**3. Diagnosis of IVAs**

#### **3.1. Imaging**

IVAs are defined as VAs originating from normal ventricular myocardium. Therefore, any association of myocardial scar with an occurrence of VAs has to be excluded for a diagnosis of IVAs. Echocardiography and exercise stress testing are basic examinations to demonstrate no evidence of SHD. However, IVAs can occur in patients with SHD. If VAs originate away from the myocardial scar, they are considered idiopathic. Therefore, an imaging study such as echocardiography, nuclear test, or cardiac magnetic resonance imaging (cMRI) should be performed to locate the site of the scar in patients with SHD. Frequent IVAs can cause tachycardia-induced cardiomyopathy. When evidence of myocardial scar is excluded by a nuclear test or cMRI despite a reduced LV function, tachycardia-induced cardiomyopathy is likely to be present. A definite diagnosis of tachycardia-induced cardiomyopathy can be made when the LV function recovers after the IVAs are well treated by medication or catheter ablation.

#### **3.2. Electrocardiogram**

IVAs usually originate from specific anatomical structures and exhibit characteristic electrocardiograms (ECGs) based on their anatomical background. In general, the first clue in 12-lead surface electrocardiograms for predicting a site of an IVA origin is a bundle branch block pattern in lead V1. A right bundle branch block (RBBB) pattern clearly suggests an origin in the LV, whereas a left bundle branch block (LBBB) pattern suggests an origin in the RV or the interventricular septum. Second, an inferior axis (dominant R waves in leads II, III, and aVF) suggests an origin in the superior aspect of the ventricle, whereas a superior axis suggests an origin in the inferior aspect. A negative QRS polarity in lead I suggests an origin in the LV free wall [2, 9], and a QS pattern in lead V6 suggests an origin near the apex (**Figures 4**, **8**, and **9**) [2, 21]. An R/S wave amplitude ratio of >1 in lead V6 suggests an origin in the base (ventricular outflow tract or annuli), whereas an R/S wave amplitude ratio of <1 suggests an origin in the middle of the ventricle (papillary muscles or left fascicles) (**Figures 4**, **8**, and **9**) [2, 21]. Twelve-lead ECGs are very helpful for predicting the likely epicardial VT origins (**Figures 10** and **11**). Because in human hearts, the Purkinje network that can quickly facilitate ventricular activation throughout the ventricles is located only in the subendocardium, ventricular activation from the epicardial origin requires more time to reach the Purkinje network, resulting in a slow onset of the QRS during epicardial VTs. Based on this mechanism, several parameters predicting epicardial VT origins have been proposed: a "pseudo-delta" wave duration of >34 ms, a QRS duration of >200 ms, a delayed intrinsicoid deflection of >85 ms, an RS complex duration of >121 ms, and a maximum deflection index (MDI) (calculated by dividing the shortest time from the QRS onset to the maximum deflection in any of the precordial leads by the total QRS duration) of >0.54 (**Figure 10**) [33, 34]. When ventricular activation propagates from an epicardial origin at the LV free wall or ventricular posterior wall, the total activation vector should go from a lateral toward medial or from an inferior toward superior direction, resulting in a QS pattern in lead I or lead aVF (**Figure 11**) [32]. On the other hand, when ventricular activation propagates from an

epicardial VAs such as the crux of the heart [30] and LV summit [31]. Anatomically, the crux of the heart is formed by the junction of the atrioventricular groove and the posterior interventricular groove and corresponds roughly to the junction of the middle cardiac vein and coronary sinus, near the origin of the posterior descending coronary artery (**Figure 6**) [30]. A region of the LV epicardial surface that occupies the most superior portion of the LV has been termed the LV summit by McAlpine (**Figure 7**) [11, 31]. The LV summit is bounded by the left anterior descending coronary artery and the left circumflex coronary artery. This region near where the great cardiac vein (GCV) ends and the anterior interventricular cardiac vein begins is one of the major sources of epicardial IVAs. The LV summit is bisected by the GCV into an area lateral to this structure that is accessible to epicardial catheter ablation (the *accessible area*) and a superior region that is inaccessible to catheter ablation due to the close proximity of the coronary arteries and a thick layer of epicardial fat that overlies the proximal portion of these vessels (the *inaccessible area*) [31]. The prevalence of LV summit VAs has been reported to account for 12% of idiopathic LV VAs. Among these VA origins, 70, 15, and 15% of them have

been identified within the GCV, accessible area, and inaccessible area, respectively.

