Diagnosis and Management of Idiopathic Ventricular Tachycardia

Diagnosis and Management of Idiopathic Ventricular Tachycardia Kurt S. Hoffmayer, PharmD, MD, and Edward P. Gerstenfeld, MD Abstract: Idiopathic ventricular tachycardia (VT) refers to VT occurring in structurally normal hearts. It is commonly seen in young patients and typically has a benign course. Because the origin is typically focal and the heart is without scar, the 12-lead electrocardiogram is extremely useful for localizing the origin of idiopathic VT. Treatment options include reassurance, medical therapy, and catheter ablation. This review describes the clinical features, electrocardiogram recognition, and management of idiopathic monomorphic VT. (Curr Probl Cardiol 2013;38:131-158.) diopathic ventricular tachycardia (VT) refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT (OT-VT), fascicular VT, papillary muscle VT, annular VT, and miscellaneous (VT from the body of the right ventricle (RV) and crux of the heart; Table 1). The prognosis is excellent in the majority of patients. Precise epidemiologic data for idiopathic VT is lacking. Early series prevalence estimates accounted for 7%-38% of all patients referred for evaluation of VT, but a more realistic estimation is closer to 10%.1-6

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Outflow Tract VT History The first descriptions of frequent repetitive monomorphic premature ventricular contractions (PVCs) were made in 1922 by Gallavardin7 and 1947 by Parkinson8. However, it was not until the work of Buxton et al.9 61 years later that the origin of these PVCs was localized to the right The authors have no conflicts of interest to disclose. Curr Probl Cardiol 2013;38:131-158. 0146-2806/$ – see front matter http://dx.doi.org/10.1016/j.cpcardiol.2013.02.002

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TABLE 1. Classification of monomorphic idiopathic VT Outflow tract VT RVOT-VT LVOT-VT Aortic cusp VT Left ventricular (fascicular) VT Left posterior fascicle VT (LPF-VT) Left anterior fascicle VT (LAV-VT) Septal VT Annular VT Mitral annular VT Tricuspid annular VT Miscellaneous Body of RV Crux of the heart

ventricular outflow tract (RVOT). Since this initial description, significant advances in our understanding of the mechanism, electrocardiogram (ECG) morphology, and treatment of idiopathic OT-VT have occurred.

Mechanism Lerman et al. have demonstrated the mechanism of OT-VT to be triggered activity due to catecholamine-mediated delayed after-depolarizations.10-13 This triggered activity results from a catecholamine-mediated increase in cyclic adenosine monophosphate, with subsequent increase in intracellular calcium from the sarcoplasmic reticulum, resulting in delayed after-depolarizations and triggered activity. This underlying mechanism leads to tachycardia initiation with catecholamines and termination with adenosine, ␤-blockers, or calcium channel blockers.

RVOT Tachycardia RVOT-VT is the most common form of idiopathic VT accounting for 70% of all cases.14,15 It is characterized by ventricular arrhythmias with a left bundle branch block (LBBB) inferior axis QRS morphology (Fig 1). There is a female predominance, with VT occurring in approximately twice as many female as male individuals.16 RVOT-VT is typically triggered by exercise or stress, and may also occur during hormonal cycles in women.17 It typically presents in the third to fifth decade of life, with the mean age at presentation in the early 40s. The most common symptom is palpitations; however, chest pain, fatigue, and presyncope or syncope may occur. Some patients may be entirely asymptomatic. Clinically, patients may present with isolated PVCs, nonsustained VT, or sustained VT. 132

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Fig 1. PVC originating from mid-septal RVOT. The ECG tracing shows frequent PVCs and couplets with an LBBB/inferior axis QRS morphology. Note that the precordial transition of the PVC is V4, whereas the sinus transition is V3/V4. Successful ablation was achieved in the mid-septal RVOT.

Anatomy of the Outflow Tract. Familiarity with outflow tract anatomy is critical for understanding RVOT-VT origin and ECG localization.18 The RVOT is anatomically leftward to the left ventricular outflow tract (LVOT). The RVOT region is defined superiorly by the pulmonic valve and inferiorly by the level of the superior aspect of the tricuspid valve. The lateral and medial borders of the RVOT are the RV free wall and interventricular septum, respectively. The RVOT passes superiorly and cephalad over the LVOT. The origin of ventricular arrhythmias from the posterior RVOT is located just below the septal aspect of the pulmonic valve, in the subpulmonary infundibulum that supports the pulmonic valve (Fig 2). Clinically, electrophysiologists separate the septal and free-wall RVOT into anterior, mid, and posterior regions. The anteroseptal RVOT is anatomically adjacent to the left ventricle (LV) epicardium near the anterior interventricular vein, and the posteroseptal RVOT overlies the right coronary cusp. The majority of RVOT-VT originates from the anteroseptal RVOT.19,20 ECG Characteristics. Ventricular arrhythmias from the RVOT region have an LBBB QRS morphology with an inferior axis in the frontal plane. Specific ECG criteria exist to help pinpoint the exact location in the RVOT.21 The precordial transition (from rS to Rs) typically occurs at lead V4 or later, and begins no earlier than lead V3. Both leads aVL and aVR Curr Probl Cardiol, April 2013

