Ventricular Tachycardia (VT) is an A-list celebrity in the arrhythmia world! When I began my involvement with EP, two cases convinced me it was worth continuing with. The first was seeing ablation of an accessory pathway but the most impressive was termination of incessant VT by ablation.
VT is a term used to describe a rapid rhythm (>100 b.p.m) originated in the ventricles (distal to the bundle of His) and lasting at least 3 beats or more. VT attracts attention because it can be life threatening and indeed it is the initiating arrhythmia in the majority of cases of sudden cardiac death (SCD). However, the risk to the patient is strongly related to the presence and degree of ventricular dysfunction (and to an extent the rate of the tachycardia) and in patients without structural heart disease VT has a much more benign prognosis.
If the rhythm lasts for >30 seconds it is described as sustained VT. The rhythm can be regular or irregular and the QRS shape (it’s morphology) can be stable or continually changing. A stable morphology is described as monomorphic VT and changing complexes as polymorphic VT. This article is about monomorphic VT.
VT is a broad complex tachycardia. The QRS complexes are broad because the impulse, which originates in ventricular muscle, spreads slowly through the tissue from myocyte to myocyte rather than being distributed rapidly by cells of the specialised conduction system. A broad QRS complex can sometimes occur during supra ventricular tachycardias (SVTs) due to bundle branch block or the presence of an anterogradely conducting accessory pathway. Features such as dissociated p waves and fusion or capture beats (narrowing of the QRS complexes due to conducted p waves activating some or all of the ventricle) strongly suggest a diagnosis of VT. The example below (fig 2) shows a fusion beat (middle complex).
All VTs are not the same
You can find descriptions of lots of different types of VT but they tend to fall into two distinct categories, with two different electrophysiological mechanisms and two different approaches to ablation.
Normal heart VT
This VT occurs in patients with a structurally normal heart as determined by tests such as echocardiography and cardiac MRI and is also referred to as idiopathic VT. The patients are typically (but not exclusively) relatively young, with a higher incidence in women. The VT is often brought on by exercise or emotion and may be present in a spectrum from frequent ectopics through to sustained VT. These are focal tachycardias where the underlying mechanism is usually triggered automaticity – where cells that should only “follow orders” start firing off repetitive impulses as if they were the sino atrial node, in response to certain stimuli. Examples include right ventricular outflow tract VT (RVOT), left ventricular outflow tract VT (LVOT) and idiopathic VTs from other parts of the left ventricle.
The flow of calcium ions across cell membranes is important in these tachycardias and drugs affecting calcium channels such as verapamil may terminate this type of VT. Other drugs such as beta blockers that reduce sympathetic tone can be effective by preventing conditions that promote the arrhythmia. One type of normal heart VT, called fascicular VT, doesn’t quite fit the mould – it has a higher incidence in men and the mechanism may involve re-entry.
This image on the right (Fig. 3) is from a patient with RVOT VT and clearly demonstrates the focal nature of the arrhythmia. Colours indicate the timing of signals recorded at various locations compared to a fixed reference. The earliest signals are coded red, followed by shades of yellow, green, blue and lastly purple. The tachycardia starts from the red point (the originating focus) and spreads outwards evenly in all directions. The map looks like a target and is used as one – to guide an ablation catheter to the red focus, which can then be ablated to get rid of the VT. The technology used to create these maps is called CARTO (Biosense-Webster) and works on a similar principle to GPS navigation, using magnetic fields.
Ablation of normal heart VT
The outlook for patients with normal heart VT is usually very good and ablation is used to eliminate symptoms from the arrythmia – either because the patient prefers this to taking long-term medication or where medical therapy is ineffective.
The ablation team study the patient’s ECG in VT for clues to the location of the focus in the right or left ventricle (there are published algorithms to help with this). During the ablation procedure an attempt is made to initiate the clinical tachycardia by pacing manoeuvres (programmed stimulation). Normal heart VT in addition often requires the administration of isprenalin to get it started. If VT is present or can be induced the team find the earliest signals (activation mapping) that occur during the tachycardia which occur just before the onset of the QRS complex on the ECG. 3D mapping systems (see above) can be used to help record and display this data more easily. Ablation at the site of earliest activation will usually eradicate the tachycardia. If inducing the rhythm becomes difficult pace-mapping can help pinpoint the focus – if the ECG during pacing looks the same as the ECG recorded during tachycardia the catheter is likely to be a the origin of the arrhythmia.
VT in structural heart disease
At least 90% of patients presenting with VT have underlying structural heart disease. Any form of heart disease that causes myocardial scarring can lead to VT because the scar tissue provides conditions necessary for re-entry. Re-entry describes the formation of circuits around or between areas of conduction block (such as scar tissue).
These circuits are very similar to a Mexican wave around a football stadium
Where there is myocardial scarring the mechanism is almost always re-entry.Conditions causing myocardial scarring and consequently VT include: MI, dilated and hypertrophic cardiomyopathy, sarcoid and arrhythmogenic right ventricular cardiomyopathy (ARVC).
Patients with VT and structural heart disease may be at risk from sudden death resulting from degeneration of VT into VF. The most important indicator of risk in these patients is the degree of ventricular dysfunction – poor function = greater risk. Patients at high risk will usually receive an implantable cardioverter defibrillator (ICD).
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Ablation of VT in structural heart disease
Reasons to ablate VT in patients with structural heart disease:
Treatment of symptomatic VT in patients who do not require an ICD
Treatment of symptomatic VT in patients with an ICD where anti-tachycardia pacing (ATP) is ineffective at terminating the arrhythmia.
Patients with an ICD shock frequency that is not acceptable to the patient. For example one of our VT ablation patients had received 18 shocks in a 3 weeks. Ablation can reduce or eliminate shocks in these patients.
Ablation in these patients is complicated because they may have serious underlying heart disease and patchy scarring can result in numerous possible circuits. VT ablation is usually more effective in ischaemic heart disease (after MI) than cardiomyopathy.
The strategy for ablation of re-entrant VT is somewhat different to normal heat VT. The best area to ablate to achieve long-term success is a narrow region of the circuit (an isthmus) with very slow conduction where the circuit passes between areas of scar tissue. In VT this critical region is called the diastolic pathway and is located by a pacing technique known as entrainment. The images below come from a patient in VT caused by a previous MI and were produced using another 3D mapping system called non-contact mapping (ESI/St. Jude). They show the propagation of the electrical wave during one beat of VT.
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The impulse is about to enter an area of diseased but still living tissue between areas of dead scar tissue from the old infarct.
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The impulse is seen moving through the narrow isthmus region of the diastolic pathway. The activation of this tissue is not sufficient to register on the surface ECG – it occurs during electrical diastole in between QRS complexes.
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The impulse leaves the infarct zone (from a point known as the exit) and moves in two directions around the two regions of scar producing the QRS complex on the ECG.
- The impulse has reached it’s starting point and the cycle begins again.
In experienced centres VT ablation for patients with a previous MI is associated with a high procedural success rate (upwards of 75%) and VT recurrence requiring ICD shocks is significantly reduced.
