Electrophyslology, Pacing, and Mythmla

Transcription

1 Clin. Cardiol. 15, (1992) Electrophyslology, Pacing, and Mythmla This section edited by A. John Camm, MD., FR.C.P., FA. C.C. Electrophysiologic Studies in Atrial flutter FRANCISCO G. COSIO, M.D., F.A.C.C., F.E.S.C., MAR~A L6PEZ-GL, M.D., ANTONIO GOICOLEA, FERNANDO ARRIBAS, M.D. Hospital Universitario de Getafe, Madrid, Spain M.D., F.E.S.C., Summary: The clinical electrophysiologic approaches to atrial flutter (F) have been activation mapping and the observation of changes induced by programmed stimulation. Sequential endocardial activation mapping has recently yielded information indicating that common F is produced by a large right atrial (RA) reentry circuit, with counterclockwise rotation in the frontal plane, including the inferior vena cava in its center. Functional block in the crista terminalis and conduction slowing in the approaches to the atrioventricular node seem to be important to support reentry. F inscribing positive deflections in the inferior leads usually follows the same path, but in a clockwise direction. Atypical F may be produced by left atrial circuits. Atrial stimulation during F entrains the circuit, resetting it with each stimulus. Collision between antidromic and orthodromic activation during entrainment produces fusion that can be identified in the surface electrocardiogram. The last paced activation restarts F, unless circuit penetration Address for reprints: Francisco G. Cosio M.D., F.A.C.C. Chief, Cardiology Service Hospital Universitario de Getafe Carretera de Toledo, km 12, Getafe Madrid, Spain Received: June 25, 1992 Accepted: July 6, 1992 has been enough to modify it by block or disorganization. Entrainment may result in F acceleration, with changes in activation sequence, suggesting a different type of reentry, possibly based on functional factors. Key words: atrial flutter, atrial reentry, flutter mapping, entrainment Introduction Atrial flutter (F) is defined on the electrocardiogram (ECG) as a regular atrial tachycardia, without a stable baseline, with rates between 240 and 350/min. These criteria are often insufficient to classify some atrial tachycardias, either because of borderline rates or because of poorly defined morphologies, and this imprecise definition has encouraged controversy about the electrophysiologic mechanisms of F. There have been two approaches to F: (1) atrial activation mapping; (2) response to atrial stimulation (reset and entrainment). The electrophysiological properties of atrial myocardium in patients with paroxysmal F are discussed elsewhere.' Activation Mapping F activation sequence was studied in the 1960s by Puech et al.,la using direct endocardial right atrial (RA) recordings and exploring the left atrium (LA) from the coronary sinus (CS) or the esophagus. The data were partial, as only a few points were timed, but there was clear evidence of an

2 668 Clin. Cardiol. Vol. 15, September 1992 FIG. 1 Postero-anterior (A) and left lateral (B) views of the catheter setup presently used for F mapping at the authors laboratory. The white square marks the anterior direction in B. Hexapolar catheters are placed in the CS and against the posteroseptal and anterolateral RA walls. A fourth exploring catheter is placed at the inferior vena cava-tricuspid ridge on the RA floor. Note an aortic prosthetic valve. ample circuit involving the right atrium and a passive role of the LA, in most cases. Recently, endocardial atrial mapping has been revived by several authors24 and a more complete picture of F circuits can be drawn, thanks to sequential pacing techniques. Multiple simultaneous endocardial recordings have obvious limitations in humans, but F offers the advantage of being a stable rhythm, with good clinical tolerance, allowing sequential mapping, with little time constraint^.^" Endocardial time references are necessary because of the relatively low voltage and lack of sharp deflections on the F waves and the superimposition of QRS complexes. This problem can be overcome by placing recording catheters in areas not subject to easy displacement, such as the RA appendage or the coronary sinus (CS). A third recording catheter can then be used for sequential mapping of the RA and, when the foramen ovale is patent, also the LA. More recently we use 7-9 intracardiac recordings, using hexapolar catheter-electrodes, placed alongside the anterolateral and posteroseptal walls and the coronary sinus (Fig. 1). We have used bipolar recordings with interelectrode separation of 1 cm in most of our studies, but catheters with 0.5 cm separation might be better in some instances. Newer catheters with deflecting tips make RA mapping much easier. Paper speeds of 100 mm/s are adequate. We have used the same filters as for His-bundle potential recording ( Hz) and whatever signal amplification is necessary for recording a local electrogram 1-3 cm in peak amplitude. Several anatomic references are helpful for catheter placement: superior and inferior venae cavae openings, fossa ovalis, coronary