Idiopathic Ventricular Tachycardia and Fibrillation

Idiopathic Ventricular Tachycardia and Fibrillation



Exercise-induced, adrenergically mediated right ventricular outflow tract (RVOT) VT serves as the mechanistic paradigm for outflow tract tachycardias. Its initiation by atrial and ventricular stimulation, facilitation by isoproterenol, and suppression by adenosine and propranolol suggest a focal mechanism dependent on catecholamine-sensitive, cAMP-mediated delayed afterdepolarizations and triggered activity.1,2 Isoproterenol (via beta receptor agonism and guanosine stimulatory proteins) activates adenyl cyclase, which promotes conversion of ATP to cAMP. This leads to a cascade of downstream events: protein kinase A phosphorylation of the L-type Ca+ channel, ryanodine receptor activation, and Ca+ release from the sarcoplasmic reticulum. Intracellular calcium overload (Ca+ induced Ca+ release and Ca+ sparks) induces delayed afterdepolarizations and triggered activity. VT can be suppressed by adenosine and vagal maneuvers (via A1 and M2 receptor agonism and guanosine inhibitory proteins) or beta blockers (via beta receptor antagonism)—all of which inhibit adenyl cyclase and cAMP formation or by L-type Ca+ channel blockers.


Right Ventricular Outflow Tract

In the embryologic heart, partitioning of the bulbus cordis and truncus arteriosus separates the pulmonary infundibulum (conus arteriosus), valve, and trunk from the aortic vestibule, valve, and aorta. Because of the spiral orientation of the aorticopulmonary septum, the RVOT wraps anteriorly and leftward around the aortic root (Fig. 19-1).3,4 Despite its name, therefore, the crescent-shaped RVOT is actually positioned leftward and anterior to the left ventricular outflow tract (LVOT). The most anterior portion of the outflow tract is the RVOT free wall, while the most leftward portion is the junction between the RVOT anteroseptum and free wall. The posteroseptum of the RVOT lies directly anterior to the right coronary cusp (RCC) of the aortic valve travelling anteriorly and leftward to meet the anteroseptum. The pulmonic valve sits anterior, leftward and 5-10 mm superior (cephalo-caudal separation) to the aortic valve. Underneath the pulmonary valve at the anteroseptum of the RVOT is the most common site for VT. VT can also arise above the valves from the pulmonary sinus cusps because of myocardial sleeves extending superiorly into the valve leaflets. The left pulmonary cusp is the most inferior, while the right and anterior cusps are situated more superiorly. The left atrial appendage is close to the anterior pulmonary artery and a possible source of far-field left atrial electrograms.

Left Ventricular Outflow Tract

The centrally positioned aortic valve sits posterior, rightward, and inferior to the pulmonic valve and whose cusp also contain arrhythmogenic myocardial sleeves. The posterior or noncoronary cusp (NCC) of the aortic valve is the most posterior leaflet; abuts the right and left atrium; and is a potential source of atrial

tachycardia (AT), accessory pathways, and only rarely VT. The commissure between the NCC/RCC lies opposite the commissure separating the septal/anterior leaflets of the tricuspid valve where the membranous portion of the interventricular septum and penetrating His bundle are located—the latter being recorded beneath the aortic valve. Both the RCC and left coronary cusp (LCC) are anterior to the NCC and potential sources of VT. The RCC directly abuts the posteroseptum of the pulmonary infundibulum posteriorly beneath the pulmonic valve. Close proximity of the right atrial appendage to the RCC can give rise to far-field atrial electrograms at this site. The LCC is posterior, leftward, and superior to the RCC and abuts the pulmonary trunk above the pulmonary valve, and therefore, the left main coronary artery travels close to the posterior pulmonary trunk. VT can also arise from the aortic vestibule beneath the valve. The aorto-mitral continuity (region between the LCC/NCC commissure and anterior leaflet of the mitral valve) is generally devoid of myocardial tissue but when present can be a source of accessory pathways and VT. The posterior-superior process of the LV or “AV septum” is the region where the right atrium abuts the LV (because of the apical displacement of the tricuspid valve relative to the mitral valve).

FIGURE 19-1 Anatomy of the outflow tracts. The RVOT wraps around the aortic root. Its free wall is the most anterior structure producing VT with a late (≥V4) precordial QRS transition. The RVOT septum sits posterior to the free wall generating VT with an earlier (V3) precordial transition. Note that the RVOT anteroseptum is the most leftward structure so that VT arising from this site is negative in lead I. Travelling more posteriorly, the RCC sits behind the RVOT posteroseptum followed by the LCC and AMC resulting in VT with progressive earlier (≤V2) precordial transition.

