RVOT

The RVOT is generally divided into rightward (free wall), anterior, leftward (septal), and posterior portions (Figure 81-1).⁹ The RVOT courses anterior and leftward of the LVOT with the distal RVOT and pulmonic valve located leftward of the distal LVOT and aortic valve, respectively. The pulmonary valve is superior to the aortic valve, such that the posteroseptal RVOT is immediately anterior and adjacent to the aortic valve, specifically the right and left coronary cusps (RCCs and LCCs).⁹ Its inferior and most rightward portion is continuous with the tricuspid annulus and the interventricular septum, where the bundle of His and the proximal right bundle branch are located, whereas its most superior and leftward portion is above the anterior pulmonary valve leaflet (Figure 81-2). Although the RVOT is muscular throughout, it is relatively thin in the rightward, anterior, and subpulmonary valve portions, and it is thicker in the proximal posterior portion, where it is directly opposite the LVOT and the anterior interventricular septum.

Relationship to Coronary Arteries

The left main coronary artery arises from the LCC, adjacent and immediately posterior to the RVOT below the pulmonary valve; therefore the potential for left main arterial damage exists during ablation both in the LCC and in the septal and posterior regions of the RVOT (see Figure 81-1). The left main coronary artery courses laterally relative to the RVOT as it branches into the left circumflex (LCx) and left anterior descending (LAD) arteries. Because the RVOT courses leftward, the right coronary artery (RCA), arising from the RCC, is closest to the proximal RVOT near the tricuspid annulus.

LVOT

Unlike the entirely muscular RVOT, part of the LVOT is muscular and part is fibrous. Most of the RCC and the anterior aspect of the LCC lie above the muscular (anterior) portion of the LVOT. The junction between the RCC and the noncoronary cusp (NCC) overlies the membranous interventricular septum (rightward portion of the LVOT), where the bundle of His and the proximal left bundle branch are located. The NCC and the posterior aspect of the LCC are continuous with the fibrous aortomitral continuity (AMC) in the posterior portion of the LVOT.

Aortic and Pulmonary Valve Cusps

The ventricular myocardium extends beyond the semilunar valves into the proximal pulmonary artery and the aortic valve cusps,¹⁰ and can be found both between and within the cusps.¹¹ Some cases of myocardial sleeves in the region of the coronary artery have also been reported.^12,13 Because the pulmonary valve is superior and leftward of the aortic valve, the RVOT beneath the pulmonary valve is at the same level as the aortic cusps. The RCC and the junction between the LCC and the RCC lie immediately adjacent to the posterior RVOT, beneath the pulmonary valve. Myocardial sleeves are found most often in the RCC and less commonly in the LCC.¹⁰ The NCC lies posterior and immediately adjacent to the interatrial septum; therefore its myocardial sleeves may be a site of origin for atrial tachycardias but not for idiopathic VTs.¹⁴

Epicardial and Perivascular Sites

Approximately 9% of idiopathic VTs originate epicardially, most often near coronary venous sites: the great cardiac vein (GCV), the anterior interventricular vein (AIV), and the middle cardiac vein (MCV).¹⁵ Immediately distal (in the retrograde direction to blood flow) to the coronary sinus (CS) os, the CS gives rise to the MCV, which courses in the posterior interventricular sulcus. The CS courses in the inferior aspect of the atrioventricular groove parallel to the mitral valve annulus, and ends at the valve of Vieussens in the region of obtuse marginal arteries. Beyond the valve of Vieussens, the vein continues as the GCV, coursing epicardially directly overlying the lateral mitral annulus. The junction of the AIV and the GCV is immediately lateral to the LCC. Proximal to distal, the AIV is adjacent to the posterolateral subvalvar RVOT, or the epicardial lateral RVOT, and the anterior epicardial space. Transpericardial mapping of the origin of epicardial idiopathic VTs has confirmed their propensity for origin near these perivascular structures.¹⁵

Left Ventricular Summit

OT VTs may also originate from the region of the LV summit, the most superior LV epicardial region at the top of the interventricular septum. The LV summit lies between the LAD and LCx arteries, near the junction of the GCV and the AIV, and superior to the aortic valve cusps.¹⁶ One series reported that 12% of idiopathic LV VTs originate from the LV summit.¹⁶ The superior-most region of the LV summit is close to the LAD and LCx arteries, along with prominent overlying epicardial fat, thus is inaccessible to epicardial catheter ablation; the lateral region is accessible via the GCV.