sinus opening, and tricuspid valve are all easily located. Taking into account the fact that both posterior atrial walls are anatomically fixed by the caval and pulmonary veins, there is little room for gross anatom- ic error. These references allow the delimitation of the septal, posterior, lateral, and anterior portions of the RA wall (Fig. 2). Several levels can be arbitrarily separated in the cranio-caudal level, taking as a visual reference the adjacent vertebrae. The spacial discrimination of this mapping technique is probably 2 1 cm. In our experience 3-5 and that of others? there is a gap of 3040% of F cycle not covered by the electrograms re- FIG. 2 Typical activation map in common F. Both atria are shown in a schematic anterior view from the atrioventricular rings. Shaded areas represent endocardium and white areas epicardium. The location of the venae cavae, CS, and pulmonary veins are shown. The septal, posterior, and lateral RA walls are represented on the endocardial side. The anterior RA wall and the CS are represented outside the tricuspid and mitral rings, respectively. Figures represent the onset of local electrograms and double figures the onset of each deflection in double electrograms. Zero reference is arbitrary. Arrows mark the suggested direction of activation. CL =cycle length.

3 F. G. Cosio er al.: Electrophysiologic studies in atrial flutter FIG. 3 Multiple simultaneous recordings in common F. From top to bottom: lead I1 and intracardiac electrograms from high anterolateral RA (HAL); mid anterolateral RA (MAL); low anterolateral RA (LAL); mid posterolateral RA (MPL); low posteroseptal RA (LPS); mid posteroseptal RA (MPS); high posteroseptal RA (HPS); mid coronary sinus (MCS); distal coronary sinus (DCS). Note the general trend of cranio-caudal activation on the anterolateral RA wall and caudo-cranial activation on the posteroseptal wall. The MPL electrogram inscribes two spikes, one of which is close in time to the LAL electrogram, while the other is close to the MPS electrogram. Wide, fragmented electrograms are recorded at LPS and MPS, suggesting local conduction delay. corded from the septal, posterior, lateral, and anterior RA walls (Fig. 3). This gap can be closed, at least partially, by mapping the RA floor, particularly the narrow area between the inferior vena cava and the tricuspid ~alve,~.~ as well as the low posteroseptal zone, close to the CS opening and atrioventricular node, where fragmented activity is usually recorded. The best approach to the inferior vena cava-tricuspid ridge, in our experience, is with a sharply curved catheter coming from the inferior vena cava, engaged in an anterior direction by gentle inferior traction (Fig. 1). A potentially confusing reference is the diaphragm, that in the AP view can be located higher or lower than the level where optimal potentials form the RA floor are recorded. In our experience, all cases of common F (defined as showing predominantly negative deflections in the inferior ECG leads) showed caudo-cranial activation of the septum and cranio-caudal activation on the lateral and anteri- or walls (counterclockwise rotation on the frontal (Figs. 2-5). Posterior wall activation basically parallels the septum, although often with a less well defined caudo-cranial direction. CS electrograms follow a right-to-left sequence and coincide roughly with septal activation. The inferior vena cava-tricuspid valve ridge appears as an obligatory path for closing the circ~it.~-~ The very reproducible configuration of F circuits suggests a strong anatomic dependence, which is further supported by the finding that rare F circuits with positive F waves in the inferior ECG leads rotate in a clockwise direction, but follow essentially the same path as common F (Figs. 4, 5).536 However, not all rare F, inscribing predominantly positive deflections in lead 11, show clockwise circuits; in some cases rotation direction is the same as in common E5 About 90% of all F is based in the RA,2,3 judging by mapping data. In a few cases of atypical flutter, generally with low voltage in the frontal plane ECG leads, activation of the CS and the septum suggests an active left atrial participation in the circuit (Fig. 6). In these cases the circular RA activation pattern, found in common and rare F, is ab~ent.~.~ Slow F due to antiarrhythmic drugs may show peculiar activation patterns with areas of continuous fragmented activity (Fig. 7), suggesting the possibility of small functional reentry circuits, based on drug-induced conduction lo wing.^ Fragmented Electrograms and Conduction Slowing or Block Local electrograms with two main deflections were already found in the caudal RA by Puech et al. in their early studies. Monophasic action potential recordings also disclosed two closely spaced potentials, located in the low RA, for each flutter cycle.7 More recently this finding has been confirmed by several a~thors~-~-*- ~ (Figs. 3, 4). Double electrograms have been attributed to a local conduction disturbance, but it is debated whether they play a significant role, supporting the reentry circuit, or rather represent nonspecific rate-dependent local conduction delays. In some instances it can be shown how intermittent block may develop between the components of a split potential, either spontaneously or under stimulation, without any change in the F cycle, ruling out an active participation of that particular conduction delay in reent~y.