Role of the Vein of Marshall in AF Recurrences After Ablation
Role of the Vein of Marshall in AF Recurrences After Ablation
Of the 61 patients consented, the VOM was successfully cannulated in 54 (89%) patients, which were included in the study. Patients had recurrent AF or atypical flutter (25 and 29, respectively). The initial arrhythmia (prior to the index PVAI) had been paroxysmal AF in 24 patients and persistent in 30. Table 1 summarizes procedure parameters.
All patients had prominent VOM electrograms recorded at baseline, which supports lack of significant VOM ablation during the previous PVAI procedure. Of note, even in patients in whom extensive left atrial scar was present, specifically at sites corresponding to the endocardial aspect of the VOM, the VOM had still prominent signal amplitudes (Fig. 1A,B). VOM recordings during AF (present at baseline or induced) were not characterized by higher activation rates than those of simultaneous adjacent coronary sinus signals (cycle lengths in the distal VOM of 187 ± 49 ms vs 195 ± 69 ms, P = NS). In 16 of 54 patients, the VOM had complex fractionated potentials during AF. Figure 1 shows examples of VOM signals during sinus rhythm, atrial flutter, and AF with and without complex potentials (Fig. 1C,D, respectively).
(Enlarge Image)
Figure 1.
Baseline signals from the VOM (labeled as VOM or CARDIMA). All patients had prominent signals from the VOM prior to ethanol infusion (pre). (A) During normal sinus rhythm. The left panel shows prominent signals in the VOM despite extensive endocardial scar, as shown by silent signals from the circular duodecapolar catheter (LASSO) in the endocardium adjacent to the VOM (right lower panel) and the 3D map (right upper panel). (B) During atrial flutter, showing complex fractionated signals in the VOM in the presence of endocardial scar as shown in the LASSO signals and the 3D map. (A and B) lack of transmurality of previous ablations, with minimal signals on the endocardial side of the VOM. (C) During AF, showing multicomponent, complex potentials in the VOM with more regular, discrete activations from the LIPV (LASSO). (D) In AF with an arrhythmogenic RSPV (LASSO), where the VOM had slower activation rate. In all cases, VOM signals were eliminated by ethanol (post).
In order to assess the possible role of VOM triggers in PVAI failure, we administered isoproterenol at 20 μg/min (n = 8), combined with adenosine (24 mg bolus, n = 5). None of these interventions induced spontaneous AF. Ectopic beats arising from the VOM were mapped in 4 patients (data not shown), one of which developed incessant focal atrial tachycardia arising from the VOM (see below). However, we were unable to demonstrate VOM triggers initiating AF.
PVAI had been achieved successfully in all patients at the index procedure. PV reconnection had occurred in the majority of patients: LSPV (30/54), LIPV (32/54), RSPV (29/54), and RIPV (30/54). When reconnected, we assessed the conduction patterns between LIPV and LSPV, coronary sinus and VOM by pacing. Figure 2A shows an example of a patient with reconnection of the LIPV in whom the VOM electrograms and response to pacing were consistent with the VOM having a connection with the LIPV: pacing from the VOM advanced the LIPV potentials relative to the atrial component of the LIPV recordings. Additionally, pacing from the LIPV led to early activation in the VOM. Of all 32 LIPV reconnections, this pattern was only present in 5 patients and in none of the LSPV reconnections. Of note, LIPV reconnection via the VOM was consistent with a discrete connecting fiber: pacing from the proximal VOM did not show connection to the LIPV, whereas pacing from the distal VOM did in 2 patients (Fig. 2C shows an example). All others had indirect connections between the PVs and the VOM via the left atrial tissue, as shown in Figure 2B. The pattern of PV and VOM connection could not be predicted based on the venographic appearance of the VOM, or its proximity to the LIPV.
(Enlarge Image)
Figure 2.