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Fig 2. Anatomy of the outflow tract. Anatomy of the typical RVOT of the heart. L, left coronary cusp; R, right coronary cusp; N, noncoronary cusp; A, anteroseptal RVOT; P, posteroseptal RVOT; RA, right atrium; RAA, right atrial appendage; LA, left atrium; RCA, right coronary artery; LMCA, left main coronary artery. Note that the pin passing through the right coronary cusp ends up in the inferoposterior RVOT.

are negative. VT of septal origin is typically narrow; lead I is positive with a posteroseptal origin and negative or flat with an anteroseptal origin. RVOT-VT of free-wall origin is uncommon, and has a less inferiorly directed and broader R-wave in the inferior leads compared with septal sites. Free-wall origin arrhythmias also typically have notching of the inferior leads and a later precordial transition (at or later than lead V4). As the origin of VT moves inferiorly toward the superior tricuspid annulus, aVL gradually becomes less negative and eventually will become flat or “w”-shaped, and lead I will become more markedly positive. William G. Stevenson. An appreciation of the complex anatomy of the outflow tracts has been critical to advancing our understanding of these arrhythmias and the approach to ablation. Excellent detailed discussions can be found in work from Yamada and Kay.22 The use of intracardiac ultrasound and computed tomography and magnetic resonance imaging (MRI) has facilitated the translation of anatomic understandings into the electrophysi134

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ology laboratory. Although we commonly refer to the “septal” portion of the RVOT, this is the region that is anterior to the aorta, and is not truly “septal.” It is worth emphasizing that the aortic annulus is rightward of the pulmonic valve annulus, explaining why VT from the RVOT can have a frontal plane axis that is directed rightward, whereas some LVOT-VTs have a frontal plane axis that is directed leftward.

Myocardial muscle fibers may extend between and above the pulmonic valve, creating a potential nidus for VT.23,24 Given the proximity to the RVOT, there are few reliable ECG criteria that suggest a pulmonary artery (PA) origin. However, ECG characteristics that favor a PA origin include taller R-wave in the inferior leads, a larger ratio of the Q-wave in aVL/aVR, and a larger R/S amplitude in lead V2.24 If after ablation of a superior RVOT-VT, the ECG morphology shifts to a more inferior axis, exploration of the PA should be undertaken. Often, the intracardiac electrogram will record a sharp prepotential at the site of successful ablation.

LVOT/Aortic Cusp Tachycardia Anatomy. The posterior RVOT is directly adjacent to the anterior wall of the LVOT and aortic root. The aortic root has a central location within the heart, and consists of 3 sinuses of valsalva: the left, right, and noncoronary cusps (Fig 2). The right and left coronary cusps make direct contact with the LV, whereas the noncoronary cusp overlies the left atrium. The right coronary cusp is posterior and rightward and lies adjacent to the posterior RVOT. The His bundle lies just inferior to the right coronary cusp. The noncoronary cusp lies anterior and superior to the paraseptal region of the left and right atria close to the atrioventricular (AV) junction. Because the noncoronary cusp does not directly contact ventricular myocardium, ventricular arrhythmias are rare.25 The base of the left and right coronary cusps lies in direct contact to the ventricular myocardium, and LV muscle fibers may extend into the aortic root, serving as a source of these PVCs. These extensions may be a remnant from embryonic development, and these myocardial fibers persist providing an arrhythmogenic substrate.23,26 When mapping more inferiorly in the aortic root, successful ablation may be related to necrosis of ventricular myocytes arising from the most superior portion of the ostium of the LV.25 Approximately 10%-15% of idiopathic VT originates from the LVOT and can be mapped to the aortic cusps, with other LV locations, including the aortomitral continuity (AMC), occurring less commonly.25,27-31 Curr Probl Cardiol, April 2013

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TABLE 2. ECG classification of RVOT-VT versus LVOT/aortic cusp VT RVOT-VT Later precordial transition (V3 or later) With V3 transition: VT transition later than sinus rhythm V2 transition ratio ⬍0.60 Narrower R-wave duration and greater R/S-wave amplitude ratio in V1 and V2

LVOT/Aortic Cusp VT Earlier precordial transition (by V3) With V3 transition: VT transition earlier than sinus V2 transition ratio ⱖ0.60 Broader R-wave duration and greater R/ S-wave amplitude ratio in V1 and V2 Notch (qrS) in V1 or V2

