Mapping of atrial activation patterns after inducing contiguous radiofrequency lesions: an experimental study.

High resolution mapping techniques are used to analyze the changes in atrial activation patterns produced by contiguous RF induced lesions. In 12 Langendorff-perfused rabbit hearts, left atrial activation maps were obtained before and after RF induction of epicardial lesions following a triple-phase sequential protocol: (phase 1) three separate lesions positioned vertically in the central zone of the left atrial wall; (phase 2) the addition of two lesions located between the central lesion and the upper and lower lesions; and (phase 3) the placement of four additional lesions between those induced in the previous phases. In six additional experiments a pathological analysis of the individual RF lesions was performed. In phase 1 (lesion diameter = 2.8+/-0.2 mm, gap between lesions = 3+/-0.8 mm), the activation process bordered the lesions line in two (250-ms cycles) and four experiments (100-ms cycles). In phase 2, activation bordered the lesions line in eight (250-ms cycles, P < 0.01 vs control) and nine experiments (100-ms cycles, P < 0.001), and in phase 3 this occurred in all experiments except one (both cycles, P < 0.001 vs control). In the experiments with conduction block, the increment of the interval between activation times proximal and distal to the lesions showed a significant correlation to the length of the lesions (r = 0.68, P < 0.05, 100-ms cycle). In two (17%) experiments, sustained regular tachycardias were induced with reentrant activation patterns around the lesions line. In conclusion, in this acute model, atrial RF lesions with intact tissue gaps of 3 mm between them interrupt conduction occasionally, and conduction block may be frequency dependent. Lesion overlap is required to achieve complete conduction block lines. Tachycardias with reentrant activation patterns around a lesions line may be induced.

[Epicardial mapping of reentrant activation during ventricular fibrillation. An experimental study]. / Cartografía epicárdica de la activación reentrante durante la fibrilación ventricular. Estudio experimental.

INTRODUCTION AND OBJECTIVES: High-resolution epicardial mapping was used in an experimental model to analyze reentrant activation during ventricular fibrillation. METHODS: In 30 isolated Langendorff-perfused rabbit hearts, recordings were made of ventricular fibrillation activity using an epicardial multiple electrode. In the activation maps with reentrant activation patterns, determinations were made of the number of consecutive rotations, the maximum length of the central core, the area encompassed by the core and two electrodes surrounding it, and the cycle defined by reentrant activation. RESULTS: Most of the activation maps analyzed showed complex patterns with two or more wave fronts that either collided or remained separated by functional block lines (514 maps, 86%). In 112 maps (19%) activation patterns compatible with epicardial breakthrough of the depolarization process were observed. Reentrant activity was recorded in 42 maps (7%) - the maximum number of consecutive rotations being 3 (mean = 1.3 +/- 0.5). The maximum length of the central core ranged from 3 to 7 mm (mean = 5 +/- 1 mm), while the area encompassed by the central core plus two electrodes surrounding it ranged from 35 to 55 mm2 (mean = 45 +/- 6 mm2). The reentrant cycle length (mean = 47 +/- 8 ms) showed a linear relation to the maximum length of the central core reentry (cycle = 4.52 x length + 24.6; r = 0.7; p < 0.0001). CONCLUSIONS: a) Epicardial mapping allowed the identification of reentrant activation patterns during ventricular fibrillation in the experimental model used; b) the reentrant activity detected is infrequent and unstable, and c) a linear relation exists between the duration of the cycles defined by reentrant activity and the maximum length of central core reentry.

[The activation patterns during atrial fibrillation in an experimental model]. / Patrones de activación durante la fibrilación auricular en un modelo experimental.

INTRODUCTION AND OBJECTIVES: In atrial fibrillation, along with the mechanisms of complete reentry and random activation focal activation patterns have been described which have been attributed both to propagation from the endocardium and to the existence of zones with automatic activity. The objectives of present study are to analyze and quantify the atrial activation patterns in an experimental model of atrial fibrillation. MATERIAL AND METHODS: In 11 Langendorff-perfused rabbit hearts atrial fibrillation was induced by atrial burst pacing after right atrial dilatation with an intra-atrial balloon. A multiple electrode consisting of 121 electrodes and positioned in the right atrial free wall was used to construct the activation maps corresponding to 10 segments of 100 ms in 11 different episodes of sustained atrial fibrillation (one per experiment). RESULTS: Of the 110 segments analyzed, 44 (40%) corresponded to random activation patterns. Fifteen segments (14%) corresponded to complete reentry, and in these cases the number of consecutive rotations ranged from 1 to 2.25 (mean 1.4 +/- 0.4). In 49 segments (44%) a single activation front was seen to pass through the recording area without block; alternatively, two simultaneous fronts were recorded that did not re-excite the zone activated by the other. In two segments (2%) there was a focal activation pattern without evidence of propagation from the epicardium surrounding the activated zone. CONCLUSIONS: a) in the experimental atrial fibrillation model used, random activation patterns are more frequent than complete reentry patterns; b) complete reentry can occur in areas smaller than 1 cm2, and c) focal activation during atrial fibrillation is rare.