VOM-mediated LIPV reconnection. Differential pacing from the VOM and LIPV was performed. (A) VOM-mediated LIPV reconnection: the left panel shows pacing from the VOM with advanced LIPV potentials—relative to the atrial signal—compared to sinus rhythm (last beat). Note that there is still delay from the stimulus artifact to the LIPV potentials, ruling out direct LIPV capture. The right panel shows VOM potentials during LIPV pacing preceding those of the coronary sinus. (B) LIPV reconnection independent of the VOM: pacing from the VOM (left panel) results in atrial signals preceding the PV potentials with identical delay as in sinus (last beat in the right panel). Pacing from the LIPV (right panel) conducts to left atrial tissue (CS) prior to the VOM. (C) Discrete VOM-LIPV connection: the left panel shows that pacing from the distal VOM results in advancement of the LIPV potentials (left beat), whereas pacing from the proximal VOM does not. Pacing from LIPV (right panel) shows signals in the distal VOM, but not in the proximal VOM. Signal labeling as in Figure 2. Conduction patterns could not be predicted by the respective locations of the quadripolar catheter in the VOM and the circular duodecapolar catheter in the LIPV (right panels).
In 23 of 32 patients (72%), ethanol infusion led to disconnection of the reconnected LIPVs. Figure 3 shows an example. In 13 of 30 (43%) patients, the LSPV was also disconnected after ethanol infusion. The venographic location of the VOM in relationship with the earliest PV potentials could predict isolation by ethanol. When the LIPV had reconnection arising from the left atrial posterior wall (as shown by the circular duodecapolar catheter), and the VOM had no posterior branches, ethanol infusion did not affect LIPV potentials. This was the case in 6 of 32 patients. Figure 3A shows an example. Partial elimination of the PV signals closest to the VOM was apparent in 3 of 32 patients, in each of whom a VOM without branches ran along the anterior aspect of the LIPV, where signals were eliminated. Figure 3B shows an example. Posteriorly directed branches of the VOM into the LIPV were present in all 23 patients in whom ethanol led to LIPV isolation. Figure 3C shows an example. Additionally, all patients in whom LSPV was isolated had VOM branches extending superiorly into the LSPV. Figure 4 shows examples of VOM branching patterns in which both LIPV and LSPV were isolated. Prior to terminating the procedure, all PVs were reassessed: in no case did we see ethanol-induced PV disconnection reverse during the procedure. The timing between ethanol infusion and final verification of left PV isolation was 47–77 minutes.
(Enlarge Image)
Figure 3.
VOM venogram characteristics and effects of ethanol infusion on LIPV connection. (A) Lack of ethanol effect. The circular catheter in LIPV shows reconnection through the LA posterior wall (left panel, earliest LIPV potentials marked with asterisk in the right panel). The VOM was small and without posterior branches. Ethanol infusion had no effects on LIPV signals. (B) Partial LIPV potential elimination by ethanol. A small VOM without posterior branches runs anterior to the LIPV (left 2 panels). At baseline, small potentials are present in the anterior LIPV (LASSO 3 through 10) during atrial flutter. Ethanol infusion led to disconnection and dissociation of this region (right panel asterisk showing a dissociated beat). (C) LIPV isolation by VOM ethanol infusion. A small VOM (left panel) had 2 posterior–superior branches directed toward the LIPV (mid-panel, circular catheter). Ethanol infusion leads to complete elimination of LIPV signals (right panel). All images are in right anterior oblique projection. Signal labeling as in Figure 2
(Enlarge Image)
Figure 4.
VOM venogram characteristics and effects of ethanol infusion on LSPV connection. (A) Small VOM branches reaching the LSPV (mid panel) were not apparent on nonselective venogram (left panel), and reached the point of LSPV reconnection (asterisk, earliest LSPV potentials in the inferior LSPV, LASSO 5–6). Ethanol infusion led to LSPV disconnection and dissociated LSPV potentials (right panels). (B) Simultaneous LIPV and LSPV disconnection by VOM ethanol. Venograms show large VOM posterior branches, directed toward the LSPV and LIPV and their reconnection sites (asterisks). Ethanol infusion led to disconnection of both veins.
