High-Resolution Mapping of Postinfarction Reentrant Ventricular Tachycardia: Electrophysiological Characterization of the Circuit

Abstract

Background: In vivo description of ventricular tachycardia (VT) circuits is limited by insufficient spatiotemporal resolution. We used a novel high-resolution mapping technology to characterize the electrophysiological properties of the postinfarction reentrant VT circuit.

Methods: In 15 swine, myocardial infarction was induced by left anterior descending artery balloon occlusion. Animals were studied 6 to 8 weeks after myocardial infarction. Activation mapping of VTs was performed by using the Rhythmia mapping system. Activation time was based on a combination of bipolar and unipolar electrograms. The response to overdrive pacing from different zones of the circuit was examined.

Results: A total of 56 monomorphic VTs were induced (3.8±2.1 per animal). Among these, 21 (37.5%) were hemodynamically stable and allowed mapping of the circuit. Isthmuses were 16.4±7.2 mm long and 7.4±2.8 mm wide. Conduction velocities were slowest at the inward curvature into the isthmus entrance (0.28±0.2 m/s), slightly faster at the outward curvature exit (0.40±0.3 m/s) and nearly normal at the central isthmus (0.62±0.2 m/s). In 3 animals, 2 VT morphologies with opposite axes sharing the same isthmus were mapped. Conduction velocities within the shared isthmus were dependent on the activation vector, consistently slower at the proximal curvature. Overdrive pacing from isthmus sites determined by activation mapping was consistent with entrainment criteria for isthmus. However, dimensions of the isthmus defined by entrainment exceeded dimensions of the isthmus measured by activation mapping by 32±18%.

Conclusions: In postinfarction reentrant VT, conduction velocities are slowest at the proximal and distal curvatures. Entrainment mapping overestimates the true size of the isthmus. High-resolution activation mapping of VT may better guide ablation therapy.

Keywords: cardiac ablation; electrophysiology; intracardiac electrograms; mapping; myocardial infarction; ventricular tachycardia.

Figure 1. Local time annotation of complex electrograms

This figure demonstrates the method of local time (activation time) annotation using combination of bipolar and unipolar electrograms. The left upper panel shows activation time annotation of a normal triphasic electrogram during sinus rhythm. Activation time is annotated at the dV/dt_max of the unipolar electrogram (Uni), coinciding with the peak of the bipolar (Bi) electrogram (red arrows). The middle upper panel shows activation time annotation of a fractionated electrogram during ventricular tachycardia (VT). The bipolar electrogram contains 2 separate high-frequency components marked with yellow and red arrows. The first component of the bipolar electrogram coincides with dV/dt_max of Uni₂ (yellow arrows) while the second component of the bipolar electrogram coincides with dV/dt_max of Uni₁ (red arrow). Thus, activation time of this bipolar electrogram is separated into two: the first component is annotated at the location of Uni₂ and the second component is annotated at the location of Uni₁. The right upper panel demonstrates local activation time of a split electrogram during VT. The local activation time coincides with the peak of the first component (yellow arrow) as determined by the dV/dt_max of the unipolar signal. The left lower panel shows activation time annotation of a multicomponent electrogram during sinus rhythm. The local activation time is marked at the terminal component of the bipolar electrogram, coinciding with the dV/dt_max of the unipolar signal (yellow arrow). The right lower panel shows activation time annotation of a complex split and multicomponent electrogram during right ventricular paced rhythm. The local activation time is marked at the late potential based on the maximal dV/dt.

Figure 2. Activation map of reentrant ventricular tachycardias

Activation maps of ventricular tachycardias (VT) in the anterior-septum of the left ventricle. The left panel shows a reentrant figure-eight circuit with a separate entrance, common channel, and exit. The entrance is characterized by convergence of the two activation wavefronts, forming a convex-shaped curvature with a wavefront propagating toward the common channel. The common channel “isthmus” is bounded by two lateral lines of block (or pseudoblock, allowing very slow conduction). The exit is characterized by concave-shaped curvature with divergence of wavefronts in front and lateral to the common-channel. The right panel is another example of figure-eight reentrant VT with an opposite axis. The arrowheads mark the proximal curvature (entrance) into the common channel.

Figure 3. Isochronal maps of reentrant ventricular tachycardia

Isochronal maps (10ms steps) derived from the unipolar dV/dt_max of the two ventricular tachycardia (VT) circuits. The left panel shows a figure-eight reentrant VT with increased isochronal density at the proximal curvature (entrance), suggestive of decreased conduction velocity (dashed white arrows). Conduction velocity within the common channel is increased as suggested by reduced isochronal density (solid white arrow). At the distal curvature (exit), conduction velocity is again slowed as demonstrated by increased isochronal density (dashed white arrows). The lateral boundaries of the isthmus are characterized by increased isochronal density suggestive of conduction of slowing (grey dashed arrows). Conduction along the outer boundaries of the isthmus, in the outer loop, is rapid and opposite in direction to the orthodromic wavefront of the common channel (white arrows). The right panel shows an isochronal map of a Y-shaped reentrant VT circuit with similar conduction velocity pattern. Conduction velocities are slowest at the proximal and distal curvatures but nearly normal in the common channel.