Reduction of atrial fibrillation inducibility by radiofrequency ablation: an experimental study.

UNLABELLED: A study is made of the antifibrillatory effects of radiofrequency (RF)-induced atrial lesions using nine Langendorff-perfused rabbit hearts in which the atrial electrophysiological properties and atrial fibrillation (AF) inducibility were modified by atrial stretching. Using a multiple electrode consisting of 121 unipolar electrodes, determinations were made of the atrial refractory periods, conduction velocity, wavelength of the atrial activation process, and the inducibility of sustained AF episodes (duration over 30 s) by atrial burst pacing in four situations: (a) control; (b) following dilatation of the right atrium; (c) after adding an RF linear lesion at the cava-tricuspid annulus isthmus; and (d) after adding two RF linear lesions rounding the base of the right atrial appendage and extending from the inferior zone of the sulcus terminalis to the anterior wall of the appendage. Under control conditions, AF was not induced in any of the experiments. The wavelengths were 10.5 +/- 1.2 cm for basic cycles of 250 ms and 6.6 +/- 0.5 cm for cycles of 100 ms. Following dilatation, a significant decrease was recorded in the atrial refractory periods, conduction velocity, and wavelength, which reached values of 6.1 +/- 0.7 cm (250-ms cycle, P < 0.01), and 3.9 +/- 0.3 cm (100-ms cycle, P < 0.01); AF was induced in five cases (P < 0.05). After producing the lesion at the cava-tricuspid isthmus, the electrophysiological modifications induced by atrial dilatation persisted (wavelength = 6.2 +/- 0.6 cm (250-ms cycle) and 4.3 +/- 0.3 cm (100-ms cycle); P < 0.01 vs the control) and AF was triggered in eight cases (P < 0.0001). In turn, on adding the two lesions at the right atrial free wall and appendage, AF was induced only in one experiment (P = NS vs control), and the dilatation-induced decrease in refractoriness and wavelength was attenuated. Nevertheless, differences remained significant with respect to the controls, with the exception of the functional refractory periods determined at cycles of 100 ms. In this phase, the wavelength was 6.6 +/- 0.7 cm (250-ms cycle, P < 0.01 vs control) and 4.9 +/- 0.5 cm (100-ms cycle; P < 0.05). Atrial conduction between the zones separated by the lesions was blocked at any frequency, or selectively at rapid atrial activation frequencies. IN CONCLUSION: (a) the production of three linear lesions in the right atrium (cava-tricuspid isthmus, atrial appendage, and inferior free wall) reduces AF inducibility in the experimental model used; (b) conduction block (either absolute or frequency dependent) through the lesions, reduction in tissue mass caused by lesion creation, and possibly the attenuation of the shortening of atrial refractoriness and wavelength in the zones not separated by the lesions are implicated in the reduction of AF inducibility; and (c) the single lesion in the cava-tricuspid isthmus does not impede AF inducibility.

[Acute changes in wavelength of the process of auricular activation induced by stretching. Experimental study]. / Modificaciones agudas de la longitud de onda del proceso de activación auricular inducidas por la dilatación. Estudio experimental.

