Functional Line Of Block Research Articles

Upper Turnover Portion of the Reentry Circuit for Typical and Reverse Typical Atrial Flutter

The posteromedial right atrium (PMRA) forms a block line during typical atrial flutter (AFL). However, whether upper turnover portion exists at the anterior or posterior superior vena cava (SVC) has not been determined. We performed right atrial mapping during AFL in 20 patients (typical AFL, n = 17; reverse typical AFL, n = 3) using an electroanatomical mapping system. Mean AFL cycle length was 224 +/- 20 ms and mean number of mapping points was 140 +/- 27. PMRA formed a block line during both typical and reverse AFL in all patients. However, in 16 of 17 patients mapped with typical AFL, PMRA did not extend superiorly to the orifice of the SVC and AFL wave propagated between the upper limit of the PMRA and the posterior SVC. In the remaining patient mapped with typical AFL, a double potential was recorded along the PMRA continuously between the orifices of the inferior vena cava (IVC) and SVC. In the three patients mapped with reverse typical AFL, a posterior barrier was detected from IVC to the upper limit of the PMRA and AFL wave propagated between the upper limit of the PMRA and the posterior SVC. Mean length from IVC to upper limit of the PMRA was 81 +/- 8% of the length from IVC to SVC. PMRA forms a functional block line during both typical and reverse typical AFL. The upper turnover portion of reentry circuit for AFL was observed between the upper limit of the PMRA and the posterior SVC in the majority of isthmus-dependent AFL patients.

Atrial Fibrillation–Atrial Flutter Interactions

An appreciation of the article by Moreira et al in the current issue of Circulation 1 requires an understanding of the close interrelationship between atrial fibrillation (AF) and atrial flutter (AFL). These authors have understood this interrelationship and applied it to their data to advance the approach to both AF and AFL ablation. Key to this understanding is the recognition that cavotricuspid isthmus (CTI)–dependent AFL almost always develops from antecedent AF of variable duration.2–5 This is because in almost all instances, it is during the AF that a functional line of block (LoB) necessary for the development of AFL forms between the superior and inferior vena cavae. This LoB acts as a critical lateral boundary that prevents short-circuiting of the AFL reentrant circuit. Thus, in the vast majority of instances, without preceding AF, there can be no AFL. The most recent additional support of this concept comes from the report by Ellis et al,6 which found that of 363 patients who presented with only CTI-dependent AFL and who underwent CTI ablation, long-term follow-up (mean of 39±11 months) demonstrated newly recognized AF in 82%. It also should be noted that, as Moreira et al1 recognize, in some patients, a LoB between the vena cavae may be fixed (ie, anatomic) rather than functional. In such patients, AF may not be required for AFL to develop. Article p 2786 As Moreira et al1 further recognize, their report does not answer all the questions about the interrelationships of AF and AFL as they relate to AF ablation, …

Electrocardiographic imaging of patients with heart failure with left bundle branch block and response to cardiac resynchronization therapy

Background Cardiac resynchronization therapy (CRT) for patients with left bundle branch block (LBBB) and left ventricular (LV) dysfunction has variable responses. We hypothesized that conduction delays in intrinsic rhythm and responses to pacing may be influenced by electrophysiologic substrate. To determine this, we used electrocardiographic imaging (ECGI), which maps epicardial ventricular excitation noninvasively. Methods and Results Electrocardiographic imaging was conducted in 8 patients undergoing CRT. During intrinsic conduction with LBBB (6 patients), ventricular activation was heterogeneous, with regions of delayed and/or absent conduction, reflecting varied LV pathology. Latest LV activation occurred in the lateral LV base in 3 patients but variably in the remainder. The anterior LV was susceptible to block and slow conduction. Cardiac resynchronization therapy usually improved interventricular electrical synchrony, but this did not correlate with changes in QRS duration. In some patients, during CRT, regions of slow conduction appeared in the LV in response to pacing, indicating functional electrical characteristics of local tissue. Conclusion In LBBB and LV dysfunction, LV activation is heterogenous and unpredictable, with areas of slow and/or absent conduction. Functional lines of block generate complex barriers and may interfere with paced wave fronts. Thus, patient-specific electrophysiologic substrate properties may determine outcome of CRT.