Among the aortic cusps, origin from the left cusp is most common, followed by the right and then the junction of the left and right cusps.25,29 As opposed to RVOT-VT, LVOT/aortic cusp VT has an almost equal gender prevalence, affecting male individuals slightly more than female individuals.16 ECG Characteristics. VTs from the LVOT or aortic cusp region share a LBBB inferior axis QRS morphology, but have a precordial transition earlier than their RVOT-VT counterpart. The precordial R-wave transition typically occurs at or before lead V3. VT originating from the left coronary cusp has an earlier R-wave transition (typically by V1/2) than the right coronary cusp (V2/3). A broader R-wave duration (⬎0.5 ms) and a taller R/S-wave amplitude in V1 and V2 favor aortic cusp location.32 When the precordial transition occurs at lead V3, a precordial transition earlier than sinus rhythm transition is suggestive of LVOT-VT.33 Other methods for distinguishing LVOT from RVOT VT have been described in the literature and are included in Table 2.34 There are many specific ECG patterns that can aid in anatomic localization (Table 3). It is important to recognize that these findings lack sensitivity, but if seen may be very helpful in localizing the origin of VT. VT originating from the left coronary cusp has a precordial transition by V1/2, may have a “W”- or “M”-shaped pattern in lead V1, and is often difficult to classify as a true left bundle branch pattern.18,35 Because the aortic valve is located cephalad to the pulmonic valve, VT of left cusp origin often also has taller R-wave amplitude in the inferior leads compared with RVOT-VT. Left cusp VT also has a greater R-wave amplitude in lead II than III (II ⬎ III) and an rS complex in lead I. VT originating from the right coronary cusp has a precordial transition later than the left cusp, typically by lead V3, and has a positive notched R-wave in lead I due to the posterior and rightward right cusp location (Fig 3). VT from the left/right cusp junction has a signature qrS pattern 136

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TABLE 3. Specific Locations and ECG Features Left cusp

Right cusp R/L cusp junction Aortomitral continuity

Epicardial

Pulmonary artery

Tricuspid annular

Tricuspid inflow or para-Hisian

“M” or “W” pattern in V1 Monophasic R by V1/2 Tall R-wave amplitude in inferior leads Greater R-wave II/III ratio or III/II?? Lead I QS or rS Monophasic R by V2/3 larger R-wave amplitude in lead I qrS in lead V1-V2 (notched downstroke), QS in lead V1 (notched downstroke) qR in lead V1 Rs/rs complex in lead I R-wave ratio ⬍1 in II/IIIqR in lead V1 Rs/rs complex in lead I R-wave ratio ⬍1 in II/III MDI ⬎55% QS in lead I QS in II, III, avF (MCV) A Q-wave ratio in avL/avR ⬎1.4 or an S-wave amplitude ⬎1.2 mV A “transition break,” specifically a loss of R from leads V1 to V2 (QS or rS) with prominent R by V3 (AIV); MDI ⬎55% QS in lead I QS in II, III, avF (MCV) A Q-wave ratio in avL/avR ⬎1.4 or an S-wave amplitude ⬎1.2 mV A “transition or pattern break,” specifically a loss of R from leads V1 to V2 (QS or rS) with prominent R by V3 (AIV) Tall R-wave in the inferior leads Larger Q-wave ratio in avL/avR Larger R/S amplitude in lead V2, larger R-wave amplitude in the inferior leads Larger Q-wave ratio in avL/avR Larger R/S amplitude in lead V2 R- or r-wave lead I R or r with overall positive polarity in aVL or r-wave I R or r with overall positive polarity in aVL Large R-wave in I, R-wave or flat in aVL, large R-wave in I, R-wave or flat in aVL

in lead V1 or V2.28 The noncoronary cusp overlies the left atrium and is more commonly a source of atrial arrhythmias, and has not been a source of VT in our experience. LVOT-VT can also originate from the LV endocardium just inferior to the aortic valve. An infrequent origin for LVOT-VT is the AMC. This VT/PVC demonstrates a pathognomonic qR pattern in lead V1, Rs/rs complex in lead I, and an R-wave ratio of ⬍1 in leads II/III25,35,36 (Fig 4). Curr Probl Cardiol, April 2013

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Fig 3. PVCs originating from the right coronary cusp. The ECG tracing shows ventricular bigeminy with an LBBB/inferior axis PVC. Note that the precordial transition of the PVC is V3, whereas the sinus transition is V4. Also of interest is the monophasic R-wave in lead I. Successful ablation was achieved in the right coronary cusp.

Fig 4. AMC PVCs. The ECG tracing shows ventricular bigeminy. The precordial leads demonstrate an R-wave V1-V6 with a small q-wave in V1. The PVC was transiently terminated with ablation in the AMC.

There are limitations to electrocardiography, and notable small changes in electrode placement may markedly affect the QRS morphology and alter the predictability of ECG localization.37 Thus, one should be cautious about interpreting VT origin in patients with nonstandard 138

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electrode positioning, such as during a stress test, and careful attention should be paid to confirm that electrodes are placed in the correct locations in the EP laboratory.

Epicardial Outflow Tract VT Rarely, VT may originate from or be accessed from the epicardial surface of the myocardium. ECG criteria have been described that suggest an epicardial VT origin. Delayed initial precordial QRS activation, as quantified by the maximum deflection index (measured as the time from the earliest QRS onset to the maximum deflection in precordial leads, divided by the total QRS duration) ⬎0.55 suggests an epicardial VT exit.38 An inferior axis with a QS in lead I may suggest an epicardial origin as well.39 A “transition or pattern break,” specifically a loss of R from leads V1 to V2 (QS or rS), with prominent R by V3, identifies a focus from the anterior LV just in front of the aortic root; when this pattern occurs together with a QS in lead I, it typically suggests an epicardial origin near the interventricular vein28 (Fig 5).

