EP 101: Ventricular Tachycardia

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 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 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 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.