OBJECTIVE: An evaluation is made of the acute modifications in the wavelength of the atrial excitation process induced by atrial stretching. MATERIAL AND METHODS: In 10 isolated Langendorff-perfused rabbit hearts and using a multiple electrode the wavelength of the atrial activation process (functional refractory period x conduction velocity) was determined in the right atrium. An analysis was also made of the inducibility of rapid repetitive atrial responses after 20 episodes of atrial burst pacing. Measurements were made under control conditions, after inducing two degrees of atrial wall stretch (D1 and D2), and following the suppression of atrial dilatation. RESULTS: Under control conditions the wavelength was 72.6 +/- 7.7 mm (250 ms cycle) and 54.0 +/- 5.1 mm (100 ms cycle). In D1 (mean longitudinal increase in atrial wall length = 24 +/- 3%) the wavelength shortened, with values of 59.8 +/- 6.6 mm (250 ms cycle; p < 0.01) and 44.9 +/- 5.1 mm (100 ms cycle; p < 0.01). In D2 (mean longitudinal increase in atrial wall length = 41 +/- 4%) the wavelength also shortened significantly, with values of 41.6 +/- 2.5 mm (250 ms cycle; p < 0.01 vs control) and 29.6 +/- 2.1 mm (100 ms cycle; p < 0.01 vs control). After suppressing atrial dilatation the wavelength was 65.7 +/- 8.0 mm (250 ms cycle, NS vs control) and 47.9 +/- 5.5 mm (100 ms cycle; NS vs control). The inducibility of rapid repetitive atrial responses increased during dilatation (22 episodes with over 30 consecutive repetitive responses in D1 [p < 0.01], 50 episodes in D2 [p < 0.001] vs 5 episodes under control conditions), and diminished after suppressing atrial dilatation (0 episodes with over 30 consecutive repetitive responses; p < 0.05). CONCLUSIONS: In the experimental model used, acute atrial dilatation produced a shortening in refractoriness and a decrease in conduction velocity. Both effects shortened the wavelength of the atrial activation process, facilitating the induction of atrial arrhythmias. The effects observed reverted upon suppressing atrial dilatation.

Quantification of the modifications in the dominant frequency of ventricular fibrillation under conditions of ischemia and reperfusion: an experimental study.

The characteristics of ventricular fibrillatory signals vary as a function of the time elapsed from the onset of arrhythmia and the maneuvers used to maintain coronary perfusion. The dominant frequency (FrD) of the power spectrum of ventricular fibrillation (VF) is known to decrease after interrupting coronary perfusion, though the corresponding recovery process upon reestablishing coronary flow has not been quantified to date. With the aim of investigating the recovery of the FrD during reperfusion after a brief ischemic period, 11 isolated and perfused rabbit heart preparations were used to analyze the signals obtained with three unipolar epicardial electrodes (E1-E3) and a bipolar electrode immersed in the thermostatized organ bath (E4), following the electrical induction of VF. Recordings were made under conditions of maintained coronary perfusion (5 min), upon interrupting perfusion (15 min), and after reperfusion (5 min). FrD was determined using Welch's method. The variations in FrD were quantified during both ischemia and reperfusion, based on an exponential model deltaFrD = A exp (-t/C). During ischemia deltaFrD is the difference between FrD and the minimum value, while t is the time elapsed from the interruption of coronary perfusion. During reperfusion deltaFrD is the difference between the maximum value and FrD, while t is the time elapsed from the restoration of perfusion. A is one of the constants of the model, and C is the time constant. FrD exhibited respective initial values of 16.20 +/- 1.67, 16.03 +/- 1.38, and 16.03 +/- 1.80 Hz in the epicardial leads, and 15.09 +/- 1.07 Hz in the bipolar lead within the bath. No significant variations were observed during maintained coronary perfusion. The fit of the FrD variations to the model during ischemia and reperfusion proved significant in nine experiments. The mean time constants C obtained on fitting to the model during ischemia were as follows: E1 = 294.4 +/- 75.6, E2 = 225.7 +/- 48.5, E3 = 327.4 +/- 79.7, and E4 = 298.7 +/- 43.9 seconds. The mean values of C obtained during reperfusion, and the significance of the differences with respect to the ischemic period were: E1 = 57.5 +/- 8.4 (P < 0.01), E2 = 64.5 +/- 11.2 (P < 0.01), E3 = 80.7 +/- 13.3 (P < 0.01), and E4 = 74.9 +/- 13.6 (P < 0.0001). The time course variations of the FrD of the VF power spectrum fit an exponential model during ischemia and reperfusion. The time constants of the model during reperfusion after a brief ischemic period are significantly shorter than those obtained during ischemia.

Acute effects of radiofrequency ablation upon atrial conduction in proximity to the lesion site.