Prognosis The prognosis for outflow tract VT is generally benign, and most patients can be reassured that the prognosis is excellent. However, two exceptions exist. These include a small percentage of patients who have a more malignant form of short-coupled PVC-induced40 polymorphic VT (Fig 6) or patients who develop LV dysfunction secondary to tachycardiainduced cardiomyopathy.41-43 Such patients should be referred for electrophysiologic evaluation. Patients with a PVC burden ⬍10% or 10,000 PVCs on a 24-hour Holter monitor have not been described to develop a PVC-mediated cardiomyopathy and require no specific therapy if asymptomatic. In a study by Bogun et al.,43 a PVC burden ⬎24% was the best predictor of developing a PVC-induced cardiomyopathy. Asymptomatic patients with a PVC burden ⬎10% should be closely followed for any signs of LV dilatation or reduction in LV function that may be a harbinger of developing a cardiomyopathy.

Evaluation and Treatment If a patient presents with a typical monomorphic outflow tract PVC, evaluation with a Holter monitor and echocardiogram is typically sufficient. If multiple PVC morphologies exist or the origin appears to be unusual (free wall), additional testing such as MRI may be warranted to exclude structural heart disease such as arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Ventricular arrhythmias from ARVD/C may share an Curr Probl Cardiol, April 2013

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Fig 5. Transition break signifying epicardial PVC origin. The above 12-lead ECG shows a “transition break,” as V1 has a monophasic R-wave, V2 RS, and V3 monophasic R-wave. This pattern along with a QS in lead I signifies an epicardial origin. On the right are fluoroscopic images showing the ablation catheter tip very close to the first diagonal branch of the left anterior descending artery.

Fig 6. Short-coupled polymorphic idiopathic VT in an idiopathic VT patient. The underlying rhythm appears to be atrial fibrillation in this rhythm strip with leads II and III shown above. A short-coupled PVC initiates polymorphic VT in a patient with a normal QT interval. The patient had a normal echocardiogram, baseline ECG, and coronary angiogram.

LBBB/inferior axis QRS morphology, and differentiation between idiopathic VT from the RVOT-VT and ARVD/C is important, given the benign nature of the former and the need for sudden cardiac risk stratification and family screening in the latter.44 ARVD/C is associated with abnormal signalaveraged ECG, and structural abnormalities (RV thinning, abnormal wall 140

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motion, aneurysms, or scarring) detected by echocardiography, MRI, RV angiogram, or RV voltage maps. On the sinus rhythm ECG, anterior T-wave inversions and/or the presence of an epsilon wave in a patient with LBBB-morphology PVCs should raise the suspicion of ARVC. A PVC with a wider QRS duration (lead I ⱖ120 ms), QRS notching in multiple leads, or very late precordial transition (⬎V5) also should raise the possibility of underlying ARVD/C.45,46 Multiple or unusual VT morphologies warrant further investigation.44 Treatment options for OT-PVCs/VT include reassurance without specific therapy, medical therapy, and catheter ablation. Treatment preference should be tailored to the individual patient– based preference, the severity and frequency of symptoms, and comorbidities. Medical Therapy. In patients with symptomatic outflow tract VT, ␤-blockers are typically first-line therapy. For patients who cannot take or tolerate ␤-blockers, non-dihydropyridine calcium channel blockers (verapamil or diltiazem) may be tried. Antiarrhythmic medications are usually reserved as second-line therapy for patients who do not wish to undergo catheter ablation.9,47 In our experience, low doses of class IC agents, such as flecainide, 50 mg twice daily, or propafenone, 75 mg three times daily, are often very effective. Catheter Ablation. Radiofrequency (RF) catheter ablation is a safe and reliable technique for curing outflow tract VT, and is a reasonable first-line alternative to medical therapy for symptomatic patients. ECG localization of the PVC origin is useful to help plan the ablation procedure and for advising patients of the potential risks and benefits of ablative therapy. The anesthesia plan should be tailored to the individual patient, as sedation may limit the frequency of PVCs or VT. Isoproterenol and burst pacing is often useful for provoking VT. Strategies for mapping include activation mapping (unipolar and bipolar) and/or pace-mapping. A 3-dimensional electroanatomic mapping system can be useful to annotate the location of earliest activation and best pace-maps. Activation mapping can be used if the patient is experiencing frequent PVCs or VT. This can be accomplished using both bipolar and unipolar electrograms. Earliest activation on the bipolar electrogram at successful ablation sites typically precedes the surface QRS onset by 20-40 ms. The bipolar electrogram usually has a sharp rapid initial deflection, and may demonstrate reversal of a late component present during sinus rhythm. Unipolar electrograms typically have a QS pattern with a sharp initial downstroke preceding the surface QRS at the successful site of ablation48 (Fig 7). Curr Probl Cardiol, April 2013

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Fig 7. Electrogram signals of successful site in RVOT-VT. Note the sharp bipolar electrogram and the QS (arrows) pattern in the unipolar electrograms.

