Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction.

OBJECTIVES: We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations. BACKGROUND: The nature of the reentrant circuit that underlies VT during acute MI is not well understood. METHODS: Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI. RESULTS: Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P < .01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P < .05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P < .05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P < .05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT. CONCLUSIONS: The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.     

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

BACKGROUND: Infarct border zone (IBZ) geometry likely affects inducibility and characteristics of postinfarction reentrant ventricular tachycardia, but the connection has not been established. OBJECTIVE: The purpose of this study was to determine characteristics of postinfarction ventricular tachycardia in the IBZ. METHODS: 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. RESULTS: 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%. CONCLUSIONS: Reentrant circuit features as determined by activation mapping can be predicted on the basis of IBZ geometrical relationships.     

Identification of unusual reentry circuit sites of nonischemic ventricular outflow tract tachycardia

Identification of Ventricular Outflow Tract Tachycardia. Background: Reentrant ventricular outflow tract (OT) tachycardia is rare in patients with nonischemic heart disease. The mechanism of ventricular tachycardia (VT) arising from the region of the aortic sinus of Valsalva (ASOV) is usually focal, rather than reentrant. Consequently, less is known about reentrant circuits in the OT and the aortic sinuses. The purpose of this study was to evaluate existence of reentry circuits in these areas using entrainment mapping techniques. Methods: We performed electrophysiological study in 51 consecutive patients with idiopathic or nonischemic symptomatic VT arising from the OT. Six of these patients were found to have VT of reentrant mechanism with 8 VT morphologies. Entrainment mapping, electroanatomical mapping (in 2 patients), and radiofrequency catheter ablation were performed. Results: Pacing entrained the VT at 93 sites, 52 of which were determined to be in the reentry circuit based on matching of the postpacing interval and VT cycle length. Of the reentry circuit sites, 6 were in the aortic sinus, 43 were below the aortic valve, and 3 were in the right OT below the pulmonary valve. Classification of reentry circuit sites identified 7 as exit, 1 as central‐proximal, 19 as inner loop, and 25 as outer loop sites. Catheter ablation terminated VT at 4 of the 6 aortic sinus sites and 4 of the 46 OT sites (P = 0.0006). Conclusions: We definitively demonstrated involvement of the ASOV in OT reentrant tachycardia using entrainment mapping. It may be useful for successful VT ablation to identify reentry circuit localization. (J Cardiovasc Electrophysiol, Vol. 23, pp. 179‐187, February 2012)     

Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia

Transient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval). The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9% (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = -0.08, p = NS). The effect of procainamide on the difference between correlated strongly with changes in the cycle length of ventricular tachycardia (r = 0.97, p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms underlying atrioventricular nodal conduction and the reentrant circuit of atrioventricular nodal reentrant tachycardia using optical mapping

The findings of multiple nondiscrete AV nodal pathways and asymmetric transitional zone provide a biophysical basis for understanding normal and abnormal AV node electrophysiology. Unidirectional block occurring at the transitional zone transforms the nondiscrete pathways model into a classic dual pathways physiology for AVNRT.     

Localization of the fast and slow pathways in atrioventricular nodal reentrant tachycardia by intraoperative ice mapping.

BACKGROUND. Atrioventricular (AV) nodal reentrant tachycardia is classically described as a reentrant rhythm entirely contained within the compact AV node. Although the concepts of longitudinal dissociation of two intranodal pathways and a distal common pathway are accepted, the proximal portion of the circuit remains undefined. Current reports suggest that the two pathways may be separable by atrial tissue and not contained entirely within the compact node. METHODS AND RESULTS. We used an ice mapping method to demonstrate the slow and fast pathways of the reentrant circuit and their relation to the atrial septum around the AV node. Six patients with the usual form (slow-fast) of AV nodal reentrant tachycardia were mapped during surgery. In most patients, antegrade slow pathway localization was posterior and inferior to the compact AV node along the tricuspid annulus; in two patients, it was superior along the tendon of Todaro. Retrograde fast pathway localization was anterior or superior to the compact AV node in all patients. In all patients, anatomic distinction was made between the two pathways and the compact node. CONCLUSIONS. We conclude that no upper common pathway exists within the compact AV node in the usual type of nodal reentrant tachycardia and that the perinodal atrial tissue is a requisite part of the tachycardia circuit.     

Development of multiform ventricular tachycardia during atrioventricular nodal reentrant tachycardia.

A woman of 18 presented with a supraventricular tachycardia, subsequently shown to be caused by atrioventricular nodal reentry, which abruptly deteriorated to a multiform ventricular tachycardia. She had not received any antiarrhythmic drugs nor did she have any of the disorders that are usually associated with this atypical ventricular tachycardia.     

Surgical treatment of ventricular tachycardia after epicardial mapping studies.

Two patients with intractable life-threatening ventricular tachycardias have been studied using intracardiac electrograms and programmed electrical stimulation of the heart. Both patients have shown to have an underlying re-entry mechanism in the ventricles as the basis for the tachycardias. Both patients underwent epicardial mapping studies at cardiac surgery, and the site of re-entry was established. In one patient the re-entry front was found to start in the posterobasal region of the left ventricle and in the other patient the re-entry front was found in the anterobasal region of the right ventricle. In both patients surgical interruption of the re-entry front was carried out. Both patients are alive and free from tachycardias at the time of writing.     

