Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp

Electrocardiographic characterization for guiding catheter ablation

Patient group

Between May 2000 and February 2001, 15 patients (8 men and 7 women; mean age 36.6 ± 20.3 years [range 11 to 78 years]) with symptomatic RMVT or frequent monomorphic VPCs were referred to our center. During clinical arrhythmia, the surface ECG showed a typical LBBB morphology with an inferior axis in all patients. All patients were refractory to anti-arrhythmic drugs (mean 3 ± 1 drugs), and six patients had previously failed ablation in the RVOT. All patients had structurally normal hearts and a normal ECG during sinus rhythm.

Electrophysiologic study

After giving written, informed consent and after withdrawal of anti-arrhythmic drugs, all patients underwent an electrophysiologic evaluation under intravenous sedation. Catheters were introduced to the right ventricular apex, RVOT and His bundle region under fluoroscopy through the femoral veins. The stimulation protocol consisted of programmed ventricular stimulation from the right ventricular apex and RVOT at two drive cycle lengths with up to three extrastimuli and incremental burst pacing at a cycle length up to 250 ms. If the clinical arrhythmia did not occur spontaneously and was not inducible during the baseline state, intravenous isoproterenol infusion (2 to 5 μg/min) was administered to provoke the clinical arrhythmia.

Electrocardiographic analysis

Spontaneous or provoked RMVT or VPCs allowed analysis of the QRS complex morphology, independent of the P and T waves. During clinical arrhythmias, analysis of the surface ECG was focused on the following (Fig. 1): 1) total QRS duration; 2) R-wave duration in leads V₁and V₂, determined from the onset of the QRS complex to the transition point between the R-wave and the isoelectric line; 3) R-wave duration index, calculated as a percentage by dividing the QRS complex duration by the longer R-wave duration in lead V₁or V₂; 4) R/S-wave amplitude ratio in leads V₁and V₂, measured from the QRS complex peak or nadir to the isoelectric line, expressed as a percentage; and 5) R/S-wave amplitude index, calculated from the greater percentage of the R/S-wave amplitude ratio in lead V₁or V₂.

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Figure 1

Example of electrocardiographic analysis of clinical arrhythmias: leads aVF, V₁and V₄of a normal sinus beat, followed by the first beat of repetitive monomorphic ventricular tachycardia. A= total QRS duration, measured from the earliest onset in lead V₄to the latest activation in lead aVF (ms); B= R-wave duration, determined in lead V₁from the QRS onset to the R-wave transaction point of the R-wave with the isoelectric line (ms); C= R-wave amplitude, measured from the peak to the isoelectric line (mV); D= S-wave amplitude measured from the cusp to the isoelectric line (mV).

Mapping and RF ablation

With spontaneous or induced RMVT or VPCs, activation mapping was performed with a 7F, 4-mm-tipped ablation catheter (Cordis-Webster, Inc., Baldwin Park, California). Activation mapping identified bipolar ventricular electrograms preceding the onset of the QRS complex. If RMVT or VPCs were infrequent, pace mapping was performed at 2 to 10 mA, and a pulse width of 0.5 to 2 ms was used to identify the site for RF catheter ablation. In all patients, initial mapping was performed in the RVOT. Whenever RVOT mapping failed to identify an early endocardial activation site, mapping of the left ventricle and ASC was performed retrogradely through the right femoral artery. The arrhythmia origin and ablation target were defined by the earliest activation. Bipolar and unipolar electrograms were filtered at 30 to 400 Hz and 0.05 to 400 Hz, respectively. The data were stored on optical disks for further analysis.

When the earliest ventricular activation was identified in the ASC, a 5F pigtail catheter was inserted into the aortic root through the left femoral artery. The aortic root and the ostia of the right coronary artery (RCA) and left main coronary artery (LMCA) were visualized by angiography. If the origin was in the left ASC, the LMCA was cannulated with a 5F left Judkin’s catheter. This was done, as a marker and for protection of the LMCA, in case of ablation catheter dislodgment during RF application.

Radiofrequency energy was delivered at the distal electrode of the thermocouple catheter and maintained for 120 s with a preselected temperature of 60°C in the RVOT or 55°C in the ASC. Radiofrequency energy was started at 30 W and increased up to 50 W in the RVOT and from 15 to 30 W in the ASC, under continuous fluoroscopy, to reach the target temperature. Radiofrequency application was immediately stopped if we observed catheter dislodgment.

