**4. Treatment of IVAs**

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

**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 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

QRS complex is often observed.

94 Cardiac Arrhythmias

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 from Ref. [5] with permission.

is present. When a PVC burden is greater than 10% (approximately 10,000 PVCs/24 h), the risk of PVC-induced cardiomyopathy is significant. Therefore, such high-burdened PVCs have to be treated when they are symptomatic. When they are asymptomatic, a close follow-up with repeat echocardiography and Holter monitoring should be considered to detect any occurrence of PVC-induced cardiomyopathy. In patients with fewer PVCs, further investigation is only necessary should the symptoms increase. For patients without SHD and mild symptoms, education of the benign nature of this arrhythmia and reassurance should be considered as the first step in the treatment of patients with PVCs. For patients whose symptoms are not effectively managed in this manner, beta-blockers or non-dihydropyridine calcium antagonists may be attempted although the efficacy of these agents is quite limited with only 10–15% of patients achieving a 90% PVC suppression, similar to placebo [4, 5]. It should also be recognized that these agents may themselves produce significant side effects rather than relieve the PVC symptoms. Membrane-active anti-arrhythmic drugs (AADs) are more effective for suppressing PVCs and can be attempted when beta-blockers or non-dihydropyridine calcium antagonists are not effective. Because these agents may increase the risk of mortality in patients with significant SHD, perhaps with the exception of amiodarone, caution is advised before using them for PVC suppression.

muscles and respond to beta-blockers or catheter ablation with a relatively low success rate [4, 5, 18–21]. Reentrant LV fascicular VTs usually present as a sustained form and can be acutely treated with intravenous verapamil or mexiletine. Oral therapy with these medicines can be used to prevent recurrence of those VTs, although the recurrence risk may be relatively high [4, 5, 26, 27]. Catheter ablation can be recommended when idiopathic VTs are highly

Idiopathic Ventricular Arrhythmias

97

http://dx.doi.org/10.5772/intechopen.77186

Catheter ablation of IVAs is usually safe and highly successful, but sometimes can be challenging because of the anatomical obstacles such as close proximity to the coronary arteries and AV conduction system, epicardial fat pads, intramural and epicardial origins, and thick muscle bands. Understanding the relevant anatomy is helpful for achieving a safe and suc-

The sites of IVA origins have been increasingly recognized for the past two decades. IVAs usually originate from specific anatomical structures, commonly endocardial but sometimes epicardial, and exhibit characteristic ECGs based on their anatomical background. IVAs are basically benign, but they require medical treatment or catheter ablation when IVAs are symp-

symptomatic and drug-refractory, especially if they are exercise-induced [1, 4, 5].

cessful catheter ablation of IVAs.

tomatic, incessant, or produce LV dysfunction.

The author declares no conflicts of interest.

Address all correspondence to: takumi-y@fb4.so-net.ne.jp

cardias. Nature Reviews. Cardiology. 2012;**9**:512-525

Division of Cardiovascular Disease, University of Alabama at Birmingham,

[1] Stevenson WG, Soejima K. Catheter ablation for ventricular tachycardia. Circulation.

[2] Yamada T, Kay GN. Optimal ablation strategies for different types of ventricular tachy-

**5. Conclusions**

**Conflict of interest**

**Author details**

Takumi Yamada

**References**

Birmingham, AL, USA

2007;**115**:2750-2760

When idiopathic PVCs are refractory to medication or patients cannot tolerate medication, catheter ablation can be a next option for their treatment. Randomized trials of PVC suppression with catheter ablation have not been performed. However, multiple studies have revealed that catheter ablation is highly successful with PVC elimination in 74–100% of highly symptomatic patients with a very high PVC burden [4, 5]. Procedural success may be dependent on the site of the VA origin with a lower efficacy reported for IVAs with epicardial foci and anatomical challenges than for other IVAs [1–5]. Although complete PVC elimination is the goal of ablation, partial success with a significant reduction in the PVC burden may still be associated with significant improvement in the symptoms as well as LV systolic function. Catheter ablation of IVAs may be less successful when multiple morphologies of PVCs present or the clinical PVC morphology cannot be induced at the time of the procedure [1–5]. The published complication rates of catheter ablation for PVC suppression are generally low (<1%) [1–5]. According to the current recommendations of the experts' consensus, catheter ablation of PVCs may be considered for highly selected patients who remain very symptomatic despite conservative treatment or for those with high PVC burdens associated with a decline in the LV systolic function [4, 5].

Idiopathic VTs are basically monomorphic and hemodynamically stable. When SHD is absent, sustained idiopathic VTs are generally associated with an excellent prognosis [1, 4, 5]. Idiopathic VTs rarely can have a malignant clinical course, usually with a very rapid rate or a short initiating coupling interval [1, 4, 5]. Idiopathic non-sustained VTs (NSVTs) usually present with frequent PVCs with the same QRS morphology, and most of them originate from the RVOT or LVOT. These arrhythmias only require treatment if they are symptomatic, incessant, or produce LV dysfunction. The treatment of these VTs is either medical with beta-blockers, non-hydropyridine calcium blockers, or class IC drugs, or catheter ablation with a high success rate and low risk of complications [1, 4, 5]. Non-sustained and sustained VTs with a focal mechanism likely based on abnormal automaticity may also occur from the papillary muscles and respond to beta-blockers or catheter ablation with a relatively low success rate [4, 5, 18–21]. Reentrant LV fascicular VTs usually present as a sustained form and can be acutely treated with intravenous verapamil or mexiletine. Oral therapy with these medicines can be used to prevent recurrence of those VTs, although the recurrence risk may be relatively high [4, 5, 26, 27]. Catheter ablation can be recommended when idiopathic VTs are highly symptomatic and drug-refractory, especially if they are exercise-induced [1, 4, 5].

Catheter ablation of IVAs is usually safe and highly successful, but sometimes can be challenging because of the anatomical obstacles such as close proximity to the coronary arteries and AV conduction system, epicardial fat pads, intramural and epicardial origins, and thick muscle bands. Understanding the relevant anatomy is helpful for achieving a safe and successful catheter ablation of IVAs.