Pace-mapping may be used as an adjunct to activation mapping or as the primary mapping strategy if PVCs/VTs are infrequent. The major limitation to pace-mapping is for PVCs/VT of aortic cusp origin. In this case, stimulation may capture far-field right or left ventricular myocardium, and a poor pace-map may still occur at an ideal ablation site. However, in the RVOT, ablation based on pace-mapping is associated with a high success rate. This strategy is performed by threshold pacing from the mapping catheter at a rate similar to the rate of the tachycardia. The paced surface 12-lead ECG is then compared with the clinical VT/PVC. The lowest possible stimulation voltage should be used to avoid far-field or anodal capture. Often, exact 12/12-lead pace-maps can be seen at sites within 4-5 mm of earliest activation.49 Careful scrutiny is needed when comparing the pace map with the clinical VT. Electrogram duration, amplitude, and notching should be inspected and ablation performed only at sites with a 12/12-lead match. Because RVOT PVC/VT origin is usually endocardial, catheter tip powers of 20-30 W are usually sufficient. With LVOT foci, the use of intracardiac echocardiography (ICE) along with 3-dimensional electroanatomic mapping allows better visualization of the LV/cusp anatomy and precise catheter tip positioning, and can help reduce the need for fluoroscopy, aortography, and coronary angiography (Fig 8). Most sites of origin of aortic cusp VT are at the base of the cusps, 142

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Fig 8. ICE of aortic cusps. The ICE image above shows the ablation catheter tip location at the junction of the right and left coronary cusps.

ⱖ1 cm below the coronary ostia, and can be visualized with ICE guidance in the longitudinal view of the LVOT.50 With aortic cusp VT, typically, a double-component electrogram is seen in sinus rhythm owing to late activation of this muscle bundle. This second component may become early during the clinical PVC or VT preceding QRS by 20-40 ms.48,49 As mentioned earlier in the text, activation mapping should be the primary technique for mapping PVCs/VT in the aortic root. Catheter ablation powers of 20-30 W are typically sufficient for ablation; however, higher powers may occasionally be needed for PVCs of deeper origin. Irrigated catheter ablation is recommended in the aortic root to avoid thrombus formation. William G. Stevenson. There has been a tendency to use actively irrigated ablation catheters for ablation in the left heart and aorta, as these catheters have a lower risk of thrombus formation. However, in high flow areas, such as the outflow regions, and using low power, this is not a significant concern, and many laboratories use solid tip electrodes that allow for better temperature monitoring.

Success rates for catheter ablation are estimated to be at least 90%-95% for RVOT-VT.51 Smaller case series have reported success rates of LVOT similar to those of RVOT-VT.25,29,50 Unsuccessful ablation may be due to (1) inability to induce the arrhythmia reliably, (2) a focus near Curr Probl Cardiol, April 2013

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a critical structure such as a coronary artery, or (3) an epicardial origin that cannot be easily accessed for ablation.48 Delivery of RF energy may lead to acceleration of the tachycardia or salvos of VT, termed “flurries,” but lack of such occurrence does not signify lack of success.52-54 Predictors of unsuccessful ablation include ⬎1 induced VT morphology, a delta wave–like onset of the QRS (potential epicardial foci), and a VT pace-map correlation ⬍11 of 12 leads.55 Complications of catheter ablation are similar to those of other ablation procedures and include vascular access complications, cardiac perforation, tamponade, stroke, and myocardial infarction due to embolus or coronary artery injury. ICE allows real-time imaging confirmation of anatomy with catheter tip positioning as well as the proximity of the catheter to left main coronary ostium. When the relationship of the catheter tip with the coronary artery is unclear or if the operator is not experienced with ICE, coronary angiography or aortography should be performed before coronary sinus or coronary cusp ablation. Ablation in the para-Hisian region of the ROVT should be performed cautiously to avoid AV block. Mapping from the right coronary cusp or use of cryoablation may be useful in these circumstances. Specific Ablation Considerations: Epicardial VT. Ablation of an epicardial VT focus may be performed through a subxiphoid approach or through the coronary venous system. We typically explore the coronary venous system first, as a subxiphoid epicardial approach is often limited by epicardial fat and the proximity to the coronary arteries. If a subxiphoid approach is chosen, the approach described by Sosa et al.56 for treating epicardial VT is used. As stated earlier in the text, before any ablation, coronary angiography must be performed to ensure that the tip of the ablation catheter is ⬎5 mm from an epicardial coronary.48,57 Epicardial cryoablation has also been described, and may be safer when in proximity to a coronary artery; however, coronary injury has been described with either approach.57 Ablation of an epicardial VT via the coronary venous system has been proven safe and effective.58-61 Typically, outflow tract arrhythmias are approached through the anterior interventricular vein. Coronary sinus venography can be helpful to outline the path and caliber of the anterior interventricular vein. Mapping with a smaller-caliber multipolar catheter may help. Coronary angiography must be performed before ablation, as the left anterior coronary artery is often in proximity to this vein.22 This is the major limitation of catheter ablation via the anterior interventricular vein. In circumstances when PVC activation time is equally early from the left coronary cusp and anterior interventricular vein, ablation should 144

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be attempted first from the left coronary cusp, as higher powers can often be delivered more safely. Predictors of success with ablation from the left cusp included a Q-wave ratio ⬍1.45 in aVL/aVR and a close anatomical distance of ⬍13.5 mm on fluoroscopy.62 William G. Stevenson. The location of the focus giving rise to idiopathic VT or PVCs is a critical determinant of success and the risk of the procedure. Because the location can often be predicted from the QRS morphology of the arrhythmia, this assessment is helpful in discussions of the risks and benefits of the procedure and deciding whether to pursue ablation. Patients should be informed that the focus may be found in a location that cannot safely be ablated, or in a location where the risks are somewhat greater than for the most common RVOT locations.