Ablation success was defined as: 1) the absence of spontaneous or inducible clinical RMVT and/or VPCs at the end of the procedure; and 2) the absence of these arrhythmias after 48 h of continuous ECG monitoring and the absence of exercise stress after ablation, without anti-arrhythmic drugs. Transthoracic echocardiography was performed before hospital discharge in all patients. Transesophageal echocardiography was also performed after the procedure in the patients with RMVT originating in the ASC. Follow-up information was obtained from either the referring physicians or direct follow-up in our clinic. Transthoracic echocardiography was performed in the patients with RMVT originating in the ASC at three and six months after ablation.

Statistical analysis

Data are expressed as the mean value ± SD. The Mann-Whitney Uand Wilcoxon tests were used for comparisons. A p value <0.05 was considered significant.

Mapping

In eight patients (group 1), the earliest ventricular activation was localized in the superior septal RVOT, preceding the onset of the QRS complex by 29.3 ± 5.5 ms (range 19 to 35 ms), with simultaneous activation in the bipolar and unipolar recordings. In this group, no presystolic or late diastolic potentials were recorded. Additional pace mapping was performed in six of these eight patients and resulted in a perfect match in all six patients.

In the remaining seven patients (group 2), the earliest ventricular activation was recorded from the ASC preceding the onset of the QRS complex by 39.3 ± 24.2 ms (range 23 to 97 ms). Two ventricular activation components were recorded at the earliest site in all patients from group 2. The first component was either presystolic or late diastolic, of high frequency and low amplitude and only present in the ASC of origin, whereas the second component was coincident with the QRS complex (Fig. 2A and 2B). The ventricular activation on the unipolar recording was always simultaneous with the second component on the bipolar recording. Interestingly, during sinus rhythm, two ventricular activation components were also recorded in the left ASC in patients with RMVT origin, but the sequence of the two components was reversed, as compared with RMVT. Pace mapping was performed at the site of the earliest ventricular activation in three patients, but in only one patient, a perfect pace map was achieved. In addition, in all patients, an atrial potential was recorded from the ASC.

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Figure 2

Mapping catheter recordings of a sinus beat and the first beat of repetitive monomorphic ventricular tachycardia (RMVT) at the successful ablation sites in two different patients. Each panel shows surface electrocardiographic leads I, III and V₄, as well as the bipolar and unipolar signals recorded from the mapping catheter. (A)Earliest ventricular activation preceding onset of the QRS complex by 34 ms in a patient with RMVT originating from the left coronary aortic sinus. The unipolar signal (AS uni) also has a QS morphology, but is activated later than the bipolar signals (AS 1–2). Please note that a low-amplitude presystolic potential (arrow)appears during RMVT, although this potential is the second component of the “ventricular signal” (asterisk)during sinus rhythm. (B)Earliest low-amplitude late-diastolic ventricular potential (arrow)preceding onset of the QRS complex by 97 ms in a patient with RMVT originating from the left coronary aortic sinus cusp. As in part A, this potential is also seen as the second component of the “ventricular signal” during sinus rhythm (asterisk). A = atrial potential; V = ventricular potential.

Electrocardiographic characteristics

Seven of eight patients from group 1 presented with rS morphology in lead V₁or V₂, or both, and an R/S-wave transition between leads V₃and V₄. In six of these patients, the earliest ventricular activation was located at the posterior part of the superior septal RVOT; in one patient, the site of earliest activation was in the anterior part of the superior septal RVOT (Fig. 3). In the remaining patient with QS morphology in leads V₁and V₂and R/S-wave transition in lead V₄, the earliest endocardial activation was located in the anterior part of the superior septal RVOT (Fig. 3).

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Figure 3

Anatomic location of the origin of the arrhythmia, with corresponding 12-lead electrocardiographic morphology. Note the different morphology in leads V₁and V₂with respect to the anatomic origin. L = left coronary aortic sinus; N = noncoronary aortic sinus; R = right coronary aortic sinus; RVOT = right ventricular outflow tract.

In group 2, six patients presented with rS morphology in lead V₁or V₂, or both, and R/S-wave transition between leads V₂and V₃. In these six patients, the earliest ventricular activation was recorded at the right ASC in two patients and at the left ASC in the other four patients (Fig. 3). The remaining patient from group 2 showed QRS morphology in lead V₁and R/S-wave transition in lead V₂. In this patient, the earliest ventricular activation was located in the left ASC (Fig. 3).