Repolarization gradients and arrhythmogenicity in the murine heart

Repolarization gradients and arrhythmogenicity in the murine heart

Model of reentrant ventricular tachycardia based on infarct border zone geometry predicts reentrant circuit features as determined by activation mapping

Infarct border zone (IBZ) geometry likely affects inducibility and characteristics of postinfarction reentrant ventricular tachycardia, but the connection has not been established. The purpose of this study was to determine characteristics of postinfarction ventricular tachycardia in the IBZ. A geometric model describing the relationship between IBZ geometry and wavefront propagation in reentrant circuits was developed. Based on the formulation, slow conduction and block were expected to coincide with areas where IBZ thickness (T) is minimal and the local spatial gradient in thickness (DeltaT) is maximal, so that the degree of wavefront curvature rho proportional, variant DeltaT/T is maximal. Regions of fastest conduction velocity were predicted to coincide with areas of minimum DeltaT. In seven arrhythmogenic postinfarction canine heart experiments, tachycardia was induced by programmed stimulation, and activation maps were constructed from multichannel recordings. IBZ thickness was measured in excised hearts from histologic analysis or magnetic resonance imaging. Reentrant circuit properties were predicted from IBZ geometry and compared with ventricular activation maps after tachycardia induction. Mean IBZ thickness was 231 +/- 140 microm at the reentry isthmus and 1440 +/- 770 microm in the outer pathway (P <0.001). Mean curvature rho was 1.63 +/- 0.45 mm(-1) at functional block line locations, 0.71 +/- 0.18 mm(-1) at isthmus entrance-exit points, and 0.33 +/- 0.13 mm(-1) in the outer reentrant circuit pathway. The mean conduction velocity about the circuit during reentrant tachycardia was 0.32 +/- 0.04 mm/ms at entrance-exit points, 0.42 +/- 0.13 mm/ms for the entire outer pathway, and 0.64 +/- 0.16 mm/ms at outer pathway regions with minimum DeltaT. Model sensitivity and specificity to detect isthmus location was 75.0% and 97.2%. Reentrant circuit features as determined by activation mapping can be predicted on the basis of IBZ geometrical relationships.

Characterization of the Effects of Single Ventricular Extrastimuli on Endocardial Activation in Human Infarct-Related Ventricular Tachycardia

The purpose of this study was to examine the resetting response in human ventricular tachycardia (VT) circuits with 3-dimensional mapping. In characterizing re-entry with the resetting response, inferences are made about interaction of single ventricular extrastimuli (SVE) with VT. Non-contact mapping was used to examine the effects of SVE from 25 sites on 10 infarct-related VT circuits. The local temporal excitable gap (EGap) was 113.8 +/- 64.3 ms, 25.8 +/- 11.2% of VT cycle length. In 7 VT circuits there was a clear difference in the EGap at different points in the circuit. All circuits could be pre-excited over a range of SVEs, resulting in either: 1) premature activation throughout the circuit resulting in reset; 2) premature activation at entry, but subsequent interval dependent conduction slowing (IDCS) resulting in a fully compensatory return cycle; or 3) change to functional lines of block and return cycle QRS morphology. The principal determinant of whether SVE resulted in reset was the degree of IDCS within the diastolic pathway (DP) of the circuit. Resetting occurred from 9 sites (7 VT) but was absent from 15 sites despite pre-excitation of a sizeable EGap in the circuit in all cases. In infarct-related VT, all circuits can be pre-excited over a range of SVEs, the effect of which is dependent on the degree of IDCS within the DP or modification of functional block defining the circuit. Failure to reset does not therefore indicate the absence of an EGap or failure of entry to the circuit. The temporal and spatial properties of the EGap vary at different sites of entry to the circuit.

Electrophysiologic and Anatomical Characteristics of the Right Atrial Posterior Wall in Patients With and Without Atrial Flutter Analysis by Intracardiac Echocardiography