~, ~ However, double electrograms recorded from the posterolateral RA in common and rare flutter (Figs. 4,5) probably represent a functionally significant line of block, enlarging the anatomic obstacle made by the inferior vena cava opening.4.5g 0 A detailed study of the posterolateral RA wall with deflecting tip catheters allows recording a caudo-cranial line of double electrograms. Activation on both sides of this line follows opposite direction^.^ F entrainment from the high RA produces fusion of the two components,

4 670 Clin. Cardiol. Vol. 15, September 1992 FIG. 4 Lead I1 and endocardial RA recordings (from top to bottom) from high, mid, and low anterolateral wall: inferior vena cava-triscupid ridge; low, mid, and high posterolateral wall and RA roof. The patient had initially a common F (left) which changed to rare F after stimulation, reversing activation sequence. Note double electrograms at the low posteroseptal site in common F and at this site and the cava-tricuspid ridge in rare F. FIG. 5 Activation maps in common F (A) and rare F (B) in a patient different from the one featured in Figure 4. For explanation see Figure 2 and text. as it would be expected if each represented the orthodromic and antidromic arms of the circ~it~. ~ (Fig. 8). A likely explanation of these findings is that anisotropic conduction in the posterior internodal pathway (crista terminalis) creates a functional barrier between the posterior and lateral RA walls which, added to the inferior vena cava opening, constitutes a large enough central obstacle to sustain reentrant activation. In some cases where clockwise and counterclockwise circuits were mapped, double potentials could be recorded from the posterolateral RA in both types of circuit. Another area where split potentials are recorded very reproducibly is the low and mid posteroseptal RA in the Proximity ofthe coronary sinus opening (Figs. 3,4), the area of confluence of all RA internodal pathways around FIG. 6 Activation map in a case of F involving the left atrium. Note CS activation sequence from left to right.

5 F. G. Cosio et al.: Electrophysiologic studies in atrial flutter 67 1 FIG. 7 Activation map of an atypical, slow rate, low voltage F in a patient taking quinidine. The double figures indicate the onset and termination of wide, fragmented electrograms, shown on the recording. The lines indicate the recording sites for the endocardia1 electrograms. the atrioventricular node. Thus, myocardial alignment in bundles and anisotropy would again explain the development of functional conduction disturbances at high rates, with activation advancing perpendicularly to the direction of the muscle bundles. It is possible that conduction slowing through this particular area may further support reentry, but to date there is no confirmation of this possibility. Entrainment and Reset The studies of Waldo eta/. * in postoperative F set the concept of entrainment of a reentrant circuit and provided evidence that reentry is the basic mechanism of human F. Pacing from the high right atrium (RA) increased atrial rate to the pacing rate, but the F waves remained negative in the inferior ECG leads despite the high pacing site (Fig. 1). After pacing interruption, the basic F rate was resumed immediately. As pacing rate increased progressively, F wave morphology changed, becoming less negative. In some cases, when a critical rate was reached, F waves became positive, and pacing interruption led to the restoration of sinus rhythm. These observations were interpreted as the result of penetration of the paced activation front orthodromically and antidromically in the F circuit. In each paced cycle, collision would occur between the antidromically directed activation and the orthodromic penetration of the previous stimulus (Fig. 9). As pacing rate shortened, more antidromic penetration occurred, and progressive fusion between the orthodromic and the antidromic fronts I ms ?- 22d 95 FIG. 8 Effect of entrainment from the high RA on double electrograms recorded in the low posterolateral RA (LPRA). The F waves remain negative F in lead Y, and double electrogram separation is decreased (45 ms) as compared with spontaneous F after pacing stops, (95 ms) indicating fusion. FIG. 9 Schematic representation of the events during common F entrainment. The open arrows represent activation spread in orthodromic and antidromic directions after the last stimulus (S). Black arrows indicate the spread of orthodromic activation from the previous paced cycle. There is collision between both at the high RA. The hatched area represents the area of functional block in the posterolateral wall.