The electrophysiological effects of RF ablation upon the areas in proximity to the lesioned zones have not yet been well characterized. An experimental model is used to investigate atrial conduction in the boundaries of RF damaged zones. In 11 isolated and perfused rabbit hearts, endocardial atrial electrograms were recorded using an 80-lead multiple electrode positioned in the left atrium. Both before and after the RF application (5 W, 8 s, 1-mm diameter unipolar epicardial electrode) in the mid-portion of the free left atrial wall, measurements were made of conduction time from the pacing zone (posterior wall of the left atrium) to three points between 7.5 and 7.9 mm distal to the damaged zone. Conduction velocity and the direction of the activation propagation vector were determined in ten groups of four electrodes positioned around the damaged zone, and at the left atrial appendage. The mean diameter (+/- SEM) of the transmural lesions produced by RF ablation and defined by macroscopic examination was 4.2 +/- 0.2 mm. The conduction times to the three points distal to the lesion site were significantly prolonged as a result of RF ablation; 7.6 +/- 0.4, 7.4 +/- 0.5, and 6.9 +/- 1.0 ms (control); and 11.3 +/- 1.0 (P < or = 0.01), 11.1 +/- 1.3 (P < 0.01), 10.6 +/- 1.4 ms (P < 0.05) (post-RF). The differences between the conduction velocities determined in the areas surrounding the lesion, before and after RF application, failed to reach statistical significance: 86.2 +/- 6.5 cm/s (control) versus 75.5 +/- 5.7 cm/s (post-RF) (NS). After RF, significant variations were only observed in the direction of impulse propagation in the proximal-inferior quadrant adjacent to the lesion site, the difference being -61 degrees +/- 18 degrees (P < 0.02). In 2 of 4 experiments in which the lesion size was increased by a second RF application (5 W, 16 s), tachycardias with activation sequence around the lesion could be induced, with cycle lengths of 56 and 50 ms, respectively. In the atrial wall, the conduction times to the regions distal to the RF lesion are significantly prolonged. No significant changes are observed in conduction velocity in the areas in proximity to the lesion. Prolonged conduction to the areas distal to the ablation site is due to the lengthened pathway traveled by the impulses in reaching these areas. Tachycardias with activation patterns that suggest reentry around the RF damaged zone may be induced.

Are double potentials markers of a specific zone of the atrioventricular junction in the isolated rabbit heart?

A study is made of the characteristics of the atrial potentials recorded in the Koch triangle and its proximity, their variations on modifying the site of cardiac pacing, and their usefulness as markers of a distinct zone of the AV junction. In 12 isolated and perfused rabbit heart preparations an analysis was made of the endocardial atrial electrograms recorded with a multiple electrode positioned in the AV junction. The electrograms were obtained during spontaneous rhythm and on pacing at the crista terminalis (CT), interatrial septum (IAS), left atrium, and right ventricle. Double potentials were frequently obtained. On pacing at the CT, high-low double potentials (DP [H-L]) were more frequent (P < 0.05) in the low CT (11% +/- 4% of the electrodes) and posterior zone of the Koch triangle (6% +/- 5%), than in the IAS (1% +/- 2%) and anterior zone of the Koch triangle (2% +/- 3%). A similar tendency was observed either on pacing at the left atrium or during spontaneous rhythm. During pacing at the IAS the percentages of low-high double potentials (DP (L-H]) were significantly higher (P < 0.05) in the low CT (7% +/- 6%). DP (H-L) were of low sensitivity in indicating a given zone; maximum sensitivity was 61% in the low CT when pacing at the CT. DP (L-H) proved even less sensitive in indicating a given zone, though their specificity was greater in the low CT (91%) during pacing at the IAS. The specific zones in which the highest percentages of DP (H-L) or DP (L-H) are obtained depend on the site of cardiac pacing. On pacing at the IAS, DP (L-H) are more specific of the low CT. During pacing at both the CT and at the IAS, DP (H-L) sensitivity in indicating a given zone is low.

Modification of atrioventricular nodal electrophysiology by selective radiofrequency delivery on the anterior or posterior approaches.