IVAs are defined as VAs originating from normal ventricular myocardium. Therefore, any association of myocardial scar with an occurrence of VAs has to be excluded for a diagnosis of IVAs. Echocardiography and exercise stress testing are basic examinations to demonstrate no evidence of SHD. However, IVAs can occur in patients with SHD. If VAs originate away from the myocardial scar, they are considered idiopathic. Therefore, an imaging study such as echocardiography, nuclear test, or cardiac magnetic resonance imaging (cMRI) should be performed to locate the site of the scar in patients with SHD. Frequent IVAs can cause tachycardia-induced cardiomyopathy. When evidence of myocardial scar is excluded by a nuclear test or cMRI despite a reduced LV function, tachycardia-induced cardiomyopathy is likely to be present. A definite diagnosis of tachycardia-induced cardiomyopathy can be made when the LV function recovers after the IVAs are well treated by medication or catheter ablation.

IVAs usually originate from specific anatomical structures and exhibit characteristic electrocardiograms (ECGs) based on their anatomical background. In general, the first clue in 12-lead surface electrocardiograms for predicting a site of an IVA origin is a bundle branch block pattern in lead V1. A right bundle branch block (RBBB) pattern clearly suggests an origin in the LV, whereas a left bundle branch block (LBBB) pattern suggests an origin in the RV or the interventricular septum. Second, an inferior axis (dominant R waves in leads II, III, and aVF) suggests an origin in the superior aspect of the ventricle, whereas a superior axis suggests an origin in the inferior aspect. A negative QRS polarity in lead I suggests an origin in the LV free wall [2, 9], and a QS pattern in lead V6 suggests an origin near the apex

**3. Diagnosis of IVAs**

**3.2. Electrocardiogram**

**3.1. Imaging**

86 Cardiac Arrhythmias

**Figure 8.** Representative 12-lead electrocardiograms of the QRS complexes during ventricular arrhythmias originating from the anterolateral region in the LV. APM, anterolateral papillary muscle; L, lateral portion; LAF, the left anterior fascicle; MA, mitral annulus; X-F, R, VAs with a focal or a macroreentrant mechanism. This figure was reproduced from Ref. [21] with permission.

**Figure 9.** Representative 12-lead electrocardiograms of the QRS complexes during ventricular arrhythmias originating from the posteroseptal region in the LV. LPF, the left posterior fascicle; MA, mitral annulus; P, posterior portion; PPM, posteromedial papillary muscle; X-F, R, VAs with a focal or a macroreentrant mechanism. This figure was reproduced from Ref. [21] with permission.

endocardial origin on the LV free wall or ventricular posterior wall, a part of the activation vector should go toward the lateral or the inferior direction, which reflects the activation conducting through the wall of the ventricular muscle toward the epicardium, resulting in the presence of an initial R wave in lead I or lead aVF (**Figure 11**). Therefore, a QS pattern in lead I or aVF suggests an epicardial origin in the LV free wall [10] or the ventricular posterior wall, respectively (**Figure 11**). All these ECG features are more accurate without SHD than with it, because without any scar tissue associated with SHD, the ventricular activation propagates away from VA origins through normal ventricular myocardium in a predictable manner. IVAs originating from the RVOT and LVOT exhibit similar ECG characteristics because anatomically, the RVOT and LVOT are located next to each other (**Figure 3**). The ECGs of idiopathic outflow tract VAs are characterized by positive R waves in all inferior leads and deep S waves in both leads aVR and aVL (almost QS pattern) (**Figures 12**–**14**). An RBBB QRS morphology clearly suggests a VA origin on the left side. However, when idiopathic outflow tract VAs exhibit an LBBB QRS morphology, it is often difficult to differentiate RVOT VAs from LVOT VAs. Because anatomically, the LVOT is located posterior to the RVOT (**Figure 3**), LVOT VAs exhibit taller and wider R waves in leads V1 and V2 than RVOT VAs. Therefore, the precordial transition is helpful for differentiating RVOT VAs from LVOT VAs. When the precordial transition is later than lead V4, the VAs are very likely to originate from the RVOT, and when the precordial transition is earlier than lead V2, the VAs are very likely to originate from the LVOT. However, when the precordial transition is in lead V3, it is most difficult to differentiate RVOT VAs from LVOT VAs. Although multiple ECG algorithms to differentiate RVOT VAs from LVOT VAs have been proposed, two ECG algorithms may be recommended, the magnitude and width of the R wave or QRS complex in leads V1 and V2