6 672 Clin. Cardiol. Vol. 15, September 1992 FIG. 10 Common F entrainment. From top to bottom lead I1 and endocardial RA recordings from low posteroseptal (LPS), mid posteroseptal (MPS), high posteroseptal (HPS), high anterior (HA), mid anterior (MA), and low anterior (LA) sites. Note fragmented activity at LPS. Baseline activation sequence and cycle length are shown on the right after pacing stops. During pacing at the RA appendage (CL 185 ms) there is antidromic penetration with complete reversal of activation sequence in MPS, HPS, and HA, with change in electrogram configuration. There is also electrogram change in MA and LA (indicating capture from a different direction), but the relative activation sequence is preserved. changed F morphology. Every time pacing was discontinued, the last orthodromic penetration would restart the F circuit. A change to a positive P wave would mean that the F circuit was broken, atrial activation starting now at the high RA pacing site. In this new situation the interruption of pacing led to the restoration of sinus rhythm. The actual events during entrainment have been documented in AV accessory pathway tachycardia13 and in F in dog model~. ~J~ Orthodromic and antidromic penetration as well as progressive fusion have been confirmed, with collision at a different point for each entrainment rate. The increased rate during entrainment modifies the properties of the circuit, mainly in terms of conduction velocity. Slow conduction may develop in different parts of the F circuit due to the faster driving rate and may progress to block of both the antidromic and orthodromic fronts, resulting in F interruption. However, in most cases of F in dogs,interruption does not follow this sequence but is preceded by disorganization into complex reentrant circuits.i5 In humans F entrainment has been demonstrated mainly on the surface ECG. Since the pathway for reentry has not been explored in detail until very recently, there are very few data on the precise changes induced by stimulation in the F circuit. Endocardia1 recordings from our laboratory5 and Waldo slo have shown some evidence of antidromic penetration and fusion in relation to the double spikes recorded in the posterolateral RA wall (Fig. 4). More recently, using multiple simultaneous recordings from within the F circuit, we have been able to demon- strate antidromic and orthodromic circuit penetration during entrainment of human F (Fig. lo). Entrainment can be conceived as continuous resetting of the F cycle by regularly spaced stimuli. Resetting by a single stimulus produces the same sequence changes as entrainrnent,i6 supporting the presence of a large circular activation pathway, although without precisely defining its limits. Type I1 Flutter Wells et al.17 described another type of postoperative F that may appear spontaneously or after entrainment of type IF. The rate of this type II F was higher (340430) and it was not possible to influence it by pacing, although occasionally it was seen to revert spontaneously to type I F. Very little information on type II F has been generated since then. With the help of multiple endocardial recordings we have observed that the appearance of a faster F after pacing type I F is accompanied by a change in electrogram sequence (Fig. 1 l), but we could not obtain complete maps of the new F. We have observed that rapid pacing may modify this faster F, changing it into a still faster F, with still another change in electrogram sequence, or returning it back to the original F. Allessie et a1.i8 showed that, under experimental conditions including vagal stimulation, F circuits can appear al-