Figure 4. Electrogram characteristics at various zones of the reentrant circuit

This figure shows four panels with electrogram characteristics of entrance, isthmus, exit, and outer loop of a reentrant ventricular tachycardia circuit. Each panel includes three surface electrocardiographic leads (I, II, V₁), bipolar (Bi) electrogram with its 2 corresponding unipolar (Uni₁ and Uni₂) electrograms. The left upper panel shows a characteristic electrogram recorded at an entrance site. The bipolar electrogram is fractionated and of long duration. This is due to increased curvature with slower conduction velocity at the entrance zone. The local activation time is at the early diastole (red arrow) as determined by the dV/dt_max of the unipolar electrogram. The left lower panel shows a characteristic electrogram recorded at an isthmus site. The bipolar electrogram displays a split signal with a near-field mid-diastolic signal (red arrow) and a far-field systolic signal (yellow arrow). The diastolic signal derives from the orthodromic wavefront propagation within the common channel while the systolic signal derives from the wavefront propagating in the opposite direction at the outer loop. This is demonstrated by the reverse electrogram polarity of the unipolar electrogram. The right upper panel shows a characteristic electrogram recorded at an exit site, displaying a fractionated signal, consistent with increased curvature with slower conduction velocity at exit sites. The right lower panel shows a characteristic electrogram recorded at outer loop sites. The bipolar electrogram is spit similar to electrograms recorded at isthmus sites. However, in contrast to electrograms recorded in the isthmus, the local near-field signal determined by the unipolar dV/dt_max occurs during ventricular activation (red arrow) while the far-field signal originating in the isthmus occurs during diastole (yellow arrow

Figure 5. Conduction velocities in the isthmus are influenced by the vector of propagation

Example of two ventricular tachycardias (VTs) with opposite axis sharing one isthmus. VT-1 had a right bundle branch block pattern with an inferior axis while VT-2 had a right bundle branch block pattern with a superior axis. The tachycardia cycle length was similar at 460 and 463ms, respectively (left and right lower panels). The isochronal map of VT-1 shows maximal isochronal density, suggestive of slowest conduction velocity, at the proximal curvature (entrance). Once the wavefront reaches the common channel “isthmus”, conduction velocity is increased as marked by lower isochronal density (solid arrow). At the distal curvature (exit), conduction velocity is slowed again as suggested by increased isochronal density (dashed arrows). During VT-2, the wavefront of propagation is reversed, such that the entrance of VT-1 becomes the exit of VT-2 and the exit of VT-1 becomes the entrance of VT-2. The isochronal map of VT-2 shows maximal isochronal density at the proximal curvature (entrance), suggesting that conduction velocity within the circuit is not fixed to the underlying substrate but rather functional, consistently slower at the proximal curvature.

Figure 6. Entrainment criteria overestimate the dimensions of the isthmus

Example of a monomorphic VT mapped using both activation and entrainment techniques (left panel). The length of the isthmus determined by activation mapping was measured from the proximal curvature (entrance) to the distal curvature (exit) and is highlighted in a red dashed ellipse. Dimensions of the isthmus were also measured using standard entrainment criteria and included sites with concealed QRS on all 12 ECG leads and PPI-TCL ≤ 30ms (gray dashed rectangle). While the two methods similarly identified the proximal curvature (entrance) and the width of the common channel, entrainment mapping overestimated the length of the isthmus, particularly at the exit site. The pseudo-exit is the zone considered part of the circuit using entrainment mapping but not part of the circuit by activation mapping (black dots). The lower panel is an example of entrainment from a pseudo-exit site (electrode, right upper panel). The bipolar electrogram at the pacing site occurs just before the QRS complex (EGM to QRS of 36ms; 9% of the TCL). Entrainment from this site resulted in concealed QRS fusion, as the stimulated pacing site assumes a similar wavefront vector to the VT (solid arrow). However, in contrast to a true exit site, pacing from a pseudo-exit site resulted in a longer PPI with PPI-TCL of 25ms. This is because the pacing site is beyond the distal curvature (white arrows) and propagation of its wavefront in the figure-8 configuration (black arrows) assume a curvature shape that encounters a partially refractory tissue, both result in slower conduction and prolonged post pacing interval.

Figure 7. Sub-threshold stimulation from a mid-isthmus site with VT termination

This is an example of a sustained monomorphic ventricular tachycardia (VT) with a cycle length of 280ms. Pacing form a mid-isthmus site at a cycle length of 240ms captured the local tissue (small dashed arrows), however failed to capture the tachycardia. The forth-pacing stimulus terminates the tachycardia without capture of the ventricle (red star). The fifth and seventh pacing stimuli capture the ventricle with QRS morphology similar to the tachycardia and a long stimulus to QRS interval. These findings are consistent with sub-threshold stimulation with VT termination at or near an isthmus site.