Jose L. Baez-Escudero, MD, FHRS and Miguel Valderr´bano, MD

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.

6. What electrocardiogram (ECG) features favor VT as the cause of a wide complex tachycardia?

    VT rhythms have rates between 100 and 280 beats/min and can be monomorphic or polymorphic. Typical ECG clues that favor VT include the following:

7. What is torsade de pointes?

    Torsade de pointes, or torsades, is a French term that literally means “twisting of the points.” It was first described by Dessertenne in 1966 and refers to a polymorphic intermediate ventricular rhythm between VT and ventricular fibrillation. It has a distinct morphology in which cycles of tachycardia with alternating peaks of QRS amplitude turn about the isoelectric line in a regular pattern (Fig. 36-3). Before the rhythm is triggered, a baseline prolonged QT interval and pathologic U waves are present, reflecting abnormal ventricular repolarization. A short-long-short sequence between the R-R interval (marked bradycardia or preceding pause) occurs before the trigger response. Drugs that prolong the QT (e.g., antiarrhythmics, some antibiotics and antifungals, and tricyclic antidepressants) and electrolyte disorders such as hypokalemia and hypomagnesemia are common triggers. When the ECG finding occurs, it should be treated as any life-threatening VT, and immediate efforts must be made to determine the underlying cause of QT lengthening.

8. What critical decisions must be made in the management of sustained VT?

    The critical decision in the management of a patient with sustained VT is the urgency with which to treat the rhythm. In a hemodynamically stable and minimally symptomatic patient, treatment should be delayed until a 12-lead ECG can be obtained. The axis and morphology help to make the diagnosis of VT, as well as shed light on the potential mechanism and origin of the rhythm. During the delay, a brief medical history and baseline laboratory values can be obtained (especially serum levels of potassium and magnesium, as well as cardiac biomarkers). Specific attention should be paid to a history of myocardial infarction, systolic heart failure, history of structural heart disease, family history of sudden cardiac death, and potentially proarrhythmic drugs.

9. What methods are used to terminate sustained VT?

    With any question of hemodynamic instability, termination should be done immediately with synchronized direct current electrical cardioversion. Hemodynamic instability is defined as hypotension resulting in shock, congestive heart failure, myocardial ischemia (infarction or angina), or signs or symptoms of inadequate cerebral perfusion. It is important to ensure that the energy is delivered in a synchronized fashion before cardioversion. Failure to do so may accelerate the rhythm or induce ventricular fibrillation. If the patient is conscious, adequate intravenous (IV) sedation should always be provided. Termination of hemodynamically stable VT may be attempted medically. Reasonable drugs of choice are IV procainamide (or ajmaline in some European countries), lidocaine, and IV amiodarone. For ischemic monomorphic VT, intravenous lidocaine is also a reasonable option. Pace termination (either through transvenous insertion of a temporary pacer or by reprogramming an implantable cardioverter-defibrillator [ICD]) can be useful to treat patients with sustained monomorphic VT that is refractory to cardioversion or is recurrent despite the use of the above-mentioned drugs. If VT is associated with acute ischemia, urgent angiography and revascularization are paramount.

10. Once the acute episode is terminated, what are the next managing strategies?

    This depends on the clinical situation and on the individual patient. Any potentially reversible cause—specifically, ischemia, heart failure, or electrolyte abnormalities—should be sought and treated aggressively. In general, beta-adrenergic blocking agents (β-blockers) are usually safe and effective and should be administered in most patients in whom concomitant antiarrhythmic drugs are indicated. Amiodarone and sotalol have been the mainstay of preventive therapy, especially in patients with left ventricle (LV) dysfunction. However, the long-term clinical success of medical regimens is low, and amiodarone carries a risk of serious side effects. All patients should be risk stratified for the likelihood of recurrence and subsequent risk of sudden cardiac death. Appropriate consultation with an electrophysiologist should be obtained to assess the need for ICD implantation (indications for ICDs are discussed in Chapter 38). Although cardiac device therapy has revolutionized treatment, providing excellent protection from sudden cardiac death, it does not prevent recurrences. Patients with defibrillators may remain symptomatic, with palpitations, syncope, and recurrent shocks for VT. Ablation of the reentrant circuits that cause VT also provides a nonpharmacologic option for the reduction of symptoms.

11. How is catheter ablation of VT performed?

    VT ablation remains challenging and is offered primarily at experienced centers. Endocardial mapping of VT to identify an optimal region for ablation can be time-consuming because of the complexity of the reentry circuits and the existence of certain circuit portions deep within the endocardium. Most ventricular reentry circuits have an exit somewhere along the border zone of the infarct scars. It is near such an exit that sinus rhythm pacing (pace mapping) is expected to produce a QRS morphology similar to that of VT. This approach, combined with modern three-dimensional voltage-mapping technologies that reconstruct and relate electrophysiologic characteristics to specific anatomy, have greatly facilitated the ablation procedure. Ablation can be achieved using traditional radiofrequency, or with other technologies, such as cryoablation or laser. When endocardial circuits are resistant to ablation, the technique of transthoracic pericardial access with epicardial mapping of VT is used. This approach facilitates localization and ablation of deep and epicardial circuits and requires the insertion of a sheath into the pericardial space, using a needle and guidewire under fluoroscopic control. If a separate indication for heart surgery is present (e.g., need for surgical revascularization, LV aneurysmectomy, mitral valve repair or replacement), surgical ablation may be considered.

12. When is catheter ablation used to treat VT?

    Ablation has traditionally been used for secondary prevention after an ICD-terminated VT and as an alternative to chronic antiarrhythmic therapy. It may also be considered as an option for reducing ICD therapies in patients with recurrent appropriate shocks and as an alternative to drug therapy for idiopathic VT. The probability of success varies, depending on an individual’s substrate for the arrhythmia. A patient with a VT arising from the right ventricular outflow tract in a structurally normal heart will have a much higher likelihood of success when compared with a patient with a severely reduced ejection fraction from a large anterior wall MI with multiple VT morphologies. The target endpoint of any VT ablation is always lack of inducible VT.

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