The posterior right atrial transverse conduction capability during typical atrial flutter (AFL) is well known, but its relationship to the anatomical characteristics remains controversial. Thirty-four AFL and 16 controls underwent intracardiac echocardiography after placement of a 20-polar catheter at the posterior block site during AFL or pacing. In 31 patients, the effective refractory period (ERP) at the block site was determined as the longest coupling interval that resulted in double potentials during extrastimuli from the mid-septal (SW) and free (FW) walls. The block site was located 3.0-29.0 mm posterior to the crista terminalis (CT) in each AFL and control patient. The CT area indexed to the body surface area was larger in AFL patients than in control patients (16.4+/-6.5 mm(2)/m(2) vs 11.3+/-6.4 mm(2)/m(2), p=0.01), and was positively correlated to age (r=0.34, p=0.02). The ERP was longer in the AFL patients than in controls (SW: median value 600 [270-725] ms vs 220 [200-253] ms; FW: 280 [230-675] ms vs 215 [188-260] ms, p<0.05 for each). A functional block line was located on the septal side of the CT in all patients. A limited conduction capability and age-related CT enlargement might have important implications for the pathogenesis in AFL.

AB36-3: Iso-duration mapping during ventricular pacing as a tool to ablate unmappable ventricular tachycardia after remote myocardial infarction

VT after MI is usually due to reentry through a protected isthmus bounded by functional lines of block (LoB). When VT is not inducible or not tolerated (unmappable VT) there is a need to unmask the isthmus by sinus mapping or pacing maneuvers. Experimental data suggest that sinus rhythm electrograms (EGM) along the central common pathway have a short duration compared to longer EGMs along LoBs. Using Carto® we aimed at identifying these isthmus-related LoBs by mapping the EGM duration during RV pacing.

Optical recording-guided pacing to create functional line of block during ventricular fibrillation

Low-energy defibrillation is very desirable in cardiac rhythm management. We previously reported that ventricular fibrillation (VF) can be synchronized with a novel synchronized pacing technique (SyncP) using low-energy pacing pulses. This study sought to create a line of block during VF using SyncP. SyncP was performed in six isolated rabbit hearts during VF using optical recording to control the delivery of pacing pulses in real time. Four pacing electrodes with interelectrode distances of 5 mm were configured in a line along and across the myocardial fiber direction. The electrodes were controlled independently (independent mode) or fired together (simultaneous mode). Significant wavefront synchronization was observed along the electrode line as indicated by a decrease in variance. With the independent SyncP protocol, the decrease in the variance was 19.3 and 13.7% (P<0.001) for the along-, and across-fiber configurations, respectively. With the simultaneous SyncP protocol, the variance was reduced by 24.2 and 10.7% (P<0.001) in the along- and across-fiber configurations. The effect of synchronization dropped off with distance from the line of pacing. We conclude that SyncP can effectively create a line of functional block that isolates regions of VF propagation. Further optimization of this technique may prove useful for low-energy ventricular defibrillation.

Pharmacological Modification of Spiral-type Reentry in the Ventricle

Spiral-type reentry is a principal mechanism for the genesis of life-threatening ventricular tachyarrhythmias. We investigated differential effects of Na channel blockers, IKr blocker (nifekalant), ICa,L blocker (verapamil), and amiodarone on the spiral reentry in rabbit hearts by using a high-resolution optical mapping system. Two-dimensional subepicardial layer of left ventricular myocardium with uniform anisotropy was prepared by endocardial cryoablation. During ventricular tachycardia (VT) elicited by cross-field stimulation, spiral-type excitations rotating around functional block lines (FBLs) were visualized.

Remodeling in Cells From Different Regions of the Reentrant Circuit During Ventricular Tachycardia

Anisotropic reentrant excitation occurs in the remodeled substrate of the epicardial border zone (EBZ) of the 5-day infarcted canine heart. Reentry is stabilized because of the formation of functional lines of block. We hypothesized that regional differences of ionic currents in cells of the EBZ form these lines of block. Therefore, we first mapped reentrant circuits of sustained tachycardias, then dispersed cells (infarct zone cells, IZs) from the central common pathway of the circuit (IZc) as well as from the other side of the line of block (outer pathway, IZo) for study. We mapped reentrant circuits in the EBZ of infarcted hearts during sustained ventricular tachycardias (>30 seconds, n=17 episodes, cycle lengths=218+/-7.9 ms). INa density was reduced in both IZc and IZo, and the kinetic properties of IZc INa were markedly altered versus IZo. Structural remodeling of the sodium channel protein Nav1.5 occurred in IZs, with cell surface localization differing from normal cells. Both IZc and IZo have similar but reduced ICaL, whereas IZc showed changes in Ca2+ current kinetics with an acceleration of current decay. Computer simulations of the 2D EBZ showed that incorporating only differences between INa in IZc and IZo prevented stability of the reentrant circuit. Incorporating only differences between ICaL in the IZc and IZo cells also prevented stability of the circuit. However, incorporating both INa and ICaL current differences stabilized the simulated reentrant circuit, and lines of block formed between the 2 distinct regions. Despite differences in INa and ICaL properties in cells of the center and outer pathways of a reentrant circuit, the resulting changes in effective refractory periods tend to stabilize reentry in this remodeled substrate.