The epicardial region of the LVOT is the LV summit and a potential source of VT. The great cardiac vein (GCV) travels epicardially near the LCC at the base of the heart, crosses the left circumflex (LCx) coronary artery, and runs alongside the left anterior descending (LAD) coronary artery to become the anterior interventricular vein. (The intersection of the GCV, LCx, and LAD forms the triangle of Brocq and Mouchet.5)



RVOT ectopy can present with different levels of arrhythmia expression (isolated PVCs, salvos of nonsustained VT, or sustained VT) that can be considered a continuum of a single mechanism (cAMP-mediated triggered activity).6 The characteristic electrocardiographic features of RVOT tachycardia include 1) left bundle branch block (LBBB) morphology and 2) inferior axis (Figs. 19-2 and 19-3). Electrocardiographic clues to identify the RVOT VT site of origin are its 1) precordial QRS transition, 2) frontal axis (particularly, QRS vector in lead I), 3) QRS width, and 4) presence/absence of notching in the inferior leads.7,8,9,10,11,12 Because the RVOT free wall is the most anterior part of the outflow tract, RVOT free wall VT shows 1) LBBB morphology with possibly an absent r wave in V1 (because V1 is an anteriorly and rightward-directed vector) and late (at or beyond V4) precordial transition; 2) short, broad QRS complexes (because of sequential right ventricular [RV] to LV activation); and 3) notching in the inferior leads. RVOT septal VT shows 1) LBBB morphology, which may show a small r wave in V1 (because the RV septum is posterior to the free wall) and earlier (V3) precordial transition; 2) narrower QRS complexes (because of simultaneous RV/LV activation); and 3) tall, smooth QRS contours. A common site for RVOT VT is the anteroseptum just beneath the pulmonic valve at its junction with the free wall—the most leftward part of the outflow tract. At this site, QRS complexes in lead I (a horizontally leftward-directed vector) are therefore negative. As the VT origin moves from anterior (left) to posterior (right) either along the septum or the free wall, lead I QRS complexes transition from negative to positive.7 Similar to aortic sinus cusps, the pulmonary sinus cusps have also been identified as an important source of RVOT VT.13,14 Mapping within the pulmonary cusps might require a supportive long sheath with a reverse U-shaped curve of the ablation tip by prolapsing it retrogradely across the pulmonic valve from the RV. A trileaflet view of the pulmonary valve from the right atrial appendage allows delineation of the three pulmonary cusps that might facilitate VT localization (see Fig. 3-19). VT arising from the pulmonary artery have higher inferior R wave amplitudes and greater aVL/aVR Q wave ratios than their subvalvular RVOT counterpart because of the more superior and leftward location of the pulmonary artery.15,16,17


From anterior to posterior, outflow tract sites for VT include 1) RV free wall, 2) RV posteroseptum, 3) RCC, 4) LCC, and 5) aorto-mitral continuity (region between the LCC/NCC commissure and anterior leaflet of the mitral valve). The RCC directly abuts the posteroseptum of the RVOT, and therefore, PVCs arising from these two sites are difficult to differentiate by ECG (LBBB morphology, V3 precordial lead transition).18,19,20 By using the normally conducted QRS complex to control for influences of cardiac rotation on precordial transition, the V2 transition ratio (V2 r/rs [VT]/V2 r/rs [NSR]) is one method to differential left- from right-sided outflow tract VT. A V2 transition ratio >0.6 suggests LVOT origin.18


Early (≤V2) precordial transition with inferior axis indicates LVOT origin.21,22,23,24,25,26,27,28,29,30,31,32,33,34,35 The absence/presence of an s wave in V5 or V6 might differentiate a supravalvular/subvalvular site, respectively.24,32 Site-specific QRS morphologies include 1) RCC: LBBB morphology with small, broad r wave in V2; 2) RCC-LCC commissure: LBBB QS (notching on the downstroke) or qrS morphology; 3) LCC: V1 M or W pattern with precordial transition ≤V2; and 4) AMC: V1 qR pattern (Figs. 19-4 and 19-5).25 (These ECG signatures, however, are based on pacemapping techniques, which have inherent limitations [preferential conduction within the LVOT, far-field capture] in reproducing true VT morphologies.) For RCC-LCC commissure VT, the V1 qrS complex represents initial posterior activation of the aortic root and LVOT (q wave) followed by anterior activation of the interventricular septum and RVOT (r wave) and then late activation of the LV (S wave).27,32 For AMC VT, V1 morphologies can transition from anterior AMC (rS [broad r] or qR) to mid-AMC (prominent R wave)—the latter showing positive concordance except for a large S wave in V2 (“rebound transition”).35 Rarely, VT can arise from the NCC.36 Epicardial VTs are broader and show slurring of the initial portion of the QRS complex (pseudo delta wave) with maximal deflection index (onset of r wave to nadir of S wave in any precordial lead/total QRS duration >55%) or a precordial break pattern (V2 R wave less than V1 and V3 R wave).37,38