Recordings from the VOM after ethanol infusion showed complete abolition of VOM electrograms except for the most proximal VOM (where the angioplasty balloon was placed for the proximal injection). Examples are shown in Figure 1. VOM ethanol infusion was performed during AF in 19 patients. A decrease in mean cycle length in the coronary sinus atrial signals was observed after ethanol infusion (mean decrease 24 ± 13 ms), but there was no AF termination (even in the 15 patients with complex potentials in the VOM), and signals at other locations were unaltered. Ethanol successfully ablated tachycardias arising from tissues around the VOM. In one patient, an LIPV tachycardia with 2:1 conduction to the neighboring left atrium was driving atrial flutter. Ethanol infusion led to termination of the LIPV tachycardia while achieving LIPV isolation (Fig. 5A). In another patient with focal atrial tachycardia arising from the VOM, ethanol infusion terminated it (Fig. 5B).
(Enlarge Image)
Figure 5.
Ethanol effect on tachycardias arising near the VOM. (A) LIPV tachycardia with 2:1 conduction to neighboring left atrial tissues. LIPV tachycardia terminates during ethanol infusion. (B) Tachycardia arising from the VOM. Activation times were earliest in the VOM recordings (fluoroscopic images in the right, showing a CS venogram and the circular catheter in the LIPV). Ethanol led to tachycardia termination and subsequent LIPV disconnection.
There were no acute complications directly attributable to VOM instrumentation or ethanol infusion. Ethanol levels measured at the end of the procedure in mixed venous blood were undetectable in all patients. One patient required drainage of a subacute hemopericardium developing 4 weeks after the procedure. At a median follow-up of 14 months (range 1–30), 8 of 54 patients (2 originally paroxysmal, 6 persistent AF) have had recurrent arrhythmias (2 recurred with AF, and 6 with atrial flutters), which have been successfully controlled with cardioversion (3), antiarrhythmic therapy (1) or repeat procedures to ablate focal atrial tachycardia (2, originating from the septum and left atrial appendage) or atrial flutter (2, left atrial roof-dependent).
Results
Patient Characteristics: AF or Flutter Recurrences
Of the 61 patients consented, the VOM was successfully cannulated in 54 (89%) patients, which were included in the study. Patients had recurrent AF or atypical flutter (25 and 29, respectively). The initial arrhythmia (prior to the index PVAI) had been paroxysmal AF in 24 patients and persistent in 30. Table 1 summarizes procedure parameters.
VOM Cannulation and VOM Baseline Electrogram Characteristics
All patients had prominent VOM electrograms recorded at baseline, which supports lack of significant VOM ablation during the previous PVAI procedure. Of note, even in patients in whom extensive left atrial scar was present, specifically at sites corresponding to the endocardial aspect of the VOM, the VOM had still prominent signal amplitudes (Fig. 1A,B). VOM recordings during AF (present at baseline or induced) were not characterized by higher activation rates than those of simultaneous adjacent coronary sinus signals (cycle lengths in the distal VOM of 187 ± 49 ms vs 195 ± 69 ms, P = NS). In 16 of 54 patients, the VOM had complex fractionated potentials during AF. Figure 1 shows examples of VOM signals during sinus rhythm, atrial flutter, and AF with and without complex potentials (Fig. 1C,D, respectively).
(Enlarge Image)
Figure 1.
Baseline signals from the VOM (labeled as VOM or CARDIMA). All patients had prominent signals from the VOM prior to ethanol infusion (pre). (A) During normal sinus rhythm. The left panel shows prominent signals in the VOM despite extensive endocardial scar, as shown by silent signals from the circular duodecapolar catheter (LASSO) in the endocardium adjacent to the VOM (right lower panel) and the 3D map (right upper panel). (B) During atrial flutter, showing complex fractionated signals in the VOM in the presence of endocardial scar as shown in the LASSO signals and the 3D map. (A and B) lack of transmurality of previous ablations, with minimal signals on the endocardial side of the VOM. (C) During AF, showing multicomponent, complex potentials in the VOM with more regular, discrete activations from the LIPV (LASSO). (D) In AF with an arrhythmogenic RSPV (LASSO), where the VOM had slower activation rate. In all cases, VOM signals were eliminated by ethanol (post).
