Dr Magdi M. Saba, Consultant in Cardiac Electrophysiology and Senior Lecturer at St George’s University of London, UK, talks to Cardio Debate about Ventricular Tachycardia and the new approaches to treatment.

Transcript

What are the criteria that define high risk VT?

The criteria that define high risk ventricular tachyarrhythmias are multiple, but if we come to think about ventricular tachycardia and its main cause it’s probably ischaemic heart disease and scar. So scar-related ventricular tachycardia is probably the most serious thing we’re looking for.

So I would suggest when we see a patient with ventricular tachycardia the first thing we want to know is what their ejection fraction looks like, if they have a history of coronary disease, myocardial infarction – so an echocardiogram, would show us some areas of hypokinesia, akinesia, or even an ECG that shows you where the Q-waves are. Prior history of ischaemic heart disease is very telling – and that’s a typical high-risk patient with ventricular tachycardia.

And other causes of ventricular tachycardia such as cardiomyopathies, non-ischaemic cardiomyopathies such as, for example arrhythmogenic cardiomyopathy, which affects mainly the right ventricle but could also involve the left ventricle, are high risk features.

The way to diagnose is a little bit more tricky. There’s ECG criteria, major and minor criteria on cardiac imaging, so cardiac MRI in that instance would probably be helpful.

And depending on the type of ventricular tachycardia we see, we can look at the ECG and say whether it is left ventricular or right ventricular. And the age of the patient, and their history – we can typically define the patient who needs further imaging.

There are less risky forms of VT – a VT that involves normal hearts, or ostensibly normal hearts on echo, typically from the outflow tracts. The right ventricular outflow tract, occasionally from the papillary muscles, and these are labeled as ‘normal heart VTs’. Of course there is something abnormal about them, but normal in terms of structure and no evidence of scar or infiltrative disease.

Is the R/T phenomenon a marker of risk?

So the R/T phenomenon is something that we see very occasionally. It’s a premature ventricular complex that happens on the T-wave, somewhere in the vulnerable window around the peak of the T-wave – just before or after the peak.

And it can lead to a fast ventricular arrhythmia, typically ventricular fibrillation. Not monomorphic VT, it’s usually related to triggered activity, not automaticity, and it can frequently occur with drug-related issues.

We don’t see it clinically that often. It’s not something that we tend to worry about in terms of the coupling interval of the ectopic beat, they typically occur after the T-wave. But when we see it happen, or if we see brief runs of non-sustained VT after that phenomenon we tend to worry about them a little bit more – but fortunately it’s not that common.

And the way to risk stratify these patients would be with a treadmill test, for example, also an ECG to see if there is anything we can predict. If on an exercise treadmill test, for example, there is more ectopy, triggered activity and more disorganised ventricular arrhythmia then these would be high risk features. But again this is not something we see that often.

Current therapeutic approaches for high risk VT

The methods we have at our disposal to treat ventricular arrhythmias are multiple. Fortunately we are in a technologically-advanced state compared to 20 years ago.

So let’s take a patient with VT. A middle-aged person with a prior history or myocardial infarction, the typical scenario.

We get an echocardiogram, we confirm, let’s say, there’s an anterior wall scar. We confirm this with an MRI to really define the topography of the scar, how deep it is, “transmural”, the patient will ultimately get a defibrillator because that’s indicated for secondary prevention. So that’s probably the mainstay, is to have the back-up of a defibrillator, an ICD implantable cardioverter defibrillator to protect them from sudden death. That’s number one.

Beta-blocker therapy is probably the mainstay of medical therapy. That would be the initial form of treatment because it raises the threshold for ventricular fibrillation. It also raises the threshold for monomorphic fast VT. So it’s the best thing you can do, especially with an ischaemic patient.

Treating their coronary disease – making sure their coronary circulation is as open as it can be, and that there are no obstructing lesions, that’s very important.

And then coming onto the arrhythmia itself. We have several options. There’s antiarrhythmic drug therapy, and there is ablation therapy.

We typically will start with antiarrhythmic drug therapy, and in cases with ischaemic heart disease or high-risk VT we stay away from class 1 drugs such as flecainide, encainide, quinidine, and we favour Class 3 drugs such as sotalol, amiodarone – those are probably the go-to drugs we use. Typically amiodarone, occasionally dronedarone. And when the patient fails these drugs, gets breakthrough VT, then we offer them an ablation procedure.

We have moved ablation further upstream in treating patients with VT in preference to drug therapy in certain cases, where a relatively young patient whom we may think maybe amiodarone may be too much for them for many, many years, we offer them primary ablation.

So after they get their ICD, a few months later we bring them back for elective VT ablation. And the way we do this is typically under general anaesthesia, we create a 3D electro-anatomic map of the ventricle “endocardially”, and occasionally “epicardially”, depending on the substrate we think based on MRI imaging and the nature of the disease, and we create a “scar map”. And we can identify the exit of the ventricular tachycardia circuit once it is induced from typically the scar border.

And that can be very successful – the success rate is easily in the 90 per cent range, acutely. But unfortunately we have the recurrence rate that can range form anything from 25 to 60 per cent depending on which study you look at.

More recently with substrate modification, which is not just targeting the VT exit site from the scar and doing a single point ablation, but we target all the possible channels within the scar and “homogenizing” the scar, if you will. We can get success rates that are over 90 per cent, acutely, and in the mid 80s, 84-85 per cent in the intermediate term looking at one year.

So there is very good data now to support VT ablation upstream before the patient gets multiple ICD shocks, before drugs fail

What is the effect of VT ablation on mortality?

Looking at the effect of VT ablation on mortality – well there’s no direct evidence from randomised controlled trials in VT ablation looking at mortality. There’s a very large series recently published from UCLA involving 12 centres worldwide, and their cumulative VT ablation experience over 1200 patients. And it confirms to us that patients who undergo VT ablation and remain free of VT afterwards, in the years afterwards – 2 year follow-up minimum – have lower mortality than those who have VT recurrence.

Now, this is observational. There could obviously be issues with bias – those (patients) who were selected for VT ablation may have been healthier. But we know that VT occurrence after an ablation is associated with higher mortality, and those who get no recurrent or less recurrence have higher survival rates.

So these are very promising results in that the efforts put into VT ablation over the past 25 years seem to be bearing fruit in that we can potentially be saving lives, and not just reducing ICD shocks.