7 X Y Z HARA MPRA PCS MCS (6) 7 FIG. 11 Pacing-induced changes in F cycle length and activation sequence. (A) A slow basal F changes to a faster F with different activation sequence. (B) The later changes to a still faster F after stimulation. HARA = high anterior RA, LLRA = low lateral RA, LPLRA = low posterolateral RA, MCS =mid coronary sinus, MPRA =mid posterior RA, PCS = proximal coronary sinus. Note changes in electrogram fragmentation, becoming more prominent as F cycle becomes shorter. Reproduced from Ref. 19 with permission. most anywhere in the dog atrium. These are basically functional circuits, not based necessarily on anatomic obstacles. It is possible that very rapid pacing may produce the same situation in humans. References F. G. Cosio et al.: Electrophysiologic studies in atrial flutter 673 1,000ms - 3. Cosio FG, Arribas F, Palacios J, Tascbn J, L6pez-Gil M: I Fragmented electrograms and continuous electrical activity in atrial flutter. Am J Cardiol57, (1986) 4 Cosio FG, Goicolea A, Lbpez-Gil M, Arribas F, Barroso JL: Atrial endocardia1 mapping in the rare form of atrial flutter. Am J Cardiol66, (1990) 5 Cosio FG, Arribas F, Barber0 JM, Kallmeyer C, Goicolea A: Validation of double spike electrograms as markers of conduction delay or block in atrial flutter. Am J Curdiol61, (1988) 6 Beckman K, Huang-Ta-Ling, Frafchek J, Wyndham CRC: Classic and concealed entrainment of typical and atypical atrial flutter. PACE 9, (1986) 7 Gravilescu S, Luca C: Right atrium monophasic action potentials during atrial flutter and fibrillation in man. Am Heart J 90, (1975) 8 Chauvin M, Brechenmacher C: Endocardial catheter fulguration for treatment of atrial flutter. Am J Cardiol 61, (1988) 9 Saoudi N, Atallah G, Kirkorian G, Touboul P Catheter ablation of the atrial myocardium in human type I atrial flutter. Circulation 81, ( 1990) 10 Olshansky B, Okumura K, Henthom RW, Waldo AL: Characterization of double potentials in human atrial flutter: Studies during transient entrainment. J Am Coll Cardiol ( 1990) 11. Spach MS, Miller WT, Dolber PC, Kootsey JM, Sommer JR, Mosher CE: The functional role of structural complexities in the propagation of depolarization in the atrium of the dog. Cardiac conduction disturbances due to discontinuities of effective axial resistivity. Circ Res 50, (1982) 12. Waldo AL, McLean WAH, Karp RB, Kouchoukos NT, James TN: Entrainment and interruption of atrial flutter with atrial pacing. Studies in man following open heart surgery. Circulation 56, (1977) 13. Waldo AL, Plumb VJ, Arciniegas JG, MacLean WAH, Cooper TB, Priest MF, James TN: Transient entrainment and interruption of A-V bypass pathway type paroxysmal atrial tachycardia. A model for understanding and identifying reentrant arrhythmias in man. Circulation 67,73-83 (1982) 14. 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 58,495-5 ll (1986) 15. Boyden PA, Frame LH, Hoffman BF: Activation mapping of reentry around an anatomic barrier in the canine atrium. Observations during entrainment and termination. Circulation 79, (1989) 16. Disertori M, Inama G, Vergara G, Guarnerio M, Del Favero A, Furlanello F: Evidence of a reentry circuit in the common type of atrial flutter in man. Circulation 67, (1983) 17. Wells JL, MacLean WAH, James TN, Waldo AL: Characterization of atrial flutter. Studies in man after open heart surgery using fixed atrial electrodes. Circulation 60, (1979) 18. Allessie MA, Lammers WJEP, Bonke FIM, Hollen J: Intra-atria1 reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog. Circulation 70, ( 1984) 19. Cosio FG, Arribas F: Role of conduction disturbances in atrial arrhythmias. In The Atrium in Health and Disease. (Eds. Attuel P, Coumel P, Janse MJ). Futura, New York (1989) I. Cosio FG: Atrial vulnerability. Clin Card 15, (1 992) la Puech P, Latour H, Grolleau R: Le flutter et ses limites. Arch Ma1 Coeur 63, (1970) 2. Chauvin M, Brechenmacher C, Voegtlin JR: Application de la cartographie endocavitaire i I ttude du flutter auriculaire. Arch Ma1 Coeur 76, (1 983)