**Figure 11.** Schema showing the mechanism to explain the difference in the QRS morphology in lead aVF during ventricular tachycardias with endocardial (left) and epicardial (right) foci. Inf, inferior; L, left; R, right; Sup, superior.

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This figure was cited from Ref. [32] with permission.

**Figure 10.** Twelve-lead electrocardiograms exhibiting a ventricular arrhythmia originating from the LV summit and the measurement of the maximal deflection index (MDI). This figure was cited from Ref. [3] with permission.

**Figure 11.** Schema showing the mechanism to explain the difference in the QRS morphology in lead aVF during ventricular tachycardias with endocardial (left) and epicardial (right) foci. Inf, inferior; L, left; R, right; Sup, superior. This figure was cited from Ref. [32] with permission.

endocardial origin on the LV free wall or ventricular posterior wall, a part of the activation vector should go toward the lateral or the inferior direction, which reflects the activation conducting through the wall of the ventricular muscle toward the epicardium, resulting in the presence of an initial R wave in lead I or lead aVF (**Figure 11**). Therefore, a QS pattern in lead I or aVF suggests an epicardial origin in the LV free wall [10] or the ventricular posterior wall, respectively (**Figure 11**). All these ECG features are more accurate without SHD than with it, because without any scar tissue associated with SHD, the ventricular activation propagates away from VA origins through normal ventricular myocardium in a predictable manner.

IVAs originating from the RVOT and LVOT exhibit similar ECG characteristics because anatomically, the RVOT and LVOT are located next to each other (**Figure 3**). The ECGs of idiopathic outflow tract VAs are characterized by positive R waves in all inferior leads and deep S waves in both leads aVR and aVL (almost QS pattern) (**Figures 12**–**14**). An RBBB QRS morphology clearly suggests a VA origin on the left side. However, when idiopathic outflow tract VAs exhibit an LBBB QRS morphology, it is often difficult to differentiate RVOT VAs from LVOT VAs. Because anatomically, the LVOT is located posterior to the RVOT (**Figure 3**), LVOT VAs exhibit taller and wider R waves in leads V1 and V2 than RVOT VAs. Therefore, the precordial transition is helpful for differentiating RVOT VAs from LVOT VAs. When the precordial transition is later than lead V4, the VAs are very likely to originate from the RVOT, and when the precordial transition is earlier than lead V2, the VAs are very likely to originate from the LVOT. However, when the precordial transition is in lead V3, it is most difficult to differentiate RVOT VAs from LVOT VAs. Although multiple ECG algorithms to differentiate RVOT VAs from LVOT VAs have been proposed, two ECG algorithms may be recommended, the magnitude and width of the R wave or QRS complex in leads V1 and V2

**Figure 10.** Twelve-lead electrocardiograms exhibiting a ventricular arrhythmia originating from the LV summit and the

**Figure 9.** Representative 12-lead electrocardiograms of the QRS complexes during ventricular arrhythmias originating from the posteroseptal region in the LV. LPF, the left posterior fascicle; MA, mitral annulus; P, posterior portion; PPM, posteromedial papillary muscle; X-F, R, VAs with a focal or a macroreentrant mechanism. This figure was reproduced

from Ref. [21] with permission.