Mechanisms underlying the reentrant circuit of atrioventricular nodal reentrant tachycardia in isolated canine atrioventricular nodal preparation using optical mapping

The reentrant pathways underlying different types of atrioventricular (AV) nodal reentrant tachycardia have not yet been elucidated. This study was performed to optically map Koch's triangle and surrounding atrial tissue in an isolated canine AV nodal preparation. Multiple preferential AV nodal input pathways were observed in all preparations (n=22) with continuous (73%, n=16) and discontinuous (27%, n=6) AV nodal function curves (AVNFCs). AV nodal echo beats (EBs) were induced in 54% (12/22) of preparations. The reentrant circuit of the slow/fast EB (36%, n=8) started as a block in fast pathway (FP) and a delay in slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP through the atrial tissue located at the base of Koch's triangle. The reentrant circuit of the fast/slow EB (9%, n=2) was in an opposite direction. In the slow/slow EB (9%, n=2), anterograde conduction was over the intermediate pathway (IP) and retrograde conduction was over the SP. Unidirectional conduction block occurred at the junction between the AV node and its input pathways. Conduction over the IP smoothed the transition from the FP to the SP, resulting in a continuous AVNFC. A "jump" in AH interval resulted from shifting of anterograde conduction from the FP to the SP (n=4) or abrupt conduction delay within the AV node through the FP (n=2). These findings indicate that (1) multiple AV nodal anterograde pathways exist in all normal hearts; (2) atrial tissue is involved in reentrant circuits; (3) unidirectional block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask the existence of FP and SP, producing continuous AVNFCs.     

Coincidence of idiopathic ventricular outflow tract tachycardia and atrioventricular nodal reentrant tachycardia.

BACKGROUND: Tachycardia-induced tachycardia appears to be a relatively rare condition. In such cases an important question arises whether catheter ablation of one arrhythmia may prevent the occurrence of another. This paper reviews single-centre experience with coincident idiopathic outflow tract ventricular tachycardia (VT) and atrioventricular (AV) nodal reentry tachycardia (AVNRT), and strategy of treatment. METHODS AND RESULTS: Seven of 46 patients (15%) with clinically documented idiopathic outflow tract VT were found to have reproducibly inducible AVNRT at the time of an electrophysiological study. There were two men and five women (mean age 35+/-9 years, range 20-44) without structural heart disease. During the study, AVNRT spontaneously triggered VT in three cases. Radiofrequency catheter ablation of the slow pathway did not suppress subsequent inducibility of VT in any of them. Successful catheter ablation of VT did not prevent clinical recurrence of AVNRT in one patient, and led to transition of VT into typical AVNRT in another. CONCLUSION: Coincidence of idiopathic outflow tract VT and AVNRT was found in 15% of cases of clinically documented idiopathic VT. Catheter ablation of one arrhythmia substrate did not prevent inducibility or clinical recurrence of the other. These data support the strategy of performing catheter ablation of both arrhythmia substrates during one session.     

Resetting of ventricular tachycardia by single extrastimuli. Relation to slow conduction within the reentrant circuit

Although both transient entrainment and resetting with single extrastimuli have been demonstrated during sustained ventricular tachycardia related to previous myocardial infarction, the relation between these phenomena has not been defined. Because transient entrainment is only demonstrated when the mechanism of a tachycardia is reentry with an excitable gap, the resetting response to timed premature extrastimuli was studied in patients with ventricular tachycardia and correlated with the ability to demonstrate transient entrainment. The importance of the location of pacing and recording electrodes relative to regions of slow conduction within the reentry circuit for demonstrating specific characteristics of the resetting response after single extrastimuli was examined in 16 patients with 21 distinct morphologies of ventricular tachycardia related to coronary artery disease. At electrophysiological study, intracardiac electrograms were recorded simultaneously from four sites in the right ventricle and four sites in the left ventricle during ventricular tachycardia. Both resetting and transient entrainment could be demonstrated for 18 of the 21 (86%) ventricular tachycardias. The resetting response at each intracardiac recording site was defined as orthodromic or antidromic, based on the conduction time from the pacing stimulus to the recording site and the morphology of the captured (advanced) electrogram. An orthodromic resetting response was associated with demonstration of transient entrainment at 76 of 82 (93%) recording sites, implying that the pacing site was proximal and the recording site was distal to a region of slow conduction. In contrast, an antidromic resetting response was associated with transient entrainment at only six of 154 (4%) recording sites, suggesting that the pacing site was not separated from the recording site by a region of slow conduction (p = 0.001). The return cycle at the site of pacing exceeded the tachycardia cycle length in all episodes of ventricular tachycardia. At orthodromically activated recording sites, however, resetting was associated with a return cycle less than the tachycardia cycle length. Thus, orthodromic resetting demonstrates that a pause is not an integral part of the resetting response but that premature extrastimuli preexcite the reentrant circuit by entering the excitable gap, conducting through a region of slow conduction, and emerging distally without a change in activation sequence. In all episodes of ventricular tachycardia, the slope of the return cycle at the pacing site was determined by the conduction properties to the orthodromically activated sites, with increasing patterns (n = 6) produced by progressive conduction delay in the reentrant circuit at shorter coupling intervals and flat patterns (n = 3) produced by a constant orthodromic conduction interval.(ABSTRACT TRUNCATED AT 400 WORDS)     

Two unusual cases of coincident atrioventricular nodal reentrant tachycardia and ventricular tachycardia.

The simultaneous occurrence of narrow and wide QRS complex tachycardias was observed in 2 patients evaluated at our electrophysiological centers. Electrophysiological testing revealed the coexistence of two types of arrhythmia (atrioventricular nodal reentrant tachycardia and verapamil-sensitive left ventricular tachycardia) in one patient and of three types of arrhythmia (atrioventricular nodal reentrant tachycardia, ventricular tachycardia originating from the right ventricular outflow tract, and left ventricular tachycardia) in the other. Both patients underwent successful radiofrequency ablation of all the types of tachycardia.