Cardiac Rhythm Management
Articles Articles 2011 July


DOI: 10.19102/icrm.2011.020708

John Day, MD, FHRS, FACC

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Dear Readers,

Managing complications and difficult clinical situations has long been a topic of interest to clinicians that manage cardiac arrhythmias. In this month's issue, we will delve into 3 of these difficult clinical scenarios- discussing how to manage device infections, neurocardiogenic syncope, and how to manage the patient with symptomatic PVCs refractory to both medical and ablative therapy.

The management of an infected device is discussed in detail from an original contribution submitted by the University of California, San Diego, along with a commentary by our Innovative Techniques Section Editor, Dr. Samuel Asirvatham. Improved management of these complications will continue to yield better outcomes in cardiac implantable electronic device procedures.

I invite you to visit the Innovations in Cardiac Rhythm Management website,, to view a follow up video presentation that further illustrates this article by one of the lead authors of the paper- Victor Pretorius, MB ChB. Please enjoy this presentation as a complimentary offering on our homepage.

Grubb and Kanjwal also provide us with an original contribution that details their observations and recommendations on how to manage the patient with medically refractory cardioinhibitory neurocardiogenic syncope. While previous studies have not shown a clear benefit of pacemaker therapy, likely due to the vasodepressor component to this condition, a relatively new pacing algorithm known as closed loop stimulation (CLS) cardiac pacing (Biotronik) may reopen this debate. Indeed, our experience in using the older pacing algorithms from the other pacemaker manufacturers has had only modest efficacy in treating cardioinhibitory neurocardiogenic syncope.

It is conceivable that previous studies have failed to show a benefit with pacemaker therapy for cardioinhibitory neurocardiogenic syncope due to the timing of the pacemaker's detection of a drop in the intrinsic sinus rate, which is too late to prevent the vasodepressor component and resulting syncope. The CLS algorithm may theoretically offer earlier intervention with atrial pacing that could blunt the vasodepressor component and possibly even prevent syncope. The CLS algorithm detects early changes in myocardial contractility and venous return (through changes to the right ventricular pacing lead impedance) thereby allowing potentially earlier atrial pacing during a neurocardiogenic syncopal event.

Within the aforementioned manuscript, Grubb and Kanjwal share their experience on how best to program the CLS algorithm, allowing 84% of their medically refractory neurocardiogenic syncope patients to be successfully treated. Unfortunately we have had limited experience with the CLS algorithm so I am unable to share any personal insights on this pacing algorithm. While very intriguing, the placebo effect of cardiac pacing for neurocardiogenic syncope remains an important consideration. Hopefully ongoing studies will help to answer the question of whether the CLS algorithm offers an improvement over the previous algorithms used by the other pacemaker manufacturers.

Lastly, the patient with highly symptomatic PVCs refractory to medical therapy and ablative therapy is another difficult clinical situation to manage. This issue of the Journal features a challenging case presented within the Innovative Collections section by Poghosyan et al. that discusses how to approach these difficult cases. Fortunately this is a rare situation, as at experienced centers 90% of PVC cases are successful.

In our experience there are generally two reasons why we cannot successfully ablate PVCs- due to difficult anatomical issues and non-inducibility of PVCs during electrophysiologic testing. There are certainly cases where the PVCs may originate very close to the AV node or to the ostium of the left main coronary artery. For patients that present para-nodal PVCs it is worth attempting cryoablation or a carefully performed radiofrequency ablation from the aortic root under the guidance of intracardiac echo to avoid injuring the left main coronary artery. Another anatomical limitation can be thick left ventricular tissue, which may require higher power settings with an irrigated tip ablation catheter. Fine catheter movement under Stereotaxis guidance may be very helpful in these cases as well.

While most PVC ablation procedures can be performed endocardially, an operator's comfort with epicardial mapping and ablation techniques can be very helpful. To perform epicardial mapping, the operator has to be sure that the severity of the clinical situation merits this aggressive approach. For patients with PVC related myocardial dysfunction or debilitating symptoms it may be reasonable to include epicardial access in the approach.

The other main reason for unsuccessful PVC ablations is non-inducability. Taking a careful history to identify exacerbating factors is of critical importance in overcoming this limitation. In addition, during the electrophysiology study it is helpful to perform a full pharmacologic evaluation including sympathetic agonists (isoproterenol, intravenous caffeine, and epinephrine) as well as parasympathomimetic agents such as neostigmine. Often, patients may need to be fully awake during the procedure if sedation suppresses the PVCs. As a guiding rule, if a patient has less than 3–5% PVCs on a 24 hour Holter study, then ablation success may be significantly compromised due to non-inducibility.

All in all, this issue is packed with information that we hope will continue to improve your practice.


John Day, MD, FHRS, FACC
The Journal of Innovations in Cardiac Rhythm Management
Director of Heart Rhythm Services
Intermountain Medical Center
Salt Lake City, UT