88 Cardiac Arrhythmias

measurement of the maximal deflection index (MDI). This figure was cited from Ref. [3] with permission.

and at the L-RCC rarely exhibit an RBBB pattern, and IVAs that can be ablated within the NCC always exhibit an LBBB pattern. The R-wave amplitude ratio in leads III–II (III/II ratio) is useful for differentiating LCC VAs from RCC VAs. When the III/II ratio is >0.9, VAs are more likely to be ablated within the LCC. A qrS pattern in the right precordial leads may be highly specific for an L-RCC VA origin (**Figure 14**) [13]. The ECG characteristics of NCC VAs are similar to those of RCC VAs (**Figure 14**) [14]. However, an S wave in lead III is present during NCC VAs although it is not during RCC VAs. When the III/II ratio is <0.65, VAs are more likely

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All MA VAs exhibit an RBBB pattern and monophasic R or Rs in leads V2–V6 (**Figure 15**) [9, 10]. Because the origins of all MA VAs are located in the posterior portion of the LV, which is distant from the precordial electrodes, the activation from the MA VA origins propagates toward these electrodes, resulting in an early precordial transition and a concordant positive QRS pattern in leads V2–V4 during MA VAs. The ECG characteristics are very helpful for predicting sites of MA VA origins [9, 10]. The polarity of the QRS complex in the inferior and lateral leads (I and aVL) is positive and negative in anterolateral MA VAs, while it is negative

**Figure 13.** Representative 12-lead electrocardiograms of VAs originating from the ventricular outflow tract. The first beat is a sinus beat and the second is a premature ventricular contraction in each panel (A–F). The S-wave amplitude in lead V2, R-wave amplitude in lead V3, and V2S/V3R index are listed below each panel. All right ventricular outflow tract (RVOT) PVCs exhibited a V2S/V3R index of >1.5, while all left ventricular outflow tract (LVOT) PVCs exhibited a V2S/ V3R index of ≤1.5. The PVCs were successfully ablated in the RVOT septum (A and B), RVOT free wall (C), left coronary cusp (D), right coronary cusp (E), and aorto-mitral continuity (F). The other abbreviation is as in the previous figure. This

to be ablated from within the NCC.

figure was cited from Ref. [35] with permission.

**Figure 12.** Examples of an electrocardiographic analysis of ventricular arrhythmias. The first beats are sinus and the second beats are ventricular arrhythmias originating from the left coronary cusp (LCC) and the right ventricular outflow tract (RVOT). **A** indicates the total QRS duration, **B** the longer R-wave duration in lead V1 or V2, determined in lead V2 from the QRS onset to the R-wave intersection point where the R-wave crosses the isoelectric line, **C** the R-wave amplitude, measured from the peak to the isoelectric line, and **D** the S-wave amplitude measured from the QRS nadir to the isoelectric line. The R/S wave amplitude ratio in lead V2 (C′/D′) is greater than that in lead V1 (C/D), and C′/D′ is determined as the R/S wave amplitude index. The R/S amplitude index is less than 0.3 and the R-wave duration index (B/A) less than 0.5 during RVOT VAs, whereas they are not during LCC VAs. This figure was cited from Ref. [6] with permission.

(R/S wave amplitude and duration indexes) [8] (**Figure 12**) and V2S/V3R amplitude ratio [35] (**Figure 13**), because they can simply and accurately perform a diagnosis by an ECG of VA only. The R/S wave amplitude in leads V1 and V2 is measured as the amplitude of the QRS complex peak or nadir to the isoelectric line. The R/S wave amplitude index, calculated from the percentage of the R/S wave amplitude ratio in lead V1 or V2 (whichever is greater), is considered more useful than the R/S wave amplitude ratio alone in lead V1 or V2. The R-wave duration index is calculated by dividing the longer R-wave duration in lead V1 or V2 by the QRS complex duration. An R/S amplitude index of <0.3 and an R-wave duration index of <0.5 may strongly suggest a VA origin on the right side (**Figure 13**) [8]. The V2S/V3R amplitude ratio is calculated by dividing the amplitude of the S wave in lead V2 by that of R wave in lead V3. A V2S/V3R amplitude ratio of ≤1.5 can predict LVOT VA origins and that of >1.5 RVOT VA origins (**Figure 13**) [35]. This ECG algorithm is useful even when the precordial transition is observed in lead V3 and has been proven to be the most accurate among the previous ECG algorithms to differentiate RVOT VA origins from LVOT VA origins.

