone may not prove that a given arrhythmia is due to reentry because of the possibility of the coexistence of conduction block with an automatic focus. Severing the reentrant ring, as it is now possible to do for a variety of reentrant tachyarrhythmias using radiofrequency ablation techniques, with interruption of the arrhythmia and the inability to reinduce the arrhythmia, is the sine qua non. By placing an orthogonal electrode catheter in the region between the coronary sinus ostium and inferior vena cava, Nakagawa et al recorded double potentials, indicating the existence of a line of block, from the site that includes the eustachian valve/ridge. This finding is similar to that recently reported by Olgin et al.16 Entrainment mapping identified the "septal isthmus," the atrial myocardium bounded by the tricuspid annulus and the coronary sinus ostium, as being within the atrial flutter circuit. Impressively, they showed that ablative lesions placed at this small site were successful in nearly all patients, and they only needed to ablate at the "posterior isthmus" (between the tricuspid annulus and inferior vena cava) in 4 patients. In addition, they used the pattern of atrial activation produced by pacing during sinus rhythm to document the successful creation of a line of bidirectional block at the septal isthmus. This finding is similar to those of Poty et al18 and Cauchemez et al19 after lesions directed to the posterior isthmus. Clearly, if one considers the eustachian valve/ridge as the extension of the line of block created by the crista terminalis, one can understand that this area of block is critical to maintenance of atrial flutter because it prevents the wave of activation from circling around the coronary sinus ostium or the inferior vena cava and short-circuiting the reentrant circuit. Targeting the septal isthmus is intriguing from a technical standpoint, as catheter contact can be maintained more easily, and the sheer volume of tissue necessary to ablate is smaller, than at the posterior isthmus. There are several concerns, however. The atrioventricular node may be vulnerable with radiofrequency lesions in this area, as discussed by Nakagawa et al.11 Also, the coronary arterial supply to the posterior ventricular wall may be at risk. Whether one chooses the posterior or the septal isthmus for initial ablation attempts will depend on clinical factors.

Both these studies beg the question of why atrial flutter occurs only in some patients, but not in all. If the anatomic structures mediating atrial flutter are normal structures existing in all normal hearts, what then are the factors that encourage the development of atrial flutter? It may be that the requisites for reentry need to develop over time20 21 or may be related to such factors as atrial hemodynamics. Is conduction through the inferior vena cava-tricuspid isthmus not slow enough in normal hearts for atrial flutter to become established? Is the line of block at the crista terminalis and eustachian valve/ridge a variable factor, existing only in some hearts? Is the addition of slow conduction in the electrical "funnel" necessary because of aging or the placement of an atriotomy for surgical repair of congenital heart defects in the anterior right atrial wall? Such questions might be answered more easily by the application of simultaneous multisite mapping studies in humans. Clearly, future studies from these and other centers will address such questions.


*    Footnotes
 
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.


*    References
up arrowTop
 up arrowIntroduction
 *References
 

  1. Waldo AL. Mechanisms of atrial fibrillation, atrial flutter, and ectopic atrial tachycardia: a brief review. Circulation. 1987;75(suppl III):III-37-III-40.
  2. Waldo AL. Animal models of atrial arrhythmias. In: DiMarco JP, Prystowsky EN, eds. Atrial Arrhythmias: State of the Art. Armonk, NY: Futura Publishing Co Inc; 1995:213-240.
  3. Frame LH, Page RL, Hoffman BF. Atrial reentry around an anatomic barrier with a partially refractory excitable gap: a canine model of atrial flutter. Circ Res. 1986;58:1233-1240.
  4. Lewis T, Feil HS, Stroud WD. Observations upon flutter and fibrillation, II: the nature of auricular flutter. Heart. 1920;7:191-245.
  5. Puech P. Le flutter et ses limites. Arch Mal Coeur. 1970;61:116-144.
  6. Cosio FC. Endocardial mapping of atrial flutter. In: Touboul P, Waldo AL, eds. Atrial Arrhythmias. St Louis, Mo: Mosby-Year Book; 1990:229-240.
  7. Olshansky B, Okumura K, Hess PG, Waldo AL. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardiol. 1990;16:1634-1648.
  8. Cosio FG, Lopez Gil M, Arribas F, Palacios J, Goicolea A, Nunez A. Mechanisms of entrainment of human common flutter studied with multiple endocardial recordings. Circulation. 1994;89:2117-2125.[Abstract/Free Full Text]
  9. Feld GK, Fleck P, Chen PS, Boyce K, Bahnson TD, Stein JB, Calisi CM, Ibarra M. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter: identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation. 1992;86:1233-1240.[Abstract/Free Full Text]
  10. Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh MD. Activation and entrainment mapping defines the tricuspid annulus as the anterior barrier in typical atrial flutter. Circulation. 1996;94:398-406.[Abstract/Free Full Text]
  11. Nakagawa H, Lazzara R, Khastgir T, Beckman KJ, McClelland JH, Imai S, Pitha JV, Becker AE, Arruda M, Gonzalez MD, Widman LE, Rome M, Neuhauser J, Wang X, Calame JD, Goudeau MD, Jackman WM. 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. Circulation. 1996;94:407-424.[Abstract/Free Full Text]
  12. Waldo AL, Plumb VJ, Arciniegas JG, MacLean WAH, Cooper TB, Priest MF, James TN. Transient entrainment and interruption of A-V bypass type paroxysmal atrial tachycardia: a model for understanding and identifying reentrant arrhythmias in man. Circulation. 1982;67:73-83.[Free Full Text]
  13. Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, Wiener I. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993;88:1647-1670.[Abstract/Free Full Text]
  14. Okumura K, Henthorn RW, Epstein AE, Plumb VJ, Waldo AL. Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit. Circulation. 1985;72:1293-1307.[Abstract/Free Full Text]
  15. Stevenson WG. Functional approach to site-by-site catheter mapping of ventricular reentry circuits in chronic infarctions. J Electrocardiol. 1995;27:130-138.
  16. Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter: activation and entrainment mapping guided by intracardiac echocardiography. Circulation. 1995;92:1839-1848.[Abstract/Free Full Text]
  17. Mines GR. On circulating excitation in heart muscles and their possible relations to tachycardia and fibrillation. Trans R Soc Can. 1914;8:43-52.
  18. Poty H, Saoudi N, Abdel Aziz A, Nair M, Letac B. Radiofrequency catheter ablation of type 1 atrial flutter: prediction of late success by electrophysiological criteria. Circulation. 1995;92:1389-1392.[Abstract/Free Full Text]
  19. Cauchemez B, Haissaguerre M, Fischer B, Thomas O, Clementy J, Coumel P. Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation. 1996;93:284-294.[Abstract/Free Full Text]
  20. Waldo AL, Cooper TB. Spontaneous onset of type I atrial flutter in patients. J Am Coll Cardiol. 1996. In press.
  21. Shimizu A, Nozaki A, Rudy Y, Waldo AL. Onset of induced atrial flutter in the canine pericarditis model. J Am Coll Cardiol. 1991;17:1223-1234.[Abstract]



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