Fascicular VT Idiopathic left fascicular VT, or fascicular VT, arises from the fascicles of the left bundle branch. It can be further subclassified based on the ECG morphology and the corresponding fascicle involved: left posterior fascicular VT, left anterior fascicular VT, and left upper septal VT. Left posterior fascicle VT is the most common, followed by left anterior fascicle VT; left upper septal VT is rare.63-66 Fascicular VT is most commonly seen in young male individuals (⬎60%), between the ages of 15 and 40 years, and typically occurs at a younger age in female individuals.16 Fascicular VT is usually paroxysmal in nature and occurs with exertion. Symptoms consist primarily of palpitations; however, more serious presentations such as syncope or tachycardia-mediated cardiomyopathy may occur.67

History In 1979, Zipes et al.68 first described the diagnostic triad of a sustained right bundle branch block (RBBB) morphology, left axis VT induced by atrial pacing in patients without structural heart disease. The verapamilsensitive nature of the tachycardia was first described by Belhassen in 1981,69 and later a second morphology with right axis deviation was described by Ohe et al.70 Shortly thereafter, multiple case series described the idiopathic nature of the tachycardia in structurally normal hearts.63,64 In 1993, Nakagawa et al.71 successfully supported the hypothesis that the tachycardia originates from the Purkinje network of the left posterior fascicle by identifying the presystolic Purkinje potentials recorded during the VT, and that the successful site of ablation was recorded at the earliest of these potentials. Curr Probl Cardiol, April 2013

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Fig 9. Left posterior fascicle VT. The ECG tracing shows left posterior fascicle VT. There is an RBBB/left superior axis. Note the narrow QRS in the lateral and inferior leads, resulting commonly in an incorrect diagnosis of this VT as SVT.

Mechanism The mechanism of verapamil-sensitive left VT is reentry, as it can be induced, entrained, and terminated by ventricular or atrial stimulation.72 As mentioned earlier, Nakagawa recorded pre-QRS potentials thought to be Purkinje in origin from the inferior posterior septum, with successful termination of the tachycardia at the site of earliest potentials with RF ablation.71 Other theories include origination from a false tendon or fibromuscular band that extends in the posterior inferior LV to the basal septum, as this has been seen in large number of patients with fascicular VT.73-76 However, Lin et al.77 found a high percentage of false tendons in normal patients, calling into question the arrhythmogenic potential of these tendons. The proposed reentrant circuit consists of an area of slow conduction that forms the orthodromic limb in the LV septum from base to apex, with the retrograde limb using the Purkinje network.72,78-80

ECG Characteristics Fascicular VT has a characteristic ECG pattern most commonly demonstrating an RBBB/left superior axis pattern (Fig 9). It is relatively narrow and may be confused for supraventricular tachycardia using wide complex tachycardia diagnostic algorithms.81-83 Left posterior fascicle VT classically demonstrates an RBBB and left axis deviation (LAFB pattern), whereas left anterior fascicular VT demonstrates an RBBB and 146

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right axis deviation (LPFB pattern); septal VT demonstrates an incomplete RBBB (QRS duration, approximately 100-110 ms) and normal axis.

Management As with outflow tract tachycardia, the long-term prognosis in idiopathic fascicular VT is excellent. Tachycardia-mediated cardiomyopathy in patients with incessant tachycardia is rare, but has been described.84

Medical Therapy Medical therapy with intravenous verapamil is effective for acute termination. Chronic oral verapamil therapy is often an effective regimen for patients with symptoms who do not wish to pursue catheter ablation. ␤-adrenergic blockers have also been used with some success.

