to the editor: This article was well written and provided the right amount of detail for primary care clinicians. However, the assertion that adenosine can be used to reliably distinguish ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberrancy is simply not true. Guidelines from the American Heart Association endorse the use of adenosine when a wide complex tachycardia is suspected to be the result of SVT with aberrancy, but arrhythmia termination with adenosine does not prove that the patient has SVT.¹

VT may also be responsive to adenosine in some situations. Although VT can be ruled in or made more or less likely using the Brugada criteria mentioned in the article, there is no way to rule it out. Adenosine likely is safe for treating a patient with VT acutely and may work to break the arrhythmia, but labeling a patient with adenosine-responsive VT as having SVT with aberrancy and sending him or her home could result in disastrous outcomes. VT is a deadly arrhythmia with serious underlying causes, such as acute coronary syndrome, dilated cardiomyopathy, myocarditis, and valvular heart disease.

Because the consequences are so grave, my practice is to treat all regular wide complex tachycardias as VT, unless I have a cardiologist immediately available to review both the old and new electrocardiographs. More information about adenosine-responsive VT is available.^2–4

in reply: Adenosine-sensitive VT, sometimes known as ventricular outflow tract VT or idiopathic VT, is a form of VT that occurs in otherwise structurally normal hearts. It is believed to occur in 10% of patients with VT.¹ It can present as exercise-induced sustained VT. Although adenosine has diverse electrophysiologic effects in supraventricular myocardium, its effect in ventricular myocardium is based solely on its inhibitory effects on adenylyl cyclase and cyclic adenosine monophosphate (cAMP).² This means that only cAMP-mediated VT is sensitive to adenosine, and that VT that originates from a focus within the ventricular outflow tract (usually the right) is caused by cAMP-mediated activity. Adenosine has no antiarrhythmic effect in catecholamine-dependent reentry or other types of VT. Accordingly, adenosine termination of VT is diagnostic of cAMP-mediated triggered activity, which is what accounts for most forms of right and left ventricular outflow tract tachycardia.

Until recently, outflow tract ventricular arrhythmias (including premature ventricular contractions) were considered benign, and this remains the case for most patients. However, it is now appreciated that some outflow tract arrhythmias trigger polymorphic VT, ventricular fibrillation, or sudden cardiac death, or result in cardiomyopathy.³

Dr. Firth is correct in asserting that this condition may be overlooked and deprive the patient of the opportunity to have the malignant arrhythmia managed with radiofrequency catheter ablation or an internal defibrillator. At present, there is not an agreed-upon parameter to distinguish between benign and malignant VT in these patients. Certainly the expertise of a cardiac electrophysiologist is indicated for management. Most experts and guidelines agree with the recommendation that all regular wide complex tachycardia should be managed as VT.