It is often said , old thoughts die hard ! It is more so in medical science as we realise , perceived fears and physician phobias have a long shelf life . A few case reports of verapamil induced acceleration of accessory pathway conduction was enough , to create a global perception among physicians and cardiologists that any drug which acts on AV node is dangerous in the management of AV nodal reëntry tachycardia (AVRT)
This is a gross perception problem due to dispropotinate importance given to a remote possibility . Thus , a great therapeutic concept was put on the back burner.
AVRT is a macro reentrant tachycardia that traverses both AV node , accessory pathway ventricle & atrium .This tachycardia can be terminated by interuppting the path way any where in the circuit .
The most easy and simple option is to block the AV node ( Verapamil, beta blockers, even digoxin !)
These drugs have cured many thousands of AVRTs in the past .As our knowledge progressed , we found , it may not be safe to block the AV node in WPW as it could divert incoming signals through accessory pathway and result in 1:1 conduction and possibility of VF
As soon as this concept was flashed all over the cardiology journals in early 1980s cardiologists took it as sermon . At the same time, lots of new anti arrhythmic drugs were developed and this concept came in handy to promote all these new class 1 c and class 3 drugs which are supposed to act more on the accessory pathway and hence projected to eliminate the risk of VF.
It was never minded , all these new group of drugs has it’s own pro arrhythmic properties like prolonging QT interval and has a potential to precipitate dangerous ventricular arrhythmias
So, by the turn of millenium calcium blockers and beta blockers have been removed form the cardiologist mind in the management of WPW/AVRT
What is the reality ?
Verapamil or betablocker induced sudden death in WPW is a grossly exaggerated concept in clinical cardiology .Treatments and procedures with many fold risks is being practiced in every walk of cardiac patients.
Complete heart block and related morbidity during RF ablation of WPW syndromes can easily exceed the of verapamil induced side effects in WPW.
How to identify potential patients who are likely to develop complications with AV nodal blockers in WPW syndrome ?
The key determinant is the accessory pathway refractory pathway . If it is < 250ms the chances of accelerated conduction is considered high. EP study is needed to measure accessory path refractory period.If it is > 300ms the accessory pathway is unlikely to condcut fast .
Is there a non invasive bedside method to estimate accessory pathway refractory period?
NO, It is not possible , but some clinical clues are available .
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All concealed accessory pathway have very high RP *thats why they are concealed .Since they can not conduct antegradely resting baseline ECG do not show any evidence for preexcitation . They are safe .
- These patients can develop only orthodromic tachycardias as the accessory pathways allow only a retrograde conduction and AV nodal blockers are ideal in them as there is no purpose to use Amiodarone and related drugs as antegrade condction thorough accessory pathway is naturally blocked .
- Intermittent WPW syndromes have negligible risk of fast antitrade conduction. As episodes of disappearance of delta wave indicate the antitrade conduction has a tendency to get blocked so no great worries.This is especially important if the WPW disappears at higher heart rates .
This clearly tells us , many times accessory pathway shares some of the decremental properties of AV node (Applying automatic electrical breaks at higher heart rates ) and it is a safety mechanism .The exact incidence of such property is not known . So , it may be a good idea to subject patients with WPW on a treadmill and look for it’s influence on delta waves and degree of pre excitation .Even a few normalised beats or prolonged PR intervals can give us assurance against rapid rates at times of AF .
*One should also remember , if a concealed WPW , manifest only during excercise it is the most dangerous group of patients in whom AV nodal blockers are absolutely contraindicated . They are immediate candidates for ablation . The above phenomenon tells us , during excercise the AV node expresses the decremental conduction properties while accessory pathway does not !
Final message
Verapamil and betablockers are not the drugs to fear upon in WPW syndrome.In fact , even in this era of hi tech cardiac care , it has a useful role to play in the chronic management of WPW .
May be , it need to be used with caution . Atleast , some efforts must be taken to estimate the refractory period of accessory pathway before prescribing these drugs.
Using with caution is not synonymous with contraindication
I attach a response to this article
Dear Dr
I refer to the above blog entry and thank you for your time. I am a doctor in the UK working in the A&E (ED in American vernicular). We recently had a case of a 27 year old ex professional soccer player who had recently moved towns and was lost to follow up. He was otherwise fit and well and came into A&E complaining of being “generally unwell”. A nurse felt his pulse was rapid and decided to do an ECG which showed an AV node reentry tachycardia. At this point he was moved to resus and a cardiac monitor attatched. His other observations including BP and sats remained normal and stable. His rate was going between 130-170 and when questioned further, he admitted to having been told he had WPW in the past but no treatment ie ablation. We subsequetly gave him two shots of iv (5MG) VERapamil and we didnt seem to be getting anywhere with regards to bring his heart rate under control. Literally 1 minute after the second dose, the patient arrested. He seemed to have a hypoxic seizure and was subsequently shocked as he had gone into VF. He came back after 30 seconds of CPR and thank fully had no deleterious side effects.
There is currently a big debate/argument going on between the cardiologists about our management. But reading your blog has given me some reassurance!
Many thanks
Dr Faisel Muhammad, Bsc (Hons) Aston BM (Soton)
In response to the above comment:
If his rate during the arrhythmia varied between 130 and 170, it sounds like he was in atrial fib or flutter, not the AVNRT you describe. This is most certainly a very different entity from the AVRT addressed in this blog post, and giving a CCB or B-blocker to a patient with WPW and a-fib/flutter is going to be the wrong move and result in just the clinical deterioration you describe.
This kind of confusion is one of the reasons why some folks are told to stay away from AV-blocking agents in WPW…