Catheter Ablation Catheter ablation is highly successful, with long-term cure estimated at ⬎90%.66,71,72 The presence of fascicular potentials preceding the QRS during PVCs/VT with F–F (fascicular potential–fascicular potential) interval driving the V–V (ventricular–ventricular) interval is important for confirming fascicular origin. Sites that demonstrate the earliest Purkinje potentials pre-QRS onset during VT are targeted for ablation. For posterior fascicular VT, this typically occurs in the posterior inferior LV septum. Ablation is usually directed at the mid-septum, at the site of earliest Purkinje potential during VT. High-dose isoproterenol is useful for provoking the arrhythmia; however, the inability to induce VT reliably may be an obstacle for successful ablation. Gentle catheter manipulation is critical to avoid mechanical suppression of the VT from “bumping” the circuit. In these circumstances, a ventricular echo beat during sinus rhythm or atrial pacing maybe useful.72 In cases in which no inducible tachycardia or echo beats are seen and a clear 12-lead ECG of fascicular VT has been documented, an empiric anatomic approach can be an effective strategy for ablation.85 RF energy ablation delivered in a linear manner along the mid-inferior septum and perpendicular to the plane of the posterior fascicle is safe and often effective. Because the fascicular system is subendocardial, ablation is typically achieved with low power; 20-30 W are often sufficient. Shifting of sinus rhythm QRS to a more rightward axis is occasionally seen after posterior fascicle ablation. Ablation of anterior fascicular VT is performed similarly, targeting the earliest anterior fascicular potential during VT at the anterior base of the LV. Catheter stability can often be challenging at this location. Curr Probl Cardiol, April 2013

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William G. Stevenson. This is an interesting VT that may be misdiagnosed as supraventricular tachycardia with aberrancy. The QRS morphology can be similar to some VTs that originate from the inferior papillary muscle, but in contrast to papillary muscle– origin VTs, this VT is almost always sustained, whereas papillary muscle arrhythmias are more commonly nonsustained. Although a portion of the reentry circuit involves antegrade conduction through the Purkinje system, the return path is more difficult to define, and is indicated by more rounded diastolic potentials that provide an alternative ablation target.79

Papillary Muscle VT In 2008, Doppalapudi et al. were the first to report idiopathic VT originating from the posterior papillary muscle of the LV in patients without underlying structural heart disease.86 Since then, others have shown VT originating from the anterior papillary muscle as well; however, a posterior papillary muscle origin is more common.22,30,87,88 Papillary muscle VT is usually exercise induced and is catecholamine sensitive, requiring isoproterenol or epinephrine for induction.22 The mechanism is typically focal in nature and not reentrant. This VT cannot be entrained, and has a lack of late potentials at the site of ablation.22 Papillary muscle VT often exhibits multiple QRS morphologies, with subtle changes seen spontaneously or during ablation. These subtle morphologic changes are thought to be from preferential conduction to different exit sites or multiple regions of origins within the complex structure of the papillary muscles.22 Successful catheter ablation usually requires irrigated ablation catheters, and ICE to visualize direct contact with the papillary muscle (Fig 10). Subtle ECG differences can help differentiate papillary muscle VT from fascicular VT. Papillary muscle VT, on average, has a wider QRS; it does not have Purkinje potentials preceding the QRS during VT; and if present, Purkinje potentials will be late in sinus rhythm compared with pre-QRS with fascicular VT. V1 morphology for posterior papillary muscle VT typically has a qR morphology or R compared with rsR’ for fascicular VT, and will notably have an absence of Q-waves in leads I and aVL.89

Annular VT Idiopathic monomorphic VT has been described originating from the mitral and tricuspid annulus. The incidence of each appears to be similar, with tricuspid annular accounting for 5%-8% of all idiopathic VT and mitral annular accounting for approximately 5%.90-92 148

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Fig 10. Papillary muscle VT ablation guided by ICE. The above ICE image shows the relationship between the tip of the ablation catheter and the posterior medial papillary muscle. ICE allows real-time visualization for catheter tip position and confirms contact between the tip of the ablation catheter and the posterior papillary muscle.

Mitral Annular VT Mitral annular VT (MAVT) can be classified by anatomic location. The majority originates from the anterior mitral annulus (in proximity to AMC), and less commonly posterior or posteroseptal annulus. The ECG in MAVT has an RBBB pattern and a monophasic R or Rs in leads V2-V6. Further ECG analysis can precisely distinguish among the different subtypes with polarity of the QRS complex in the inferior and lateral leads.90 In anterior MAVT, the polarity of the QRS complex is positive in the inferior leads and negative in leads I and aVL (Fig 11), in comparison with a negative polarity in the inferior leads and positive polarity in leads I and aVL in posterior or posteroseptal MAVT. The presence of a negative component in the QRS complex in leads I and V1 or a greater Q-wave amplitude ratio of lead III to lead II is useful for differentiating posteroseptal MAVT from posterior MAVT. Kumagi et al.93 described MAVTs with a delta wave–like beginning of the QRS complex. The R-wave transition occurred between V1 and V2 in all cases, and they described a 12-lead ECG algorithm for presumption of site of origin. Catheter ablation is highly successful with ablation delivered at the site of earliest ventricular activation or sites with a 12/12 pace-map match. In approximately 40% of patients, a discrete potential preceding the QRS complex was recorded during VT, preceding the surface QRS by as early Curr Probl Cardiol, April 2013

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Fig 11. Mitral annular VT/PVCs. The ECG tracing shows mitral annular PVCs. There is an RBBB/inferior axis, with a dominant R-wave seen in leads V1-V6. Note the inferior positive polarity. This was successfully terminated with ablation at the anterior mitral valve.

as 70 ms.48 Most cases may be successfully ablated via an endocardial approach, but ablation in the coronary venous system, specifically the great cardiac vein, has been described.60