Although the three ASCs are located next to each other, IVAs that can be ablated within each ASC may be differentiated by ECGs (**Figure 14**) [7]. IVAs that can be ablated within the RCC and at the L-RCC rarely exhibit an RBBB pattern, and IVAs that can be ablated within the NCC always exhibit an LBBB pattern. The R-wave amplitude ratio in leads III–II (III/II ratio) is useful for differentiating LCC VAs from RCC VAs. When the III/II ratio is >0.9, VAs are more likely to be ablated within the LCC. A qrS pattern in the right precordial leads may be highly specific for an L-RCC VA origin (**Figure 14**) [13]. The ECG characteristics of NCC VAs are similar to those of RCC VAs (**Figure 14**) [14]. However, an S wave in lead III is present during NCC VAs although it is not during RCC VAs. When the III/II ratio is <0.65, VAs are more likely to be ablated from within the NCC.

All MA VAs exhibit an RBBB pattern and monophasic R or Rs in leads V2–V6 (**Figure 15**) [9, 10]. Because the origins of all MA VAs are located in the posterior portion of the LV, which is distant from the precordial electrodes, the activation from the MA VA origins propagates toward these electrodes, resulting in an early precordial transition and a concordant positive QRS pattern in leads V2–V4 during MA VAs. The ECG characteristics are very helpful for predicting sites of MA VA origins [9, 10]. The polarity of the QRS complex in the inferior and lateral leads (I and aVL) is positive and negative in anterolateral MA VAs, while it is negative

(R/S wave amplitude and duration indexes) [8] (**Figure 12**) and V2S/V3R amplitude ratio [35] (**Figure 13**), because they can simply and accurately perform a diagnosis by an ECG of VA only. The R/S wave amplitude in leads V1 and V2 is measured as the amplitude of the QRS complex peak or nadir to the isoelectric line. The R/S wave amplitude index, calculated from the percentage of the R/S wave amplitude ratio in lead V1 or V2 (whichever is greater), is considered more useful than the R/S wave amplitude ratio alone in lead V1 or V2. The R-wave duration index is calculated by dividing the longer R-wave duration in lead V1 or V2 by the QRS complex duration. An R/S amplitude index of <0.3 and an R-wave duration index of <0.5 may strongly suggest a VA origin on the right side (**Figure 13**) [8]. The V2S/V3R amplitude ratio is calculated by dividing the amplitude of the S wave in lead V2 by that of R wave in lead V3. A V2S/V3R amplitude ratio of ≤1.5 can predict LVOT VA origins and that of >1.5 RVOT VA origins (**Figure 13**) [35]. This ECG algorithm is useful even when the precordial transition is observed in lead V3 and has been proven to be the most accurate among the previous ECG

**Figure 12.** Examples of an electrocardiographic analysis of ventricular arrhythmias. The first beats are sinus and the second beats are ventricular arrhythmias originating from the left coronary cusp (LCC) and the right ventricular outflow tract (RVOT). **A** indicates the total QRS duration, **B** the longer R-wave duration in lead V1 or V2, determined in lead V2 from the QRS onset to the R-wave intersection point where the R-wave crosses the isoelectric line, **C** the R-wave amplitude, measured from the peak to the isoelectric line, and **D** the S-wave amplitude measured from the QRS nadir to the isoelectric line. The R/S wave amplitude ratio in lead V2 (C′/D′) is greater than that in lead V1 (C/D), and C′/D′ is determined as the R/S wave amplitude index. The R/S amplitude index is less than 0.3 and the R-wave duration index (B/A) less than 0.5 during RVOT VAs, whereas they are not during LCC VAs. This figure was cited from Ref. [6] with

Although the three ASCs are located next to each other, IVAs that can be ablated within each ASC may be differentiated by ECGs (**Figure 14**) [7]. IVAs that can be ablated within the RCC

algorithms to differentiate RVOT VA origins from LVOT VA origins.

permission.