Optical imaging of spiral waves: pharmacological modification of spiral-type excitations in a 2-dimensional layer of ventricular myocardium

Differential effects of sodium channel blockers, an I Kr blocker (nifekalant) and amiodarone on the spiral-type reentry, were investigated in rabbit hearts by using a high-resolution optical mapping system. Two-dimensional subepicardial layer of left ventricular myocardium with uniform anisotropy was prepared by endocardial cryoablation. During ventricular tachycardia (VT) elicited by cross-field stimulation, spiral-type excitations rotating around functional block lines (FBLs) were visualized. All the sodium channel blockers stabilized rotors; VT duration was prolonged in association with increases of FBLs and VT cycle length. The rotors in the presence of nifekalant were characterized by large meandering, long FBLs, and frequent front-tail interactions generating wave breaks. Amiodarone (acute application) increased FBLs and VT cycle length, but shortened the VT duration with minimal front-tail interaction. These results suggest that multifaceted drug action on both depolarization and repolarization may be required for the early termination of spiral-type reentry without causing breakup of rotors.

Characteristics of action potentials in the posteromedial right atrium: New insight into the mechanism of conduction block during atrial flutter

Background: Functional line of block is often seen at the posteromedial (sinus venosa region) right atrium (RA) during common atrial flutter (AFL), forming a posterior loop of reentrant circuit (JCE 2004; 15). Action potential propeties in the posteromedial RA may explain such phenomenon, since no anatomical obstacle exists in this region. However, little information is available on this issue in human patients.

Combined Effects of Nifekalant and Lidocaine on the Spiral-Type Re-Entry in a Perfused 2-Dimensional Layer of Rabbit Ventricular Myocardium

Spiral re-entry plays the principal role in the genesis of ventricular tachycardia and ventricular fibrillation (VT/VF). The specific I(Kr) blocker, nifekakant (NIF) has, often in combination with lidocaine (LID), recently been used in Japan to prevent recurrent VT/VF, but the combined effects of these drugs on spiral re-entry had never been investigated. A ventricular epicardial sheet was obtained from 13 Langendorff-perfused rabbit hearts by means of a cryoprocedure, and epicardial excitations were analyzed with a high-resolution optical mapping system. Nifekakant (0.5 micromol/L) caused significant prolongation of action potential duration (APD) and LID (3 micromol/L) attenuated the APD prolongation without affecting the conduction velocity. VT were induced in 6 hearts by cross-field stimulation, and single- or double-loop spirals circulating around variable functional block lines were visualized during the VT. Nifekakant reduced VT cycle length and caused early termination in association with destabilization of the spiral dynamics (prolongation of functional block line, frequent local conduction block, and extensive meandering). These modifications of spiral-type re-entrant VT by NIF were prevented by addition of LID. The effects of NIF on the spiral excitations are reversed by LID. This interaction should be taken into account when these drugs are used in combination to treat VT/VF.

Relationship Between Anatomic Location of the Crista Terminalis and Double Potentials Recorded During Atrial Flutter:

The activation sequence in typical atrial flutter (AFL) around the tricuspid annulus is well described. However, activation of the remainder of the right atrium (RA) is not well defined. Previous studies have shown a linear block at the crista terminalis (CT) during AFL. The aim of this study was to evaluate the relationship between the location of the CT and the line of block by intracardiac echocardiography (ICE). Twenty-one patients with typical AFL were included in the study. The ICE imaging catheter (9-French with 9-MHz ultrasound transducer) was advanced to the RA. Under ICE guidance, a 20-pole roving catheter was used to map double potentials (DPs) during AFL, and three-dimensional images of the RA were reconstructed. During counterclockwise (CCW), clockwise (CW) AFL, or both, a line of conduction block manifested by DPs was identified at a septal site adjacent to the CT in 12 patients and in the posteroseptal RA in 9 patients. The functional line of block in CCW and CW AFL is localized not at the CT but at the septal edge of the CT or in the posteroseptal RA.