Tricuspid Annular VT In 2 large series of idiopathic arrhythmias, origin from the tricuspid annulus was seen in 8% of all patients referred (including right- and left-sided VT)91 and approximately 5% of all patients with right-sided VT origin.92 Septal sites were more common than free-wall sites in the series reported by Tada (74%),91 and less common in the series presented by Van Herendael et al. (43%).92 Of the septal locations, the majority was anteroseptal or para-Hisian. The ECG shared many features with RVOTVT, with a few important distinctions. In all cases arising from the tricuspid annulus, an R or r pattern in lead I was recorded. A positive component (any r or R) was recorded in lead aVL in 95% of patients, and the overall polarity in aVL was positive in 89%. Among all tricuspid annular VTs, QRS duration and Q-wave amplitude in each of leads V1-V3 were greater in VT/PVCs arising from the free wall of the tricuspid annulus compared with the septum. Notching of the QRS complex was seen more often in free-wall sites, as well as later precordial transition. A Q-wave in lead V1 was observed more often in 150

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septal tricuspid annular VTs. In the Tada series,91 RF catheter ablation was successful more often for the free wall (90%) compared with the septal (57%) group. Low success rate in the septal tricuspid annular group was thought to be due to the likelihood of impairing AV nodal conduction with RF ablation. This is in contrast to 100% acute success rate in the Van Herendael series.92

Miscellaneous Origin Arrhythmias Arising from the Body of the Right Ventricle In recent years, there have been descriptions of idiopathic right ventricular arrhythmias arising from the body of the RV.91,92 Van Herendael et al.92 demonstrated that in a large series of patients (n ⫽ 278) presenting with idiopathic VT arising from the RV, 10% had VT/PVCs from the lower RV body. Of these, 48% were within 2 cm of the tricuspid annulus, 28% from the basal RV, and 24% from the apical RV. All but one from the basal and apical RV originated from the free wall. VT/PVC from the RV free wall had a longer QRS duration and deeper S-wave in lead V2/V3. Apical VT/PVC more often had precordial R-wave transition ⱖV6, smaller R-waves in lead II, and an S-wave in aVR. RF catheter ablation was acutely successful in 96% of patients. As previously discussed, exclusion of ARVC/D is often important for patients with VT origin from unusual sites or multiple PVC/VT origins.

Crux of the Heart Doppalapudi et al.94 described 4 cases among 340 patients referred for idiopathic VT originating from the crux of the heart. Anatomically, this area is an epicardial location near the junction of the middle cardiac vein and the coronary sinus. In all four patients, VT was sustained and was associated with syncope or presyncope. VT was induced with programmed stimulation or burst pacing from the RV, and often required isoproterenol. The ECG demonstrates a leftward superior axis QRS morphology with an early precordial transition and delayed intrinsicoid deflection. The earliest activation was present in the middle cardiac vein or proximal coronary sinus. Ablation from the coronary sinus or middle cardiac vein was attempted in all, but was successful in only one. Percutaneous epicardial ablation was attempted in two of the remaining three, and successfully abolished VT in both. Coronary angiography demonstrated the site of earliest activation within 5-10 mm of the proximal posterior descending artery. Curr Probl Cardiol, April 2013

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Summary Idiopathic VT refers to VT occurring in structurally normal hearts in the absence of myocardial scarring. Classification of monomorphic idiopathic VT includes outflow tract VT, fascicular VT, papillary muscle VT, annular VT, and miscellaneous (VT from the body of the RV and crux of the heart). It is commonly seen in young patients and usually has a benign course. The 12-lead electrocardiogram is critical in distinguishing the specific form and locations of idiopathic VT. Treatment options include medical therapy specific to the underlying mechanism of VT or catheter ablation. William G. Stevenson. Dr Hoffmayer and Dr Gerstenfeld provide an excellent summary of ventricular arrhythmias that are encountered in structurally normal hearts. Although the focus is on VT, for many of these arrhythmias, PVCs and nonsustained VT are more common. Sudden death is rare, but it is critical to exclude the presence of underlying heart disease. For outflow tract arrhythmias, the major concerns are arrhythmogenic RV cardiomyopathy and cardiac involvement with sarcoidosis. Any abnormality of the sinus rhythm ECG, such as T-wave inversions in the anterior precordium, or first-degree AV block warrants further evaluation for these diseases. Cardiac MRI can be helpful in this regard, but a normal MR study does not absolutely exclude a small region of scar from a myopathic process that may progress. PVCs that are closely coupled to the preceding QRS, interrupting the T-wave or runs of rapid VT that becomes polymorphic, are unusual and concerning for a risk of ventricular fibrillation and warrant review by an electrophysiologist. A family history of sudden death also warrants careful consideration, as there are an increasing number of genetic syndromes, both with and without structural heart disease, that warrant careful consideration. For those with no high-risk features, many require only reassurance and attention to removal of aggravating factors, such as caffeine and other stimulants, as are now commonly prescribed for adult attention deficit disorder. Some patients remain very symptomatic, and the arrhythmias can have a major impact on quality of life, requiring suppression with drugs or ablation as is nicely discussed in this review.

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