VOM Triggers of AF
In order to assess the possible role of VOM triggers in PVAI failure, we administered isoproterenol at 20 μg/min (n = 8), combined with adenosine (24 mg bolus, n = 5). None of these interventions induced spontaneous AF. Ectopic beats arising from the VOM were mapped in 4 patients (data not shown), one of which developed incessant focal atrial tachycardia arising from the VOM (see below). However, we were unable to demonstrate VOM triggers initiating AF.
PV Reconnection: Role of VOM
PVAI had been achieved successfully in all patients at the index procedure. PV reconnection had occurred in the majority of patients: LSPV (30/54), LIPV (32/54), RSPV (29/54), and RIPV (30/54). When reconnected, we assessed the conduction patterns between LIPV and LSPV, coronary sinus and VOM by pacing. Figure 2A shows an example of a patient with reconnection of the LIPV in whom the VOM electrograms and response to pacing were consistent with the VOM having a connection with the LIPV: pacing from the VOM advanced the LIPV potentials relative to the atrial component of the LIPV recordings. Additionally, pacing from the LIPV led to early activation in the VOM. Of all 32 LIPV reconnections, this pattern was only present in 5 patients and in none of the LSPV reconnections. Of note, LIPV reconnection via the VOM was consistent with a discrete connecting fiber: pacing from the proximal VOM did not show connection to the LIPV, whereas pacing from the distal VOM did in 2 patients (Fig. 2C shows an example). All others had indirect connections between the PVs and the VOM via the left atrial tissue, as shown in Figure 2B. The pattern of PV and VOM connection could not be predicted based on the venographic appearance of the VOM, or its proximity to the LIPV.
(Enlarge Image)
Figure 2.
VOM-mediated LIPV reconnection. Differential pacing from the VOM and LIPV was performed. (A) VOM-mediated LIPV reconnection: the left panel shows pacing from the VOM with advanced LIPV potentials—relative to the atrial signal—compared to sinus rhythm (last beat). Note that there is still delay from the stimulus artifact to the LIPV potentials, ruling out direct LIPV capture. The right panel shows VOM potentials during LIPV pacing preceding those of the coronary sinus. (B) LIPV reconnection independent of the VOM: pacing from the VOM (left panel) results in atrial signals preceding the PV potentials with identical delay as in sinus (last beat in the right panel). Pacing from the LIPV (right panel) conducts to left atrial tissue (CS) prior to the VOM. (C) Discrete VOM-LIPV connection: the left panel shows that pacing from the distal VOM results in advancement of the LIPV potentials (left beat), whereas pacing from the proximal VOM does not. Pacing from LIPV (right panel) shows signals in the distal VOM, but not in the proximal VOM. Signal labeling as in Figure 2. Conduction patterns could not be predicted by the respective locations of the quadripolar catheter in the VOM and the circular duodecapolar catheter in the LIPV (right panels).
Ethanol Infusion: Effect on Left PV Reconnection
In 23 of 32 patients (72%), ethanol infusion led to disconnection of the reconnected LIPVs. Figure 3 shows an example. In 13 of 30 (43%) patients, the LSPV was also disconnected after ethanol infusion. The venographic location of the VOM in relationship with the earliest PV potentials could predict isolation by ethanol. When the LIPV had reconnection arising from the left atrial posterior wall (as shown by the circular duodecapolar catheter), and the VOM had no posterior branches, ethanol infusion did not affect LIPV potentials. This was the case in 6 of 32 patients. Figure 3A shows an example. Partial elimination of the PV signals closest to the VOM was apparent in 3 of 32 patients, in each of whom a VOM without branches ran along the anterior aspect of the LIPV, where signals were eliminated. Figure 3B shows an example. Posteriorly directed branches of the VOM into the LIPV were present in all 23 patients in whom ethanol led to LIPV isolation. Figure 3C shows an example. Additionally, all patients in whom LSPV was isolated had VOM branches extending superiorly into the LSPV. Figure 4 shows examples of VOM branching patterns in which both LIPV and LSPV were isolated. Prior to terminating the procedure, all PVs were reassessed: in no case did we see ethanol-induced PV disconnection reverse during the procedure. The timing between ethanol infusion and final verification of left PV isolation was 47–77 minutes.
