In the next installment of the EP 101 series, author Dr. Liem discusses the mechanisms and management of ventricular tachycardia (VT).

Mechanism of Ventricular Tachycardia
       Ventricular tachycardia is, in general, considered to be a “malignant” arrhythmia, as it is most commonly found in a diseased heart and is associated with increased cardiovascular mortality. The typical setting is a patient with prior myocardial infarction (MI) or other forms of cardiomyopathy (CM). The most common mechanism for VT is reentry; a diseased ventricular myocardium provides the key elements for reentry, namely conduction and repolarization disparity, opportunity for unidirectional block, and the prevalence of premature ventricular complexes (PVCs) as the initiator. This type of VT can readily “degenerate” into ventricular fibrillation (VF), which almost always results into sudden death. The propensity for VT-to-VF degeneration is greatly influenced by the degree of left ventricular (LV) dysfunction. Patients with significant LV dysfunction (in general, those with left ventricular ejection fraction [LVEF] of < 35%) cannot tolerate any type of tachycardia and tend to suffer from hypotension caused by significantly reduced cardiac output, which in turn activates a significant increase in cathecolamine response.
       In a subset of patients with LV dysfunction from cardiomyopathy, the reentry is through specialized bundle branches. This VT is called bundle branch reentry VT (BBR-VT). This distinction is important, because BBR-VT is curable with catheter ablation (usually of the right bundle branch). However, depending on the severity of underlying LV function, these patients may also benefit from primary sudden death prevention (see below).
       There are several other types of VT. One type that is less common than the typical reentry kind mentioned above is the so-called “idiopathic” VT. The term idiopathic denotes the lack of an obvious cause for the arrhythmia. The VT is present in healthy myocardium or ventricles with minimal abnormalities. Idiopathic VT is believed to be caused by one or two other arrhythmia mechanism(s), namely automaticity and/or triggered activity. This distinction in mechanism is important to keep in mind, as both automaticity and triggered activity events are more likely to self-terminate than reentry events. Furthermore, the absence of underlying structural heart disease provides a different hemodynamic milieu when compared to a diseased ventricular myocardium with a significant LV dysfunction. This type of VT rarely degenerates into VF.
       There is also a subset of patients with no structural heart disease but who are still at risk for sudden death. These patients have an inherent electrical instability despite the absence of underlying myocardial damage. These two conditions are called long QT syndrome and Brugada syndrome. Both syndromes involve abnormality in repolarization, either from potassium-channel defect, sodium-channel defect, or both. Typically there is a family history of sudden death at a very young age (less than 40 years old). In these patients, the presenting (or induced) arrhythmia is typically polymorphic VT rapidly degenerating into VF.

Management of Ventricular Tachycardia
       With a better understanding of VT mechanism, the management can be tailored to the specific pathophysiology. The advent of medical technology has provided significant improvement in the approach and success in this field of medicine. The obvious advancement is the implantable cardioverter-defibrillator (ICD). At its inception, this treatment method was not well-received, because it was not aimed at correcting or preventing the VT itself. Nonetheless, it was later shown to be the most effective form of treatment in preventing the real threat of VT, namely premature sudden death from cardiac arrest. Hence, ICD is now considered the treatment of choice for the subset of patients at risk for sudden death, namely those with significant LV dysfunction (LVEF < 35%).^1,2 In fact, the ICD is indicated in such patients, even before having a VT episode (primary prevention). This topic will be discussed in other issues of EP Lab Digest.

Electrophysiology Study
       The electrophysiology study (EPS) as a diagnostic tool is, in general, not required for the decision to implant an ICD in patients who qualify for the device, because the requirement criteria include mainly the degree of LV dysfunction and the absence of reversible cause for the arrhythmia. However, diagnostic EPS in these patients is still useful for identifying other arrhythmias that may co-exist and potentially complicate general ICD programming, and for assessing the rate of VT for accurate programming of the ICD detection zones. EPS is indicated in patients with mild LV dysfunction (those with LVEF > 35%), if VT is suspected to be the cause for syncope. EPS is also performed in preparation of catheter ablation. VT ablation is indicated in patients with frequent episodes of VT. ICD therapy alone in such a patient, while effective in preventing sudden death, can be detrimental to the quality of life, because repeated syncope or pre-syncope cannot be prevented and repeated shocks frequently occur.
       The protocol for a VT study is quite simple.³ The basic principle is to reproduce the clinical scenario that would promote reentry. Thus, pacing is performed, usually from two sites in the right ventricle (right ventricular apex [RVA], and right ventricular outflow tract [RVOT]), at two “drive cycle lengths (CL)” of 600 ms and 400 ms for 8–10 beats, followed by one, two, or three “extra-stimuli (ES)” with increasing degrees of prematurity until refractoriness is encountered. This type of “programmed electrical stimulus (PES)” is a well-accepted method for induction of any type of reentry arrhythmia as the premature beats are expected to create slower conduction and unidirectional block promoting the initiation of such arrhythmia. Caution should be exercised to avoid “too aggressive” pacing protocol, as very rapid pacing (CL of < 300 ms) and extreme degree of extra-stimulus prematurity (< 180 ms) can cause the induction of VF. The induction of VF in EPS is considered of low specificity and is clinically less significant than the induction of monomorphic VT. However, very rapid monomorphic VT can rapidly degenerate into polymorphic VT and VF, and if it occurs at relative ease (such as using only double extra-stimuli or less), it may be clinically significant.
       In patients undergoing VT ablation, the VT is usually inducible with just a single extra-stimulus. What is important in this setting is to maintain stability of blood pressure during prolonged episodes of VT, which is necessary for mapping of VT “focus,” In the event the induced VT is too rapid, intravenous procainamide can be administered (at 10 mg/kg body weight). VT ablation will also be discussed in a separate issue.
       For induction of “idiopathic” VT, PES is usually performed using burst pacing. This type of pacing is more suitable for triggered-activity mechanism. Rapid pacing at a fixed DCL is performed for 15–20 beats at a starting CL of 350 ms, and repeated with each burst at shorter CL, down to a CL of 250 ms, again to avoid induction of VF. Idiopathic VT can also be induced using isoproterenol infusion alone or with burst pacing.
       The pacing protocol for patients with long QT or Brugada syndrome is not yet uniform. More important than the pacing protocol is the identification of repolarization abnormality. Long QT syndrome would present with a markedly long QT interval (usually > 500 ms) and abnormal T-U wave morphology. The VT is usually already present and documented clinically, with the twisting morphology known as Torsade de Pointes (TdP). Thus, EPS is frequently not necessary. Clinical presentation and family history are more important. Brugada syndrome manifests as slightly delayed depolarization (rSr’) typically on ECG leads V1-V3 and ST elevation on those leads as well. The abnormality can be unmasked by placing the ECG electrodes of those leads one intercostal space higher, or by administering a sodium-channel blocker. This is best performed in the EP laboratory, as PES can then be applied for VT induction. The induced VT is typically also polymorphic.

Summary
       A ventricular tachycardia study in the EP laboratory is rarely performed nowadays, as ICD therapy is considered the mainstay of therapy as secondary and primary prevention of sudden death. VT study is usually performed for VT ablation preparation. VT ablation is performed for both reentry VT and idiopathic VT. VT study is also performed for patients with primary electrical disease such as Brugada syndrome.