Mechanism of pacing-induced ventricular fibrillation in the infarcted human heart.

The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined. Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.

Identification of functional block line in atrial flutter using three-dimensional intracardiac echocardiography.

The crista terminalis (CT) is reportedly a critical barrier for maintaining typical atrial flutter (AFL), but recent observations have suggested the presence of posteromedial functional block, as well as crista conduction. Therefore, this study was designed to identify the correlation between the posterior boundary of AFL and anatomical architecture in the human right atrium (RA) using 3-dimensional (D) intracardiac echocardiography (ICE). In 11 patients with AFL (typical 9, reverse typical 2), mapping with a 10-pole (n=5) or 32-pole (n=6) catheter was performed during AFL. ICE was used to determine the catheter's position relative to the intra-atrial structures. In all patients, double potentials were recorded at the posteromedial RA and the catheter positions were recognized as posterior to the CT by 3-D ICE. Double potentials were not recorded on the CT, and the activation sequence revealed a craniocaudal direction in the 9 patients with typical AFL and caudocranial direction in the 2 patients with reverse typical AFL. These findings demonstrate that the posterior boundary of the AFL circuit is in the sinus venosa region posterior to the CT, which may provide an important insight into the mechanism of maintaining AFL.

Mechanism of conversion of atypical right atrial flutter to atrial fibrillation

The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional “breaks” in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 ± 9 months for the atypical group and 18 ± 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.

Isochronal difference mapping: an approach for mapping dynamic changes during reentrant ventricular tachycardia.

During clinical electrophysiological study for treatment of reentrant ventricular tachycardia, activation maps constructed from the acquired electrophysiological data can be difficult to interpret when the reentrant circuit is changing from one cardiac cycle to the next. Reduction of complexity would be beneficial but has been difficult. A new technical method termed isochronal difference mapping (IDM) was devised to reduce complexity and enhance distinctive conduction patterns present in the data. Electrograms were acquired from 196 sites using a canine model of a reentrant ventricular tachycardia circuit with a figure eight conduction pattern occurring in the epicardial border zone. Activation maps were constructed for all cardiac cycles during episodes of tachycardia in five experiments. IDM maps were then created, which are subtractive comparisons of the activation maps from two different cardiac cycles during a given tachycardia episode. In each map the electrical activation occurring for only one or for both of the cardiac cycles was separately highlighted in distinct spatial areas of the border zone during an isochronal interval. Based on the mappings, areas of conduction velocity change, regions of breakthrough of the wavefront across functional lines of block, regions with coherent activation, and regions with irregular activation became readily apparent. IDM maps showed that when cycle length prolonged due to deceleration of conduction within the reentrant circuit isthmus, conduction velocity increased elsewhere in the circuit. IDM accentuates cycle-to-cycle differences in multi-channel electrophysiological data and can be used to reduce complexity and enhance distinctive conduction patterns.

Mechanisms for spontaneous changes in QRS morphology sometimes resembling torsades de pointes during reentrant ventricular tachycardia in a canine infarct model.

Spontaneous changes in QRS morphology during sustained reentrant ventricular tachycardia, occurring gradually or abruptly, causing the tachycardia to be polymorphic, have been described in clinical cases. The purpose of this study was to determine the mechanism for such changes in a canine infarct model. Reentrant circuits were mapped in the epicardial border zone during sustained ventricular tachycardia in the canine heart, 4 days after left anterior descending coronary occlusion. In 10 tachycardias, there was either an abrupt change in QRS morphology or a gradual change that took up to 25 cycles. When the latter occurred, the ECG resembled torsades de pointes. Maps showed that the predominant mechanism for the change in QRS was a shift in the exit route by which the impulse left the reentrant circuit to activate the ventricles (9/10 tachycardias). Such shifts resulted from small changes in conduction velocity in segments of the circuit, either speeding or slowing, which modified the length of the functional lines of block. Movement of the circuit to a different region was responsible for the change in QRS in only one of these experiments, in which the reentrant mechanism also changed from functional to anatomic. Subtle changes in conduction in reentrant circuits can alter QRS morphology. Changes in the exit route from a stable reentrant circuit can cause the ECG characteristics to resemble torsades de pointes.