The total QRS duration, R-wave duration and R/S-wave amplitude ratio in leads V₁and V₂, for both groups, are shown in Table 1. No difference in the total QRS duration was seen between the two groups. In contrast, the R-wave duration and R/S-wave amplitude ratio in leads V₁and V₂were significantly greater in group 2, which resulted in significantly higher indexes of R-wave duration and R/S-wave amplitude (Fig. 4). Cut-off values for an R-wave duration index ≥50% and for an R/S-wave amplitude index ≥30% allowed us to identify six of seven patients with RMVT origin from the ASC. One patient with RMVT originating from the right ASC had an R-wave duration of 46% and an R/S-wave amplitude index of 27%. No overlap of R-wave duration and R/S-wave amplitude indexes was noted between the two groups.

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Figure 4

Plot of the indexes of R-wave duration (A)and R/S amplitude (B)in patients with repetitive monomorphic ventricular tachycardia originating from the superior septal right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC).

Radiofrequency ablation

Five of seven patients with RMVT originating from the ASC, compared with only one of eight patients with RVOT originating from the ASC, had a previously failed ablation in the RVOT. The clinical arrhythmia was successfully ablated in all 15 patients. No significant difference was seen in the number of RF applications between the two groups (Table 1). In group 1, frequent VPCs and/or short runs of ventricular tachycardia with a very similar QRS morphology were observed during RF application. All ventricular arrhythmias were successfully abolished by RF applications.

In five patients from group 2, RF energy was applied at the left ASC below the LMCA ostium (Fig. 5). The distance from the tip of the ablation catheter to the LMCA ostium was 12.2 ± 3.2 mm (range 7.3 to 16.1 mm). In the remaining two patients, RF energy was applied in the right ASC, 8.8 and 11.1 mm antero-inferior to the RCA ostium. Radiofrequency current terminated RMVT in <3 s in 6 patients and within 8 s in one patient. No increase of ventricular ectopy was observed during RF delivery in group 2.

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Figure 5

Right (30°) and left (45°) anterior oblique (RAO and LAO, respectively) radiographic views of the mapping catheter (Map) at the successful ablation site in the left coronary sinus cusp. The mapping catheter was located below the ostium of the left main coronary artery (LMCA). CS = decapolar catheter inside the coronary sinus, with the distal electrode inside the great cardiac vein; His = decapolar catheter at the His bundle region; JC = 5F left Judkin’s catheter.

In all 15 patients, no procedure-related complications occurred, and no damage of the aortic valve was found by echocardiography. In addition, all 15 patients were free of arrhythmias, without anti-arrhythmic drugs, during a follow-up period of 9 ± 3 months.

Electrocardiographic characteristics and arrhythmia origin

Using quantitative ECG analysis, we could differentiate between RMVT originating from the RVOT and ASC. In the present study, the arrhythmia origin was in the superior septal RVOT in eight patients and in the ASC in seven patients. The indexes of R-wave duration and R/S-wave amplitude, calculated from lead V₁or V₂during arrhythmia, were significantly different between these two origins. These differences can be explained by their anatomic location. The arrhythmia originating from the ASC produces a slightly different vector, because the anatomic location is more posterior and rightward, which results in a longer R-wave duration and higher R/S-wave amplitude ratio in leads V₁and V₂. However, the right ASC is in close anatomic proximity to the so-called superior septal RVOT. This may explain why one patient with RMVT originating from the right ASC had lower indexes of R-wave duration and R/S-wave amplitude. Furthermore, the value for an R-wave duration index ≥50% and for an R/S-wave amplitude index ≥30% strongly suggest the ASC origin in patients with a typical LBBB morphology and an inferior axis.

In addition to the significant difference in the indexes of R-wave duration and R/S-wave amplitude, a low-amplitude, high-frequency potential was always found in patients with the ASC origin of RMVT. In patients with RMVT originating from the left ASC during tachycardia, this potential presented as either presystolic or late diastolic activation, whereas during sinus rhythm, it was the second ventricular activation component, which suggests that there was a slow conduction area between the ventricle and the left ASC. Again, this finding can be explained by the anatomic data. Myocardium from the septum and left ventricle is present in the right and left ASCs (17). In some patients, such myocardium can be arrhythmogenic and produce RMVT.