An analysis was made in 14 isolated and perfused rabbit hearts of the electrophysiological effects of selective radiofrequency (RF) delivery in the anterior (group I, n = 7) or posterior zone (group II, n = 7) of the Koch triangle, with the aim of modifying atrioventricular nodal (AVN) conduction without suppressing 1:1 transmission. After opening the right atrium, RF was delivered (0.5 W) with a 1-mm diameter unipolar electrode positioned in the selected zone until a prolongation of no less than 15% was obtained in the Wenckebach cycle length (WCL). Before and after (30 min) RF, anterograde and retrograde AVN refractoriness and conduction were evaluated, stimulating from the crista terminalis (CT), the interatrial septum (IAS), and from the RV epicardium. After RF, the following percentage increments were observed in group I: AH(CT) = 36% +/- 9%, AH(IAS) = 38% +/- 11%, WCL(CT) = 28% +/- 8%, WCL(IAS) = 22% +/- 6%, functional refractory period (FRP) of the AVN(CT) = 13% +/- 11%, FRP-AVN(IAS) = 13% +/- 8%, retrograde WCL = 20% +/- 19%, and retrograde FRPVA = 13% +/- 16%. The increments observed in group II and the significances of the differences with respect to group I were: AH(CT) = 11% +/- 14% (P < 0.01), AH(IAS) = 19% +/- 32% (NS), WCL(CT) = 42% +/- 14% (P < 0.05), WCL(IAS) = 42% +/- 16% (P < 0.01), FRP-AVN(CT) = 28% +/- 28% (NS), FRP-AVN(LAS) = 21% +/- 19% (NS), retrograde WCL = 35% +/- 24% (NS), and retrograde FRP = 16% +/- 13% (NS). In both groups, the AH interval variations were not correlated with those of the rest of the parameters analyzed. Truncated nodal function curves suggestive of a dual AV nodal pathway were obtained in three experiments, though in only one of them was this observed under basal conditions. In the other two experiments, with dual AV nodal physiology only after RF (one from each group), AV nodal reentrant tachycardias were triggered with atrial extrastimulus at coupling intervals equal to or shorter than at those that cause a sudden lengthening of the AH interval, RF delivered in the anterior and posterior zones of the Koch triangle produced effects of different magnitude on the AH interval and Wenckebach cycle length. In the anterior zone the AH interval was prolonged to a greater extent, while in the posterior zone the effects were greater on the Wenckebach cycle length. No correlation existed between the variations in AH interval and Wenckebach cycle length, regardless of where RF was delivered. The evaluation of anterograde AV nodal refractoriness was similar when stimulating from the crista terminalis or from the interatrial septum. By delivering RF, it was possible to induce dual AV nodal physiology and reentrant tachycardias.

Recovery curve and concealed conduction in the His-Purkinje system of the rabbit heart: effects of radiofrequency modification of the low AV junction.

UNLABELLED: The aim of this study was to analyze the recovery curve and concealed conduction in the normal His-Purkinje system and after delivering radiofrequency current in the low AV junction, in the perfused rabbit heart. Twenty-one rabbit hearts were studied. Radiofrequency current (5 W) was delivered in the low AV junction to induce an incomplete His-Purkinje AV block (HV prolongation with 1:1 AV conduction); this was achieved in 9 experiments (Group I), while 12 experiments developed a complete block (Group II). Atrial stimulation was performed in both Groups at baseline, and in Group I after radiofrequency delivery, as follows: (1) pacing at increasing rates to determine the His-Purkinje AV block cycle length; (2) atrial extrastimulus test (A1A2) to calculate the His-Purkinje effective refractory period and the fitting of the recovery curve (H1H2 vs H2V2) to the exponential equation delta HV = a.e(-b)x(H1H2); (3) concealed conduction protocol (in 15 experiments) consisting of an atrial extrastimulus test with an interposed beat (A1-A0-A2) at a fixed A1A0 coupling interval. The baseline recovery curve fitted an exponential equation in 17 experiments (with a 93% +/- 42% maximum H2V2 increase at the shortest H1H2), but did not in 4 experiments (the maximum H2V2 increase being only 22% +/- 7%). Radiofrequency application prolonged the HV interval (25 +/- 6 ms vs 46 +/- 16 ms; P = 0.001) and His-Purkinje effective refractory period (167 +/- 28 ms vs 217 +/- 57 ms; P = 0.02). The percentage increment was greater for HV than for refractory period (99% +/- 65% vs 35% +/- 32%; P = 0.02); however, the increment of the His-Purkinje block cycle length (77% +/- 74%) only correlated with that of the refractory period (r = 0.95; P = 0.0001). The recovery curve after radiofrequency delivery fitted an exponential equation in all experiments, showing a rightward shift expressed by an increment of the constant ln a (2.7 +/- 1.9 vs 5.5 +/- 5.5; P = 0.02). Concealed conduction appeared in only three experiments at baseline. After radiofrequency, however, it was observed in all experiments, producing a rightward shift of the recovery curve and an ln a increase (2.87 +/- 1.2 vs 9.9 +/- 2.7; P = 0.0001). When Ho was conducted, the curve rightward shift and ln a increase (26 +/- 7.5; P = 0.0001) were greater. CONCLUSION: (1) His-Purkinje physiology, as in AV nodal physiology, can be described by a recovery curve that fits an exponential equation, especially if conduction becomes depressed with radiofrequency current. (2) Radiofrequency application in the low AV junction modifies His-Purkinje conduction more than refractoriness, though the refractoriness increase determines the degree of block at fast atrial rates. (3) Concealed conduction is uncommon in the normal His-Purkinje system during atrial pacing, but very frequent after modifying the low AV junction with radiofrequency current.