Ventricular Tachyarrhythmias in Normal Hearts Overview and Classification

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VT is usually associated with structural cardiac disease. The most common anatomic substrate of ventricular arrhythmias is chronic ischemic heart disease. Other structural disorders associated with VT are valvular and congenital heart disease, cardiac tumors, myocarditis, and cardiomyopathies. Only approximately 10% of arrhythmias occur in the absence of structural heart disease assessed by clinical examination and imaging studies. Some of them may be caused by inherited cardiac diseases such as catecholaminergic polymorphic VT syndrome, long QT syndrome, and the Brugada syndrome [13].

VT occurring in subjects without any clinically demonstrable underlying cardiac abnormality is referred to as "idiopathic" [2]. The clinical manifestations range from nonsustained, asymptomatic VT to sustained arrhythmias, which rarely can cause hemodynamic compromise and cardiac arrest. It can be classified with respect to the site of origin, the morphologic features (QRS configuration and axis), evidence for catecholamine-dependence, as well as the response to programmed stimulation and to pharmacological agents (adenosine, verapamil, and propranolol) [14].

Probably due to an embryological origin [15], that differs from the other heart structures, 90% of idiopathic VT originate from the RVOT, whereas 10% arise from the left (LVOT). As an alternative, defective sympathetic innervation of these regions may be the underlying substrate predisposing to enhanced arrhythmogenicity [16]. Somatic cell mutation in the RVOT leading to increased concentration of intracellular cAMP in response to beta-adrener-gic stimulation may also predispose to some forms of RVOT tachycardia [17].

Over the last two decades, the cellular mechanisms of idiopathic VT have been under investigation in experimental models and in humans. The potential electrophysiological mechanisms that have been proposed include triggered activity, re-entry, and abnormal automaticity.

According to current knowledge, idiopathic VT can be classified in three main categories based on cellular and electrophysiological mechanism (Table 12.1):

1. Adenosine-sensitive VT due to triggered activity

(delayed afterdepolarizations);

  1. Propranolol-sensitive (automatic);
  2. Verapamil-sensitive (due to intrafascicular re-entry).

Currently, the cellular mechanism of idiopathic tachycardias from RVOT and LVOT is thought to be cyclic AMP-mediated triggered activity that is dependent on delayed afterdepolarizations. These tachycardias are characterized by sensitivity to adenosine [18, 19]. The mechanism of idiopathic outflow tract VT may be explained by adrenergic mediated automaticity (propranolol-sensitive tachycardias) in only a small number of patients. In contrast, re-entry is the most common mechanism of ventricular arrhythmias in structural cardiac disorders (myocardial infarction, congenital heart disease, and cardiomyopathies including ARVC/D). The mechanism of verapamil-sensitive-fascicular-tachycardia seems to be re-entry involving the fascicles of the left bundle branch. Re-entry involving Purkinje tissue in or adjacent to a left ventricular false tendon has been also proposed. This arrhythmia originates from the LV and has a distinct RBBB morphology with left-axis configuration (suggesting exit site from the left posterior fascicle) or with right-axis configuration (exit site from the left anterior fascicle).

Although RVOT and LVOT are anatomically separate, they have an embryologic origin from a common solitary outflow tract (Fig. 12.1) [15]. The myocardium of the outflow tract has different properties as compared with the atrial or ventricular myocardium. Myocardial cells of the outflow tract are reminiscent of early development. The outflow tract has a lower rate of proliferation, a more "primitive" contractile phenotype (poorly developed sarcomeric and sarcoplasmic reticular structures, persistent expression of smooth muscle alpha-actin), and slower impulse conduction consistent with its role as a sphincter in the embryonic heart tube [20]. Based on these common features, it has been suggested that RVOT and LVOT arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias" [21]. There is a recent evidence that the pulmonary trunk can also give rise to VT, suggesting a common etiology of these tachycardias [22, 23]. Aortic cusp tachycardia and epicardial LV tachycardia are considered variants of outflow tract arrhythmias [24, 25].

Table 12.1 • Types of idiopathic ventricular tachycardia. Modified from [14]

Adenosine-sensitive (triggered activity)

Propranolol-sensitive (automatic)

Verapamil-sensitive (intrafascicular re-entry)


LBBB, inferior axis


RBBB, superior axis

RBBB, inferior axis

RBBB, polymorphic

RBBB, inferior axis

Clinical characteristics

RMVT; exercise-induced,


May be incessant






Intrafascicular, exit site:

left posterior fascicle,

left anterior fascicle

Drug response



Transient suppression

No effect








No effect




Enhanced automaticity


Triggered activity



Programmed stimulation


Programmed stimulation

+/- catecholamines

+/- catecholamines





EPS, electrophysiological study; LBBB, left bundle branch block; LVOT, left ventricula outflow tract; PA, pulmonary artery; RBBB, right bundle branch block; RMVT, repetitive monomorphic ventricular tachycardia; RVOT, right ventricular outflow tract

Fig. 12.1 • Embryological origin of the ventricles. In the tubular heart the atrioventricular canal and the outflow tract are separated by ventricular primordial, whereas in the formed heart they are connected. Left: embryonic heart tube. Right: the formed heart. oft, outflow tract (blue); RV, right ventricle (red); LV, left ventricle (green); avc, atrio-ventricular canal (yellow). Reproduced from [15]

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