Symptoms

Palpitations, chest pain, dyspnea, and light-headedness during episodes are common, and rarely syncope can occur; some patients may be entirely asymptomatic.¹⁸

Triggers

Episodes are often triggered by caffeine, emotional stress, or exercise, typically during the recovery period after exercise.18,20,21 In women, hormonal flux (e.g., premenstrual, perimenopausal) may be a particular trigger.²¹ Circadian variation with morning and late afternoon peaks of occurrence of outflow tract PVCs has also been reported.²² These suggest the importance of sympathetic activity and circulating catecholamines in the mechanism of OT VTs.

RVOT

The most common origin of OT VT is the septal aspect of the RVOT, just inferior to the pulmonic valve (see Figure 81-2).²⁷ Because the PVC/VT exits from the superior-most region of the right ventricle, the inferior leads in stereotypical ECG morphology are markedly positive and narrow (see Figure 81-3). Leads aVR and aVL are markedly negative with a QS pattern. All RVOT PVCs/VT have left bundle branch block morphology in lead V₁ (rS or QS; see Figure 81-3). The precordial lead transition from net negative to net positive (from r<S to R>s) is critical for distinguishing RVOT from LVOT origin. The transition for PVCs of RV origin typically occurs at or later than lead V₃. Lead I is typically of low amplitude and is useful for differentiating posteroseptal (positive) from midseptal (multiphasic) or anteroseptal (negative) origin (Figure 81-4). The more leftward location of the anterior RVOT compared with the posterior RVOT accounts for the differences in lead I polarity (see Figures 81-1 and 81-4). The most common site of PVC origin is the anteroseptal or midseptal region.²⁷ Less than 10% of RVOT PVCs originate from the free wall.²⁸ For free-wall RVOT PVCs, the QRS remains inferiorly directed but is wider and notched compared with those of septal origin (see Figure 81-4). In the study by Dixit and colleagues,²⁹ no QRS width cutoff clearly separated free-wall from septal origin; however, relative QRS widening with free-wall compared with septal origin was clearly noted within each patient. Because the RV free wall is more anteriorly located, the precordial transition is seen later than that of VT with septal origin, nearly always at or later than lead V₄ (see Figure 81-4). Similar to septal PVCs, lead I is useful for differentiating anterior (negative) from posterior (positive) free-wall origin. Because a free-wall origin is very uncommon in patients with a structurally normal heart, the presence of PVCs of free-wall morphology should elicit a more thorough search for underlying structural heart disease, in particular arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D).

PVCs may also originate lower in the OT, further beneath the pulmonic valve. As the origin becomes more inferior, a series of changes to the ECG occurs: The inferior leads become less positive (first lead III, then lead aVF, and finally lead II), lead aVL becomes less negative, and lead I becomes more positive (as the origin becomes more posterior toward the tricuspid valve; Figure 81-2). An ECG morphology that is slightly inferiorly directed (positive in II and aVF and biphasic or positive in III), flat, or w-shaped in lead aVL and is more positive in lead I than in the typical posteroseptal PVC is typical for a PVC that originates from the RV inflow tract at the level of the His bundle³⁰ (see Figure 81-4). These para-Hisian PVCs are less common than OT PVCs but do occur in structurally normal hearts. The origin may be just superior or free-wall to the His bundle region, and careful mapping is critical to avoid heart block during ablation.

Even more infrequently, PVCs may originate superior to the pulmonic valve from myocardial fibers that extend into or just above the pulmonary valve.³¹ Few ECG features are helpful in distinguishing pulmonary artery (PA) from RVOT PVCs, other than a markedly inferior axis, earlier precordial transition (>R/S ratio in lead V₂), and the presence of a small atrial and ventricular potential on the mapping catheter at the site of successful ablation.³² Pulmonary artery origin can be confirmed with right ventriculography or intracardiac echocardiography (ICE).