Anatomic considerations

For a better understanding of the origins of arrhythmias and approaches for catheter ablation, the anatomic arrangement between the RVOT and aortic sinus is relevant. Spatially, the aortic root occupies a central location within the heart, with the left and right coronary aortic sinuses adjacent to the left and right atrial appendages, respectively (Fig. 6a and 6b). The anteriorly situated RVOT passes slightly superior to and leftward of the aortic valve. The conical-shaped infundibulum of the right ventricular muscle is like a free-standing sleeve that elevates the pulmonary valve above the ventricular septum and superior to the aortic valve. Although commonly referred to as the “superior septal RVOT,” the posterior wall of the infundibulum is not septal, because an extracardiac tissue plane interposes between its epicardial surface and the right and left coronary aortic sinuses, as clearly seen on simulated long-axis sections of the heart (Fig. 6c and 6d). The circular ventriculo-arterial junction between the muscle of the infundibulum and the wall of the pulmonary trunk is crossed by the semilunar hinge lines of the leaflets of the pulmonary valve. This arrangement leaves three semilunar areas of muscle in the troughs of the sinuses (18). The left ventricular outflow tract, in contrast, has part muscular and part fibrous walls (Fig. 6c). The fibrous continuity between the aortic and mitral valves lies between the noncoronary leaflet and the posterior part of the left coronary leaflet, to a greater or lesser extent. The larger part of the right coronary and a portion of the left coronary aortic leaflets are related to the ventricular septum and the free wall of the left ventricle, respectively (17). Therefore, in these areas, the semilunar leaflets are hinged superior to the aortic wall but inferior to the muscle, enclosing ventricular muscle at the cusps of the sinuses (Fig. 6c to 6e). The posterior part of the right ASC is adjacent to the central fibrous body, which carries within it the penetrating His bundle. Anteriorly, the right ASC is related to the bifurcating atrioventricular bundle and the origin of the left bundle branch (Fig. 6d). The complex spatial relationships between the RVOT and ASC may explain the arrhythmia’s ECG characteristics.

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Figure 6

Heart specimens illustrating the anatomic arrangement between the right ventricular outflow tract (RVOT) and the aortic sinuses. (a)Viewed anteriorly, the RVOT passes leftward and superior to the aortic valve. (b)The posterior view shows the left (L) and right (R) coronary aortic sinuses adjacent to the pulmonary infundibulum. The noncoronary (N) aortic sinus is remote from the RVOT, but is related to the mitral valve (MV) and central fibrous body. The dotted linemarks the ventriculo-arterial junction (VAJ) between the wall of the pulmonary trunk (PT) and right ventricular muscle. Note the cleavage plane behind the pulmonary infundibulum and in front of the aortic root. (c and d)These simulated parasternal long-axis sections show two halves of the same heart and display the left and right coronary orifices. The right- and left-facing pulmonary sinuses (R and L in circles, respectively) are situated superior to the aortic sinuses. The dotted linemarks the epicardial aspect of the subpulmonary infundibulum in the so-called “septal” area. LAA = left atrial appendage; LCA = left coronary artery; LV = left ventricle; RAA = right atrial appendage; RCA = right coronary artery; SCV = superior vena cava; TV = tricuspid valve; VS = ventricular septum.

Radiofrequency ablation

Previous studies have shown that RMVT originating from the ASC can be successfully ablated (14–16), although aortic valve and coronary artery damage represent potential risks. In our patients, RF current was applied in the ASC 7.3 to 16.1 mm below the coronary artery ostium, and RMVT was terminated within 3 s in six patients and within 8 s in one patient. The immediate termination of tachycardia, in conjunction with the findings of autopsied hearts, is highly supportive of the arrhythmogenic substrate located superficially within the ASC. On the basis of these data, we suggest that RF application should be stopped if the RMVT cannot be terminated after 10 s. In addition, continuously visualizing the mapping catheter by fluoroscopy, with an angiographic catheter in the LMCA as a marker and for protection, was used in our patients to decrease the risk of complications during RF application in the ASC.

Study limitations

This small series has several limitations: 1) our patients did not represent the natural incidence of RMVT or VPCs, with LBBB morphology and an inferior axis, because patients with complex arrhythmias were usually referred to our center. However, quantitative ECG analysis from this study provides practical criteria for distinguishing between RVOT and ASC origins; and 2) the pace mapping used in this study was not systematically performed, although all clinical arrhythmias were identified by activation mapping under isoproterenol infusion.

Conclusions

In this study, all 15 patients with LBBB morphology and an inferior axis were referred for ablation of “RVOT” arrhythmias. Our data suggest that in some patients, RMVT can originate from the left and right ASC 7.3 to 16.1 mm below the coronary artery ostium. Repetitive monomorphic ventricular tachycardia originating from the ASC shows a QRS morphology very similar to that of RVOT arrhythmias on the surface ECG. However, the indexes of R-wave duration and R/S-wave amplitude can distinguish between the two arrhythmias. Mapping within the ASC is mandatory in patients with higher indexes of R-wave duration and R/S-wave amplitude, especially in those with previously failed RF ablation in the RVOT. If the RMVT origin is located in the left coronary ASC, RF ablation can be safely performed with a catheter used to cannulate the LMCA as a marker and for protection.