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Radial Artery Catheterization Causes Pacemaker Oversensing in Rate-Adaptive Cardiac Pacemakers

Mark E. Lanzieri, MD and Joseph Sala, PA-C

Mark E. Lanzieri, MD and Joseph Sala, PA-C

ABSTRACT: Cardiac catheterization from radial artery access is observed to cause increased heart rate via oversensing in ipsilateral rate adaptive pacemaker. The mechanism of this phenomenon is discussed. This interaction was not observed in the setting of an implanted cardiac defibrillator.

J INVASIVE CARDIOL 2013;25(11):E205-E206

Key words: radial artery access, PCI complications

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Radial artery access for cardiac catheterization or intervention presents challenges distinct from femoral arterial access. Presented is an unexpected interaction with implanted rate-adaptive cardiac pacemakers.

Case Reports. Patient #1. A 72-year-old male was referred for coronary angiography in the setting of acute coronary syndrome. Past history was remarkable for chronic atrial fibrillation and activity sensing VVIR pacemaker from left subclavian vein access. Catheterization was performed from the left radial artery due to operator preference under conscious sedation. Passage of catheters resulted in pacemaker-driven tachycardia at the upper sensor rate of 120 ppm. Employed catheters included 6 Fr Judkins right 4 cm, Judkins left 3.5 cm, and pigtail catheter. Coronary intervention was performed with a 3.5 CLS (Boston Scientific) without complication. Each pacemaker tachyarrhythmia began upon catheter entry into the mid-portion of the subclavian artery and every QRS was preceded by a pacemaker spike. Each event terminated spontaneously after approximately 30 seconds. Episodes were asymptomatic and could not be reproduced when a magnet was applied over the device to disable sensing during catheter passage.

Patient #2. A 67-year-old male was referred for coronary angiography for atypical chest pain. Past history included placement of a single-chamber implantable cardioverter defibrillator (ICD) in the left chest with postshock VVI pacing at a rate of 40 and ventricular tachycardia detection rate of 150. Angiography was performed with Judkins right 4 cm and Judkins left 3.5 cm catheters without arrhythmia. His device was reprogrammed to VVIR with maximally sensitive activity threshold and slope. Simultaneous programming to a maximum sensitivity zone for ventricular tachycardia between rates of 120-150 was performed. A Judkins left 4 cm catheter was passed over a wire retained in the aorta. There was repeated induction of ventricular pacing at rates up to 90 ppm during catheter movement in the left subclavian artery via left radial artery access (Figure 1). Postprocedure interrogation after completion of angiography confirmed sensor-driven ventricular pacing and did not reveal sensing within any VT zone. The patient was reprogrammed to his baseline parameters.

Discussion. Inappropriate sensor-mediated activity-based pacing due to oversensing of environmental stimuli is a well-recognized complication of activity-sensing pacemakers.1,2 First-generation sensors consisted of a piezoelectric crystal bonded to the inner surface of the pulse generator and utilized can vibration as a surrogate for activity. These proved unacceptably susceptible to external sources of vibration, resulting in non-physiologic sensor-driven pacing. Current-generation accelerometer-sensor driven pacemakers utilize a freely moveable cantilevered bridge (“springboard”) capable of deforming under acceleration forces. Mechanical deformation of the bridge by acceleration is converted to an electrical signal (in our patients via a piezoelectric membrane), which is interpreted by pacemaker circuitry as activity and results in sensor-driven pacing. Since it is mounted within the circuit board, the bridge will predominantly sense acceleration in the anterior-posterior axis when the pacemaker is implanted parallel to the chest wall and more closely correlates with the physiologically indicated pacing rate.3-5 It is less subject to deformation resulting from motion in the superior-inferior or lateral axes and low-frequency vibration (typically 0.5-3 Hz). Although the exact stimulus for oversensing cannot be determined, we postulate that mechanical forces transmitted by a catheter within the subclavian artery either produced sufficient anterior motion of the pulse generator to deform the accelerometer or produced sufficient low-frequency vibration to simulate activity. In either case, we anticipate such a response to be more likely the closer the pulse generator is implanted to the clavicle. One might anticipate a similar response in the presence of a piezoelectric-crystal based vibration sensing rate response pacemaker based on over sensed vibration rather than mechanical deformation. While this phenomenon is probably clinically benign, its recognition may assist in the interpretation of spontaneous wide-complex tachycardia during radial access catheterization in the presence of an ipsilateral rate adaptive pacemaker. 