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**Figure 13.** Representative 12-lead electrocardiograms of VAs originating from the ventricular outflow tract. The first beat is a sinus beat and the second is a premature ventricular contraction in each panel (A–F). The S-wave amplitude in lead V2, R-wave amplitude in lead V3, and V2S/V3R index are listed below each panel. All right ventricular outflow tract (RVOT) PVCs exhibited a V2S/V3R index of >1.5, while all left ventricular outflow tract (LVOT) PVCs exhibited a V2S/ V3R index of ≤1.5. The PVCs were successfully ablated in the RVOT septum (A and B), RVOT free wall (C), left coronary cusp (D), right coronary cusp (E), and aorto-mitral continuity (F). The other abbreviation is as in the previous figure. This figure was cited from Ref. [35] with permission.

**Figure 14.** Two-dimensional CT images and representative 12-lead electrocardiograms of ventricular arrhythmias originating from the aortic root. L, left coronary cusp; N, noncoronary cusp; R, right coronary cusp. The other abbreviations are as in the previous figures. This figure was cited from Ref. [7] with permission.

waves in lead V1, and the presence of notching in the inferior leads (the timing of the second peak of the notched QRS complex in the inferior leads corresponds precisely with the LV free wall activation) (**Figure 16**). A negative QRS polarity in the inferior leads predicts VA origins in the posterior aspect of the TA, and otherwise, VA origins in the mid- to anterior aspects of

**Figure 15.** Representative 12-lead electrocardiograms of the premature ventricular contractions originating from the anterolateral (a), posterior (b), and posteroseptal (c) aspects of the mitral annulus. The arrows indicate "notching" of the

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late phase of the QRS complex in the inferior leads. This figure was cited from Ref. [10] with permission.

IVAs originating from the anterolateral and posteromedial PAMs in the LV exhibit RBBB and right inferior and left or right superior axis QRS morphologies, respectively (**Figures 8** and **9**) [18–21]. IVAs originating from the posterior or anterior RV PAMs more often exhibit a superior axis with a late precordial transition (>lead V4) as compared with septal RV PAM VAs, which more often exhibit an inferior axis with an earlier precordial transition (≤lead V4) [22]. Because of the close anatomical relationship, it is important to distinguish PAM VAs from MA VAs and LV fascicular VAs by ECGs (**Figures 8** and **9**) [21]. The ECG features such as an rS in lead I, an rS in lead aVR (for only the LV anterolateral region), a qR in lead aVL, a Q in lead V1, an S wave amplitude ratio in leads III to II <1.5, and an R/S ratio of ≤1 in lead V6 (the last two parameters are for only the LV posteroseptal region) can accurately distinguish MA VAs from PAM and LV fascicular VAs [21]. However, the ECG features are very similar for PAM and LV fascicular VAs, and an R/S ratio of ≤1 in lead V6 in the LV anterolateral region and a QRS duration of >160 ms, and qR or R waves in lead V1 (as compared with an rsR' for fascicular VTs) in the LV posteroseptal region may be the only reliable predictors for differentiating

the TA are suggested.

PAM VAs from LV fascicular VAs [21].

and positive in posterior and posterolateral MA VAs, respectively. MA VAs originating from the free wall of the MA are characterized by a longer QRS duration sometimes with pseudodelta waves and notching in the late phase of the R or Q wave in the inferior leads, which may result from phased excitation from the LV free wall to the RV (**Figure 15**). Posterior MA VAs exhibit a dominant R wave in lead V1, whereas posteroseptal MA VAs exhibit a negative QRS component in lead V1 (qR, qr, rs, rS, or QS).

All TA VAs exhibit an LBBB QRS morphology and positive QRS polarity in leads I, V5, and V6 (**Figure 16**) [17] because the TA VA origins are located on the right anterior side of the heart, and the activation propagating from TA VA origins toward the apex generates a positive QRS polarity in leads V5 and V6. The R wave in lead I is usually taller during TA VAs than during RVOT VAs because the TA is located more rightward and inferior to the RVOT. For the same reason, a positive QRS polarity in all of the inferior leads is rare in TA VAs but common in all RVOT VAs. During TA VAs, a QS or an rS pattern in lead aVL is rare, and the QRS polarity in lead aVL is positive in almost all TA VAs, which is not the case for RVOT VAs. Among all TA VAs, the QRS duration and Q wave amplitude in each of the leads V1–V3 are greater in TA VAs originating from the free wall of the TA than in those from the septal wall of the TA [17]. Septal TA VAs exhibit an early precordial transition (lead V3), a narrower QRS duration, and QS in lead V1 with the absence of notching in the inferior leads while the free wall TA VAs are associated with a late precordial transition (>lead V3), a wider QRS duration, the absence of Q