(Enlarge Image)
Figure 3.
VOM venogram characteristics and effects of ethanol infusion on LIPV connection. (A) Lack of ethanol effect. The circular catheter in LIPV shows reconnection through the LA posterior wall (left panel, earliest LIPV potentials marked with asterisk in the right panel). The VOM was small and without posterior branches. Ethanol infusion had no effects on LIPV signals. (B) Partial LIPV potential elimination by ethanol. A small VOM without posterior branches runs anterior to the LIPV (left 2 panels). At baseline, small potentials are present in the anterior LIPV (LASSO 3 through 10) during atrial flutter. Ethanol infusion led to disconnection and dissociation of this region (right panel asterisk showing a dissociated beat). (C) LIPV isolation by VOM ethanol infusion. A small VOM (left panel) had 2 posterior–superior branches directed toward the LIPV (mid-panel, circular catheter). Ethanol infusion leads to complete elimination of LIPV signals (right panel). All images are in right anterior oblique projection. Signal labeling as in Figure 2
(Enlarge Image)
Figure 4.
VOM venogram characteristics and effects of ethanol infusion on LSPV connection. (A) Small VOM branches reaching the LSPV (mid panel) were not apparent on nonselective venogram (left panel), and reached the point of LSPV reconnection (asterisk, earliest LSPV potentials in the inferior LSPV, LASSO 5–6). Ethanol infusion led to LSPV disconnection and dissociated LSPV potentials (right panels). (B) Simultaneous LIPV and LSPV disconnection by VOM ethanol. Venograms show large VOM posterior branches, directed toward the LSPV and LIPV and their reconnection sites (asterisks). Ethanol infusion led to disconnection of both veins.
Ethanol Infusion: Effect on AF and Peri-VOM Arrhythmogenesis
Recordings from the VOM after ethanol infusion showed complete abolition of VOM electrograms except for the most proximal VOM (where the angioplasty balloon was placed for the proximal injection). Examples are shown in Figure 1. VOM ethanol infusion was performed during AF in 19 patients. A decrease in mean cycle length in the coronary sinus atrial signals was observed after ethanol infusion (mean decrease 24 ± 13 ms), but there was no AF termination (even in the 15 patients with complex potentials in the VOM), and signals at other locations were unaltered. Ethanol successfully ablated tachycardias arising from tissues around the VOM. In one patient, an LIPV tachycardia with 2:1 conduction to the neighboring left atrium was driving atrial flutter. Ethanol infusion led to termination of the LIPV tachycardia while achieving LIPV isolation (Fig. 5A). In another patient with focal atrial tachycardia arising from the VOM, ethanol infusion terminated it (Fig. 5B).
(Enlarge Image)
Figure 5.
Ethanol effect on tachycardias arising near the VOM. (A) LIPV tachycardia with 2:1 conduction to neighboring left atrial tissues. LIPV tachycardia terminates during ethanol infusion. (B) Tachycardia arising from the VOM. Activation times were earliest in the VOM recordings (fluoroscopic images in the right, showing a CS venogram and the circular catheter in the LIPV). Ethanol led to tachycardia termination and subsequent LIPV disconnection.
Patient Follow-up
There were no acute complications directly attributable to VOM instrumentation or ethanol infusion. Ethanol levels measured at the end of the procedure in mixed venous blood were undetectable in all patients. One patient required drainage of a subacute hemopericardium developing 4 weeks after the procedure. At a median follow-up of 14 months (range 1–30), 8 of 54 patients (2 originally paroxysmal, 6 persistent AF) have had recurrent arrhythmias (2 recurred with AF, and 6 with atrial flutters), which have been successfully controlled with cardioversion (3), antiarrhythmic therapy (1) or repeat procedures to ablate focal atrial tachycardia (2, originating from the septum and left atrial appendage) or atrial flutter (2, left atrial roof-dependent).