FIGURE 19-2 RVOT PVCs. All manifest LBBB morphology. The RVOT anteroseptal (AS) PVC shows a tall/smooth contour with V3-V4 transition and right inferior axis (negative QRS in lead I). The RVOT posteroseptal (PS) PVC shows a tall/smooth contour with V2-V3 transition and left inferior axis (positive QRS in lead I). The RVOT free wall (FW) PVC shows a short/broad contour with inferior notching and V5 transition. An r wave in V1 is absent.

FIGURE 19-3 RVOT VT. Both manifest LBBB morphology. RVOT anteroseptal (AS) VT shows a tall/smooth contour, V2-V3 transition, and right inferior axis (negative QRS in lead I). RVOT free wall (FW) VT shows broad QRS complexes with inferior notching and V4 transition.

FIGURE 19-4 LVOT PVCs. The RCC PVC shows an LBBB morphology but broad r wave in V2. The RCC-LCC PVC has a distinctive V1 QS complex with notching on its downstroke. The LCC PVC shows a “W” type pattern. The AMC PVC manifests RBBB morphology with positive precordial concordance except for a “rebound transition” pattern (S wave in V2 but not V1 or V3).

FIGURE 19-5 Different RBBB PVCs. The AMC PVC shows a V1 qR pattern with positive precordial concordance except for a “rebound transition” pattern (small S wave in V2). The posteroseptal (PS) mitral valve (MV) PVC shows V1 rSR′ morphology and left superior axis. The posteromedial papillary muscle (PMP) PVCs are interpolated and show atypical qR pattern and left superior axis.


When mapping and ablation is performed in the RVOT, it is important to be aware that the wall of the RVOT is thin and the left main coronary artery runs close to the posterior pulmonary trunk above the pulmonary valve. Because of the close anatomic proximity of the RVOT posteroseptum and RCC, the ECG morphology of VT arising from these two sites is similar and differentiating RVOT versus LVOT site of origin can be difficult. The following suggest an LVOT origin: PVC onset − RV apex electrogram (QRS − RVA) ≥49 ms, diffuse breakout pattern along the RVOT posteroseptum, and only transient VT suppression with ablation along the RVOT posteroseptum.39 The small, confined space of the LVOT and aortic cusps can make catheter manipulation and torqueing relatively difficult, while their close proximity to sensitive structures (His bundle and coronary artery ostium [˜1.5 cm above the nadir of the cusps]) makes ablation in this region potentially dangerous. A properly positioned His bundle catheter provides the location of both the penetrating His bundle and aortic root. The location of the coronary artery ostia should be identified prior to ablation (aortic root or selective coronary artery angiography or intracardiac echocardiography [ICE] imaging), and radiofrequency (RF) delivery should be avoided within 5 mm of the coronary artery.

Activation Mapping

The focal origin of tachycardia allows activation mapping by identifying the earliest site of near-field bipolar ventricular activation (near-field earliest electrogram determination) and/or local unipolar “QS” configuration relative to PVC onset (RVOT: Figs. 19-6, 19-7, 19-8, 19-9 and 19-10; LVOT: Figs. 19-11, 19-12, 19-13, 19-14, 19-15, 19-16, 19-17, 19-18, 19-19, 19-20 and 19-21). Successful electrograms often precede QRS onset by 30-50 ms, although there is no degree of electrogram prematurity predictive of success.11,12 For supravalvular VT (aortic cusps, pulmonary artery), two-component electrograms can be seen: sharp “spike” potentials (near-field) followed by low-frequency ventricular electrogram (far-field) preceding VT QRS complexes with their reversal (far-field/near-field) during sinus rhythm (analogous to pulmonary vein sleeve potentials) (Figs. 19-8, 19-9, 19-12, and 19-13).15,16 With PA mapping, a far-field atrial electrogram (left atrial appendage) can be recorded.

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Oct 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Idiopathic Ventricular Tachycardia and Fibrillation
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