#### Idiopathic Ventricular Arrhythmias http://dx.doi.org/10.5772/intechopen.77186 93

**Figure 15.** Representative 12-lead electrocardiograms of the premature ventricular contractions originating from the anterolateral (a), posterior (b), and posteroseptal (c) aspects of the mitral annulus. The arrows indicate "notching" of the late phase of the QRS complex in the inferior leads. This figure was cited from Ref. [10] with permission.

waves in lead V1, and the presence of notching in the inferior leads (the timing of the second peak of the notched QRS complex in the inferior leads corresponds precisely with the LV free wall activation) (**Figure 16**). A negative QRS polarity in the inferior leads predicts VA origins in the posterior aspect of the TA, and otherwise, VA origins in the mid- to anterior aspects of the TA are suggested.

and positive in posterior and posterolateral MA VAs, respectively. MA VAs originating from the free wall of the MA are characterized by a longer QRS duration sometimes with pseudodelta waves and notching in the late phase of the R or Q wave in the inferior leads, which may result from phased excitation from the LV free wall to the RV (**Figure 15**). Posterior MA VAs exhibit a dominant R wave in lead V1, whereas posteroseptal MA VAs exhibit a negative QRS

**Figure 14.** Two-dimensional CT images and representative 12-lead electrocardiograms of ventricular arrhythmias originating from the aortic root. L, left coronary cusp; N, noncoronary cusp; R, right coronary cusp. The other

abbreviations are as in the previous figures. This figure was cited from Ref. [7] with permission.

All TA VAs exhibit an LBBB QRS morphology and positive QRS polarity in leads I, V5, and V6 (**Figure 16**) [17] because the TA VA origins are located on the right anterior side of the heart, and the activation propagating from TA VA origins toward the apex generates a positive QRS polarity in leads V5 and V6. The R wave in lead I is usually taller during TA VAs than during RVOT VAs because the TA is located more rightward and inferior to the RVOT. For the same reason, a positive QRS polarity in all of the inferior leads is rare in TA VAs but common in all RVOT VAs. During TA VAs, a QS or an rS pattern in lead aVL is rare, and the QRS polarity in lead aVL is positive in almost all TA VAs, which is not the case for RVOT VAs. Among all TA VAs, the QRS duration and Q wave amplitude in each of the leads V1–V3 are greater in TA VAs originating from the free wall of the TA than in those from the septal wall of the TA [17]. Septal TA VAs exhibit an early precordial transition (lead V3), a narrower QRS duration, and QS in lead V1 with the absence of notching in the inferior leads while the free wall TA VAs are associated with a late precordial transition (>lead V3), a wider QRS duration, the absence of Q

component in lead V1 (qR, qr, rs, rS, or QS).

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IVAs originating from the anterolateral and posteromedial PAMs in the LV exhibit RBBB and right inferior and left or right superior axis QRS morphologies, respectively (**Figures 8** and **9**) [18–21]. IVAs originating from the posterior or anterior RV PAMs more often exhibit a superior axis with a late precordial transition (>lead V4) as compared with septal RV PAM VAs, which more often exhibit an inferior axis with an earlier precordial transition (≤lead V4) [22].

