Ventricular Tachycardia

Published on 15/05/2015 by admin

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Chapter 36

Ventricular Tachycardia

1. What is the differential diagnosis of a wide complex tachycardia (WCT)?

    The differential includes the following:

Of note, a wide-QRS tachycardia should always be presumed to be VT if the diagnosis is unclear. VT is defined as three or more consecutive QRS complexes arising from the ventricles. Sustained VT is that which causes symptoms or lasts more than 30 seconds.

2. What is the pathophysiologic substrate of VT?

    It depends on the clinical scenario, but the most common mechanism is reentry, followed by automaticity.

3. What is the most common underlying heart disease predisposing to VT?

    The most common conditions predisposing to VT are coronary artery disease and coronary ischemia. VT in the setting of acute ischemia and immediately after myocardial infarction (MI) is related to excess ventricular ectopy as a result of increased automaticity (Na+,K+-ATPase malfunction, increase in intracellular calcium, tissue acidosis, and locally released catecholamines). After completion of an infarct, patients with resultant ischemic cardiomyopathy can suffer from recurrent sustained monomorphic VT. In this case, VT originates in scarred myocardium where islands of infarcted tissue surrounded by strands of functional myocytes provide the substrate for the creation of a reentrant circuit.

4. Can VT occur in other nonischemic heart diseases?

    Scar-related VT can occur in other nonischemic conditions whenever an inflammatory or infiltrative disorder damages the myocardium. Sarcoidosis or Chagas disease are typical examples in which VT can occur as a result of such nonischemic scars. Fatty infiltration of the right ventricle leads to areas of unexcitable myocardium that can generate reentrant circuits in patients with arrhythmogenic right ventricular dysplasia. Myocardial scars leading to reentry also occur after surgical correction of congenital heart diseases. Dilated cardiomyopathies can lead to reentry within the diseased conduction system, the so-called bundle-branch reentry, where impulses use the right and left bundles as antegrade and retrograde pathways (less commonly in the opposite direction). Conceivably, any structural heart disease can lead to reentry.

5. Can VT occur in the absence of structural heart disease?

    VT can occur in the structurally normal heart. Monomorphic VT occurs in two distinct clinical entities in the absence of heart disease. One is outflow tract VT. This condition leads to VT typically during or after exercise or in enhanced catecholamine states. It is thought to be generated by triggered activity in the form of delayed after-depolarizations, typically created in situations of calcium overload. It originates most commonly from the right ventricular outflow tract but occasionally can arise from the left ventricular outflow tract and even the aortic cusps. The second condition is idiopathic fascicular VT (also known as verapamil-sensitive or Belhassen VT). It typically occurs in young, healthy individuals with normal hearts, and most commonly involves a right bundle branch block (RBBB) and left anterior fascicular block pattern, because it arises from the left posterior fascicle. Both these forms are curable with mapping and ablation.

    Primary electrical disorders can also lead to VT. Familial long QT syndromes typically lead to torsades des pointes, as does short QT syndrome. Brugada syndrome leads to primary ventricular fibrillation (Fig. 36-2). Catecholaminergic polymorphic ventricular tachycardia (CPVT) is the result of a mutation of the ryanodine receptor and typically causes exercise-induced bidirectional and polymorphic VT.

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