LVOT

Recognition that OT PVCs can also originate from the LVOT is increasing.³³ The most common origin is from myocardial fibers within or adjacent to the aortic root,^34,35 but PVCs may also originate from the left ventricular (LV) myocardium just below the aortic valve, from the LV summit at the top of the interventricular septum, from the region of the AMC, or from the LV outflow epicardium.³⁶ LVOT PVCs also have a left bundle branch block pattern in lead V₁ (usually rS) with an inferior axis. Because the aortic root is immediately posterior to the RVOT (see Figure 81-1), LVOT PVCs have an earlier precordial transition, typically at or before lead V₃.^11,37 Further analysis can be performed to identify the origin within the aortic root. PVCs from the LCC region typically have an rS in lead I and an earlier precordial transition (lead V₁ or V₂) than those from the RCC (see Figure 81-4). PVCs from the RCC typically are positive and notched in lead I, with a precordial transition at lead V₂ or V₃.³⁸ The region at the junction of the RCC and LCC is a common site of aortic root PVC origin and has a signature “notch” or qrS pattern in lead V₁ or V₂^39,40 (see Figure 81-4).

As was already mentioned, PVCs with a precordial transition before lead V₃ typically originate in the LVOT, and those with a transition after V₃ typically originate in the RVOT. PVCs with a transition at lead V₃ are therefore challenging to localize.⁴¹ In addition, cardiac rotation or precordial lead misplacement can confound most ECG localization algorithms. One study found that comparing the precordial transition of the PVC with that in sinus rhythm can be helpful in localizing PVCs with a V₃ transition. If the PVC transition occurs after the sinus rhythm transition, the origin is RVOT with 93% specificity.⁴² Other algorithms are available for distinguishing RVOT from LVOT arrhythmias^43,44 (Table 81-1, Distinguishing ECG Features of LVOT vs. RVOT PVCs).

Rarely, PVCs can originate just below the aortic valve at the AMC—the region between the aortic and mitral valves. These PVCs have a marked inferior axis with a “signature” qR pattern in lead V₁ and a positive QRS complex in all precordial leads (see Figure 81-4).⁴⁵

Several criteria can be used to identify an epicardial exit to OT PVCs. The typical morphology is a left bundle branch block/inferior axis with an early precordial transition, delayed or “slurred” intrinsicoid deflection, and a QS pattern in lead I. A criterion called the maximal deflection index (MDI) takes advantage of the slower intrinsicoid deflection for arrhythmias of epicardial origin.¹⁵ The MDI measures the time from onset to the latest R wave peak in any precordial lead divided by the QRS duration; an MDI greater than 0.55 suggests an epicardial origin that is best approached via the coronary venous system or epicardium rather than via the aortic cusps. The typical PVC morphology originating closest to the GCV or the AIV has an early transition (V₁ or V₂) with a slurred initial r wave in V₁ and an rS or QS in lead I.⁴⁶ Another common morphology for an epicardial OT PVC is a right bundle branch block pattern in V₁, where a “pattern break” occurs from V₁ to V₃ (i.e., an R in V₁ and V₃ and an Rs or rS in V₂).

One should always be aware of the location of the ECG electrodes on the chest when analyzing a 12-lead ECG of OT VT, particularly in the EP laboratory, where other patches on the chest may affect usual ECG lead placement. Limb lead placement in the anterior chest during a stress test or precordial lead placement at the wrong interspace may lead to a significant change in ECG morphology that may confound any PVC localization algorithm.⁴⁷

Medical Therapy

OT VTs generally respond well to β-blockers or calcium channel blockers. These medications are typically first-line treatment because they have mild side effect profiles as compared with other antiarrhythmic medications, along with success rates in the range of 65%.¹⁸ Side effects such as fatigue may limit patient adherence. Calcium channel blockers may be tried in patients with asthma or intolerance to β-blockers but are typically less effective.

For patients who do not respond to β-blockers or calcium channel blockers, the addition or substitution of a class IC antiarrhythmic drug (flecainide, propafenone) may be useful.19,61 In refractory patients, class III drugs (sotalol or amiodarone) may also be considered.⁶¹ Because class I medications are contraindicated in the setting of ischemic heart disease, coronary artery disease should be excluded in patients with intermediate or higher risk before administration of such medications is considered. The efficacy of drug therapy can be monitored by patient symptoms, Holter monitoring, or stress testing. We typically perform a routine stress test every other year in patients on class IC antiarrhythmic drugs.

Mapping and Catheter Ablation

Catheter ablation is now considered an alternative first-line option for treatment of symptomatic PVCs and is detailed here. For patients with recurrent syncope due to rapid VT- or PVC-induced torsade de pointes VT, catheter ablation should be considered strongly early in the course of therapy. In some patients who suffer cardiac arrest caused by short-coupled PVC-induced torsade, an ICD may be recommended. In general though, ICD therapy is not warranted for most OT PVCs because they are typically associated with a benign prognosis and frequently can be cured with catheter ablation.