Both devices were implanted over 2 years prior to catheterization, excluding pocket swelling or hematoma as a factor facilitating oversensing. Device parameters (including pacing thresholds and lead impedances) were normal, excluding lead displacement, lead fracture, or insulation degradation to explain our observations. All pacing and sensing configurations were bipolar, eliminating random patient myopotentials as the cause of oversensing. Both devices we observed utilize accelerometers as the rate-adaptive sensor. All catheters utilized could be made to produce the same tachycardic response. It was most reliably produced with the catheter tip facing anterior, and was initially observed and effortlessly produced with the Judkins left catheter with anterior-oriented tip. This observation has implications regarding the best way to avoid this response. The failure to previously observe this phenomenon during the Sones brachial catheterization era (when larger French sizes should have produced a similar response) is due to the absence of rate-adaptive pacing, which was not introduced to pacing therapy until the mid-1980s. 

Our initial observations raised concern regarding the potential for a similar oversensing response in a device with defibrillation capacity resulting in inappropriate classification of sensed mechanical stimulation as ventricular arrhythmia and device delivered therapy.6,7 As such, we temporarily reprogrammed the ICD device to a third ventricular tachycardia (VT) detection zone to determine if oversensing could potentially result in unexpected shock. ICD interrogation after catheterization revealed no detected arrhythmia in any VT zone and programming was restored to baseline. Since the majority of ICD oversensing is due to electromagnetic rather than mechanical energy, and given the role we believe the activity sensor plays in the response, this was not completely unanticipated. Based on our observations in patient #1, temporarily programming rate-adaptive parameters in patient #2 produced sensor-driven pacing confirmed by pacemaker interrogation immediately after its observation.

In patient #1, the tachyarrhythmia occurred at precisely the programmed upper sensor-driven rate and terminated at the programmed offset interval of 30 seconds. The inability to reproduce the arrhythmia that disabled sensing during magnet application in patient #1 indicates sensing as the initiating event in arrhythmia generation. 

Conclusion. Catheter passage through the subclavian artery can produce sensor-driven cardiac pacing from a device implanted via the adjacent subclavian vein. Although this appears to be a benign consequence, its recognition avoids unnecessary treatment of a pathologic arrhythmia. Its occurrence is possibly avoidable by directing catheter tips posteriorly. Consideration of radial arterial access contralateral to an implanted rate-adaptive pacemaker or preprocedure device reprogramming to a non-rate adaptive mode might  be considered during ipsilateral access in patients for whom intermittent tachycardia is undesirable. While a clinically benign occurrence, unexpected device behavior following such an event should warrant device interrogation to ensure absence of spontaneous device reprogramming to a noise-reversion mode. 

References

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  6. Olsen WH. The effects of external interference on ICDs and PMs. In: Implantable cardioverter-defibrillators: A Comprehensive Text. Wang PJ, Estes NAM, Manolis AS, eds. New York: Marcel Dekker: 1994.
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From Central Maine Medical Center, Lewiston, Maine.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 9, 2013, provisional acceptance given June 10, 2013, final version accepted June 28, 2013.
Address for correspondence: Mark E. Lanzieri, MD, FACC, FSCAI, Central Maine Medical Center, 60 High Sr, Lewiston, ME 04240. Email: marklanzieri73@hotmail.com