Because of the close anatomical relationship, it is important to distinguish PAM VAs from MA VAs and LV fascicular VAs by ECGs (**Figures 8** and **9**) [21]. The ECG features such as an rS in lead I, an rS in lead aVR (for only the LV anterolateral region), a qR in lead aVL, a Q in lead V1, an S wave amplitude ratio in leads III to II <1.5, and an R/S ratio of ≤1 in lead V6 (the last two parameters are for only the LV posteroseptal region) can accurately distinguish MA VAs from PAM and LV fascicular VAs [21]. However, the ECG features are very similar for PAM and LV fascicular VAs, and an R/S ratio of ≤1 in lead V6 in the LV anterolateral region and a QRS duration of >160 ms, and qR or R waves in lead V1 (as compared with an rsR' for fascicular VTs) in the LV posteroseptal region may be the only reliable predictors for differentiating PAM VAs from LV fascicular VAs [21].

preferential conduction, and the presence of intramural VA origins, it is challenging to predict where LVOT VAs can be ablated among those three sites by an ECG algorithm [28, 29].

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Treatment of IVAs should be tailored according to the presentation type of VAs, PVCs, or VTs, and the patient characteristics (**Figure 17**) [4, 5]. When SHD is absent, the most common indication for treating PVCs remains the presence of symptoms. The severity of the symptoms from PVCs is not closely related to the frequency of PVCs. Even when the PVCs are infrequent, some patients are very symptomatic. When PVCs are not frequent, the physician has to explain and reassure that there is a benign nature of idiopathic PVCs. It is a common experience that symptoms from PVCs can improve without any treatment in most patients with infrequent PVCs. Exercise stress testing should be considered to determine whether PVCs are potentiated or suppressed by exercise, to assess whether longer duration VAs are provoked especially when symptoms are associated with exercise. PVCs that worsen with exercise should prompt further investigation as these patients are more likely to require treatment. Frequent asymptomatic PVCs may have to be treated if PVC-induced cardiomyopathy

**Figure 17.** Schema exhibiting the management of premature ventricular contractions (PVCs). (a) Absence of a high-scar burden suggests reversibility; (b) medical therapy + implantable cardioverter-defibrillator. CRT, cardiac resynchronization therapy; LV, left ventricular; MRI-DE, magnetic resonance imaging with delayed enhancement; PE, physical examination; Rx, therapy; SHD, structural heart disease; VAs, ventricular arrhythmias. This figure was cited

**4. Treatment of IVAs**

from Ref. [5] with permission.

**Figure 16.** Representative 12-lead electrocardiograms of the premature ventricular contractions originating from the posterolateral (a), anterior (b), and anteroseptal (c) aspects of the tricuspid annulus. The arrows indicate "notching" of the late phase of the QRS complex in the limb leads. This figure was cited from Ref. [10] with permission.

IVAs arising from the MB exhibit a distinctive ECG morphology, LBBB and left superior axis QRS morphology, a sharp downstroke of the QRS in the precordial leads, and a relatively narrow QRS duration (**Figure 4**) [23]. MB VAs not only have a late precordial transition pattern, typically after lead V4, but also the transition is always later than that of the sinus QRS. Among the idiopathic RV VAs, a late precordial transition and a superiorly directed nature are helpful for distinguishing MB VAs from VAs originating from the RV base or septum [23]. The ECG characteristics of the IVAs originating from the infundibular muscles are similar to those of IVAs originating from the RVOT and the anterior to anteroseptal aspect of the TA [24, 25]. However, the precordial transition is relatively early, and a slow onset of the QRS complex is often observed.

IVAs arising from the crux of the heart exhibit a left superior axis QRS morphology with deeply negative deltoid waves (QS pattern) in the inferior leads and an early precordial transition (a prominent R wave in lead V2), which may be associated with a polarity reversal between leads V1 and V2 (**Figure 6**) [30]. It is noted that crux VAs often exhibit a QS or a large S wave in lead V6 although they arise from the LV base. This is likely because the activation from the crux VA origins first conducts to the ventricular apex where it enters the Purkinje system and then propagates throughout the ventricles. The common ECG characteristics of LV summit VAs are a right inferior axis QRS morphology, a wider QRS, and a larger MDI than the other idiopathic LVOT VAs [31]. The MDI [34] of these epicardial IVAs is usually >0.55. The AMC and LV summit face each other with the superior end of the LV muscle between them, which is attached to the LCC. Because of the anatomical proximity, the presence of preferential conduction, and the presence of intramural VA origins, it is challenging to predict where LVOT VAs can be ablated among those three sites by an ECG algorithm [28, 29].