Mapping of PVCs in the EP laboratory requires fluoroscopy and an electrophysiological recording system that is typically coupled with an electroanatomical mapping system. For cases of aortic root or LVOT arrhythmia, phased-array ICE can be invaluable. PVCs can be mapped with pace mapping or activation mapping. If PVCs occur spontaneously and frequently, activation mapping can be used to identify the earliest bipolar electrogram preceding the surface QRS. For typical OT PVCs, a bipolar activation time longer than 20 to 25 milliseconds before QRS is usually sufficient for successful ablation. A QS pattern on the unipolar electrogram can also be recorded at the site of origin of the PVC/VT. Pace mapping should also be performed at the earliest site—recording of a pace map that does not match the clinical PVC at the earliest recorded site suggests that the PVC may originate from an adjacent cardiac chamber (e.g., LVOT when recording from posterior RVOT or epicardium). In cases of infrequent PVCs, pace mapping alone can be used to localize PVC origin. Pacing output should be set to twice diastolic threshold to avoid far-field or anodal capture. Pace mapping should begin in the area of suspected VT origin based on the 12-lead ECG and the catheter manipulated to achieve a 12/12 lead pace-map match with clinic VT (Figure 81-5). The first beat of sustained VT can sometimes have a slightly different morphology than the sustained run as the result of repolarization changes during initiation; therefore the morphology during sustained VT should be targeted. In addition, sometimes a pace map can appear similar over a sizable distance (1 to 3 cm^2,62,63). Attempts to match notching and QRS amplitude in all 12 leads will yield better ablation success.

For nearly all patients, mapping of the RVOT should occur first, given the low risk and high prevalence of RVOT origin PVCs. When the RVOT is mapped, positioning a catheter at the RV apex helps to delineate septal from free-wall RVOT location in the left anterior oblique projection. Typically the site of earliest activation will also have a perfect 12-lead pace-map match; if activation is longer than 20 ms before QRS with qS on the unipolar electrogram, then radiofrequency (RF) energy should be applied. A standard nonirrigated 4-mm RF energy ablation catheter can be used in the RVOT. Because the origin of these PVCs is superficial, powers of 25 to 30 watts are usually sufficient. An early “flurry” of PVCs during ablation is often considered a good sign, although this may occur with catheter ablation in any region. Very high-power lesions should be used cautiously, given the proximity of the superior RVOT, and particularly the proximal pulmonary artery, to the coronary arteries.⁶⁴ If the earliest activation is less than 20 milliseconds before QRS, if a small initial r wave is present on the unipolar electrogram at the earliest site, and/or if the pace map has a later precordial transition than the clinical PVC, mapping of the LVOT should be performed. Because the aortic valve plane is inferior to the plane of the pulmonic valve (Figure 81-6), when PVC activation is earliest in the low posterior RVOT and is less than 20 milliseconds before QRS, mapping of the aortic cusps should be performed. Typically the RCC is directly posterior to the inferoposterior RVOT, and the LCC is posterior to the anterior RVOT (see Figure 81-1). Unsuccessful ablation in these RVOT regions should lead to exploration of the corresponding aortic sinus regions. If after ablation in the superior RVOT, a change in PVC morphology is noted with a more inferior axis, the septal aspect of the pulmonary artery should be explored.⁶⁵ Coronary angiography should be performed before ablation in the PA. Cryoablation of RVOT and of pulmonary artery PVCs has been described but offers few advantages over RF ablation unless one is close to the His bundle.⁶⁶ Cryoablation may have a role in para-Hisian PVCs, although before ablation is performed in the para-Hisian region, the RCC should be explored, because this region lies just above the His region and may serve as a safer location for catheter ablation.⁶⁷

For LVOT mapping catheter localization, unless the operator has experience with aortography for identifying the coronary cusps, ICE is extremely useful for identifying the aortic cusps and the catheter position within the cusps (Figure 81-7). Fluoroscopy alone can often be misleading. The aortic root is typically mapped using the retrograde aortic approach, and it should be mapped as a separate cardiac chamber, with multiple activation points and pace maps taken throughout each coronary cusp at the valve level and up to 2 cm above the valve. The NCC overlies the left atrium and has never been associated with PVC origin in our experience. However, sites throughout the RCC, R/LCC junction, and LCC have been described. In contrast to the RVOT, pace maps in the aortic root are often unreliable because pace mapping can capture distant structures rather than the thin sleeves of myocardium in the aortic root that may be the source of PVCs. The precordial transition will often be a closer match than the RVOT, and although a poor pace map should not dissuade ablation, a perfect pace map is a useful guide for suggesting an aortic root origin.

