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Further data needed for the optimal diagnosis and management of ventricular tachycardia

Doctor Katja Zeppenfeld (Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands) spoke to Congress News about current approaches for managing ventricular tachycardia and the need for further data in this area.

Ventricular Tachycardia

What is the incidence of ventricular tachycardia in Europe?

That is very difficult to answer as there are different groups of patients with ventricular tachycardia. One group of patients will experience sudden cardiac arrest and will require resuscitation. Those that survive the acute event will receive an implantable cardioverter defibrillator (ICD) for secondary prevention. We often do not know whether the initial event was a monomorphic VT or primary ventricular fibrillation. There are also patients who present with stable monomorphic ventricular tachycardia without haemodynamic compromise. Current European Society of Cardiology (ESC) guidelines advise that everyone with ventricular tachycardia—regardless of left ventricular function—should receive an ICD, but not all countries and not all physicians follow these recommendations. Finally, there is a third group of patients who received an ICD as primary prevention.  We have data from patients who receive an ICD for primary or secondary prevention; however, this figure does not represent the true incidence of monomorphic ventricular tachycardia.

How do we identify patients at risk of ventricular tachycardia?

We need to screen patients after myocardial infarction as the main cause of ventricular tachycardia is myocardial scar as the result of the myocardial infarction. At the moment, we rely on the ejection fraction to identify those at risk but there are probably other important criteria that could help to identify or exclude patients at risk—we need further data to determine those criteria.

We also need to identify patients within the heterogeneous group of non-ischaemic cardiomyopathies who are at risk. There are the patients with known genetic mutations but there are also those who have ventricular impairment because of an inflammatory disease: patients who have had a viral myocarditis or those with sarcoidosis, for example. These patients have different substrates and require potentially different risk stratification.

We do know that a lot of patients unnecessarily receive an ICD for primary prevention; for most patients, we just have information about their ejection fraction. The investigators in the DANISH study, which did not find an overall survival benefit for ICDs in patients with non-ischaemic heart failure, took quite a while to identify enough cardiac events for a proper analysis because such events are rare. However, a subgroup of younger patients did receive a benefit from the ICD. I think this shows that identifying which patients are at risk is very challenging.

How could imaging help to identify patients at risk?

Imaging plays an important role in identifying substrates that could lead to ventricular tachycardia, and contrast-enhanced magnetic resonance (MR) imaging is a core part of this. Also, some studies have suggested that certain scar characteristics can be used to determine risk but the current data are conflicting and may be not applicable to all patients.

However, I strongly believe that, in the future, more sophisticated imaging protocols will play an important role in identifying the relevant substrates. Once we can visualise the substrate by imaging, we can identify an individual patient at risk and we may be able to target those substrates with ablation or other interventions.

What are the challenges of using ablation to treat ventricular tachycardia?

One challenge is our lack of knowledge, particularly in patients with non-ischaemic cardiomyopathies. We often treat them like post-infarct patients while we only know a little about their specific substrate/scar characteristics.

Therefore, the first challenge is to understand the substrate. When we understand the substrate, we need to localise it. As mentioned, we can use imaging to do this but another possibility is to characterise and localise the substrate based on electrogram analysis during catheter mapping. This means trying to identify relevant areas based on signal characteristics and we are getting better at that. We now have multielectrode catheters that use small electrodes that are able to give more detailed information about the subendocardial scar. But we are still limited regarding intramural scars or scars in the subepicardium in areas covered by fat or coronary arteries.

In addition, once we identify a scar, we need to understand how to reach it and how to eliminate the arrhythmogenic parts. Although we would like to abolish the entire substrate, there are limitations. We cannot reach everything easily.

Overall, ablation continues to play an important role in the management of ventricular tachycardia, and we have some good technologies for ventricular tachycardia ablation. However, we need some better ones. For example, we still do not have the perfect energy source to abolish the substrate of ventricular tachycardia without causing collateral damage.

One promising technology in this area is needle catheters, which allow you to record intramural electrograms and ablate within the ventricular wall. This is important because parts of the ventricular wall are quite thick, so we are limited if we only record and ablate from the endocardial and/or epicardial surface. However, again, we need further data.

What about the role of ICDs in this patient population?

ICDs are the most important therapy for any patient who we believe to be at risk of sudden cardiac death because of a ventricular arrhythmia. However, we also know that there are patients with ventricular tachycardia who will not benefit from an ICD—particularly those with ejection fraction >35%. Additionally, ICDs do not prevent ventricular tachycardia and despite modern programming, a significant number of patients will receive ICD shocks with potential implications for quality of life and mortality.

There are very limited data on drugs for managing ventricular tachycardia, in particular in patients with non-ischaemic cardiomyopathy. Long-term studies indicate patients tend to stop taking medication such as amiodarone or sotalol because of the side-effects. Therefore, at present, we urgently need new drugs to treat ventricular tachycardia and prevent ICD shocks that have also fewer side-effects.

Left untreated, what are the risks associated with ventricular tachycardia?

It depends on the function of the heart and on the rate of the ventricular tachycardia. A rapid ventricular tachycardia, even with preserved ejection fraction, can be fatal—sudden cardiac death is the greatest concern. A fast ventricular tachycardia can cause low blood pressure, which can lead to coronary hypoperfusion, ischaemia, and even secondary ventricular fibrillation.

A slow ventricular tachycardia can be tolerated for a long time. However, some patients may present in the hospital with decompensated heart failure as a result of a slow ventricular tachycardia; they may not experience palpitations or syncope.

Looking to the future, what further data are needed?

We need data on how ventricular tachycardia is managed in Europe because at the moment we do not have a clue! We need outcome data of patients with well tolerated ventricular tachycardias who have never been included in clinical trials. We need data and new randomised trials to evaluate the benefit of ICDs in contemporary patients after myocardial infarction. Most trials were conducted in the 1990s and patient management has changed dramatically since then with early revascularisation and improvement in heart failure treatment. We also need more randomised trials that compare drugs with ventricular tachycardia ablation, and we need to identify the patients who will benefit from ablation at an early stage.

Importantly, at the moment, we see a lot of patients with ventricular tachycardia at a very late stage. Therefore, they often have a poor prognosis and a high mortality because of advanced heart failure and the best we can hope to do is improve the quality of life. If we were able to identify and treat patients at an earlier stage, we could probably also impact mortality.

Finally, we need to better understand the substrate in the different aetiologies; therefore, we need to work together with basic scientists and with the industry to develop new technologies and devices for substrate visualisation and elimination.