The primary tool used for mapping in the aortic root is activation mapping. As can be seen with RVOT sites, early sites are typically greater than 20 milliseconds before QRS. In the aortic root, “reversal” of a sharp potential from late during sinus rhythm to early during a PVC confirms the origin as aortic root and often suggests a successful ablation site⁶⁸ (see Figure 81-5). Because of the proximity of the aortic valve region to the coronary arteries, coronary angiography is recommended before ablation is performed in the aortic root. If ICE is being used by an experienced operator, coronary angiography may be omitted if the site of earliest activation at the R/LCC junction or at the LCC if the coronary artery can be visualized farther than 1 cm away from the left main coronary artery. Registering the electroanatomical map with another imaging modality such as computed tomography (CT) angiography can facilitate identification of the proximal coronary arteries (see Figure 81-5). Visualizing the RCA with ICE is difficult; therefore coronary angiography should be performed before ablation within the right cusp. If ablation at an early site is ineffective, changing the angle of the catheter or looping the catheter into the LV cavity and back up into the aortic root can sometimes help. Mapping in the aortic root should be performed under systemic heparinization, and ablation should be performed with the use of irrigated ablation catheters, because any thrombus can potentially embolize down a coronary artery. Power usually is initiated at 15 to 20 watts and is slowly titrated up to 30 watts. Higher powers usually are not needed, although for an intramyocardial or epicardial focus, powers of up to 50 watts may be used. The impedance drop should be carefully observed and power discontinued at any sign of a rise in impedance.

The aortic cusps are the most common sites of LVOT PVCs; other sites include the LVOT myocardium just beneath the aortic valve and the LVOT epicardium, which can be approached via the aortic root or the coronary venous system or by subxiphoid epicardial access. Mapping and ablation of the LVOT endocardium beneath the aortic valve can be undertaken using conventional activation and pace mapping as described for the RVOT, although catheter stability is often challenging. For PVCs with a suggested epicardial exit by ECG or mapping, we often first explore the coronary venous system (GCV or AIV) and the left aortic sinus before considering epicardial access, because epicardial fat and proximity to the coronary arteries often limit the ability to perform epicardial ablation. A coronary sinus venogram can be performed to delineate the caliber and anatomy of the distal AIV. We place a small coronary sinus catheter as far distally as possible in the AIV for all LV outflow tract PVCs, to compare activation timing during the PVC with the use of catheters in the RVOT and the aortic root (see Figure 81-7). The main limitations of ablation within the GCV/AIV include the following: (1) the small size may not allow access with the ablation catheter; (2) low flow within a small vein may limit the power delivered, even with irrigated RF ablation; and (3) the proximity to the left main and LAD coronary arteries (Figure 81-8). Coronary angiography should always be performed before ablation is begun in the GCV/AIV so that closeness to the LAD coronary artery may be noted and ablation avoided if the catheter tip is less than 5 mm from the coronary artery. If activation is noted as equally early in AIV and LCC, ablation in the LCC can be safer and more effective because higher power can be safely delivered.⁶⁹ In some cases, the AIV has been the only site in which PVC elimination has occurred.^46,70

Percutaneous subxiphoid access can also be used to gain transpericardial access to map the epicardial surface of the OT. Although this is often limited by epicardial fat and proximity to the epicardial coronary arteries, a safe site that results in PVC elimination can be identified occasionally. It should be emphasized that even in expert hands, some PVCs of epicardial or intramyocardial origin near a major coronary artery cannot be eliminated with catheter ablation. Cryoablation has been performed for lesions near epicardial coronary arteries or the His bundle.⁷¹ In theory the warm blood pool would protect the coronary arteries, making cryoablation safer than RF energy when near a coronary vessel. However, animal studies have demonstrated that chronic coronary artery damage can occur after cryoablation directly on top of coronary arteries.⁷² In cases of unsuccessful ablation, treatment with drug therapy, including 1C agents, sotalol, or, if necessary, amiodarone, can then be undertaken. Minimally invasive surgical cryoablation under direct visualization has also been described for malignant PVCs originating near a coronary artery.⁷³

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