High Voltage Riata ST Defibrillator Lead Failure and Its Implications for Durata

It came from a case report published online before print in PACE from Dr. John Marenco of Tufts University in Springfield, Massachusetts:

A 60-year-old man had a single-chamber St.Jude Atlas VR defibrillator (St. Jude Medical, St. Paul, MN, USA) with a dual coil St. Jude Riata 7001 defibrillator lead (My note: this is actually a downsized, second-generation 7 Fr Riata ST model whose internal construct shares many similarities to St. Jude's currently-marketed third-generation 7 Fr Durata lead) placed in 2006 for primary prevention secondary to an ischemic cardiomyopathy and prior myocardial infarction.  All routine device interrogations, both remote and in-office, had been normal with stable sensing amplitude, lead impedances, and capture thresholds. The device was programmed with two zones: a ventricular tachycardia (VT) zone from 340 ms (176 beats/min) and a ventricular fibrillation (VF) zone from 260 ms (231 beats/min).  The VT zone had a morphology discriminator “on” with interval stability and sudden onset “passive.” Five years from implant, he presents with palpitations, light-headedness, and a single implantable cardioverter defibrillator (ICD) discharge.  He has a friend drive him to the emergency room and is found to be in ventricular tachycardia over 200 beats/min. The ventricular tachycardia terminated with intravenous amiodarone bolus before need for external defibrillation. Device interrogation demonstrated an initial rhythm of atrial fibrillation with the appropriate detection of the onset of ventricular tachycardia with a cycle length of 245 ms, within the device’s VF zone (Fig. 1). Discriminators were not activated in the VF zone, but the morphology discriminator clearly demonstrates a failure of the electrogram signal to match the template (indicated by the “x” in the marker channel). After detection of 12 intervals (interval average) within the VF zone an episode is declared and a 25-Joule (693 V) shock is delivered, failing to restore sinus rhythm.  No additional shocks are delivered despite appropriate redetection within the VF zone (Fig. 2).  After a fifth detection, the device declares “no more therapies” with VT continuing indefinitely. Device interrogation in the emergency department reveals a pacing lead impedance was 465 ohms, signal amplitude 1.8 mV, and capture threshold 0.75 V at the rate of 0.5 ms. What is the differential diagnosis of failure to deliver appropriate therapy and why did this device fail to deliver more than a single shock?

Further review of the case's figure disclosed appropriate VT detection, a high voltage impedance of 0 ohms, and an "aborted charge because of possible output circuit damage" on device interrogation after the event.  Importantly, at the time of lead revision, "there was no fluoroscopic insulation breach and no obvious insulation breach in the pocket."  Fluoroscopic screening of these leads, therefore, would not have detected pending lead failure.  Further, as far as we can tell from the report, no antecedent device alerts were triggered before this event.

This case report discloses several important issues. (1) High voltage coil damage in a 7Fr  Riata ST lead can lead to either ineffective high voltage therapy delivery, withholding of further therapies, or both despite appropriate arrhythmia detection.  St. Jude defibrillators are engineered to automatically withhold energy delivery in low high-voltage lead impedance situations to avoid excessive current delivery and device overheating in such circumstances (personal communication).  (2) This failure mechanism, while curently very rare, may affect implanters decisions regarding whether or not to replace existing Riata leads irrespective of their performance characteristics and flouroscopic appearance at the time of battery change.  Already there have been other reported high voltage failures in Riata leads with externalized wires.  Some have advocated testing the high voltage leads as part of Riata lead follow-up to screen for this failure mechanism, especially since the therapeutic implications of high voltage lead failure is much more significant and difficult to detect than low-voltage (sensing lead) failures. 

Perhaps most important for St. Jude going forward is how this case will influence implanters' choice of later-generation 7 Fr St. Jude defibrillator leads with their Optim coating but similarly-downsized inner lumen dimensions.  I look forward to St. Jude's update of their Riata Communications website regarding these recently published case reports.

-Wes

References:

Marenco JP. "Failure to Deliver ICD Shocks after a Failed Discharge Despite Redetection of Rapid Ventricular Tachycardia? What Is the Cause?" PACE DOI: 10.1111/j.1540-8159.2012.03484.x Published online 21 July 2012.

For an excellent overview of the Riata ICD lead recall by Dr. Jay Schloss: http://cardiobrief.org/2012/02/22/guest-post-more-lessons-from-the-riata-icd-lead-recall/

The Riata ICD Lead Recall: Two Perspectives

Robert Hauser, MD published a perspective piece in the New England Journal of Medicine today entitled "Here We Go Again — Another Failure of Postmarketing Device Surveillance." In the piece, he offers these suggestions on how to detect these failures earlier:

Opportunities have emerged for automated tools to prospectively monitor multicenter device databases for early, low-frequency adverse events and to compare suspect devices with established products that have been shown to be reliable.(4) The goal is a postmarketing surveillance system that not only detects device problems early but also accumulates the data needed to guide patient care. Until such a system exists, St. Jude Medical should initiate a study with these attributes for recalled Riata and Riata ST leads and for the currently marketed Durata leads. Indeed, all manufacturers should conduct postmarketing studies of this type for marketed class III devices that sustain or support life.

It has been 3 years since the FDA launched the Sentinel Initiative, as Congress, in 2007, directed it to do.(5) The intent of this new system is to supplement the current passive adverse-event reporting with an active, real-time network capable of identifying any safety or efficacy issues soon after a new drug or device is marketed and then communicating the information in a timely manner to health care providers and the public. Creating such a system is an ambitious undertaking, and the initiative aims to gather electronic health data from 100 million people by the end of 2012. Formidable challenges lie ahead, such as setting priorities, developing analytic tools, and deciding when and how to alert the public if a safety signal is detected. Thus, we are years away from a fully operational Sentinel Network.

Jay Schloss, MD offers another thoughtful perspective on this issue in his guest post over on Cardiobrief:

It is worth noting that all high impact device failures in the cardiac rhythm device industry have occurred well after device approval. In most cases, failures have been rare events occurring many years after these devices became clinically available. The industry is littered with high profile device failures, some of which serve now as footnotes or memories from the more gray haired members of the EP community: Medtronic polyurethane pacing leads, Ventitex Cadence ICDs, and Telectronics Accufix pacing leads were all devices that failed well after they had been introduced to the market. It was through case reports from concerned doctors – not the FDA — that these problems were brought to light.

Trying to absolutely prevent the failure of medical devices through the FDA approval process would be challenging to say the least. This would require an anticipation of the potential failure mechanism before the fact to design a study that would detect said defect. Moreover, the number of patients and length of study for these trials would be daunting, impractical and quite likely prohibitively expensive.

Hauser’s call to enforce a robust active postmarket surveillance system would allow ongoing innovation and appropriately timed approval of new technology. With the ability to carefully monitor a large population of approved devices “in the field,” sentinel failures could be detected and acted upon as they occur. With public reporting of these events, doctors could draw their own conclusion of whether to keep implanting these devices and prospective studies could then be designed promptly to determine the scope of the problem. That would be a system that protects patients while still allowing innovation.

Neither author mentions how their approaches might be funded. Nor is there a clear consensus on how to determine a threshold for sounding a recall (or "advisory"). Should it be announced before a root cause of the problem is known or suspected, or after? Pulling a recall trigger too early before a root cause of the defect is identified leaves doctors and patients completely in the dark about how to manage these complicated situations. These issues are still debated today.

What is clear, though, is that the efforts to prevent such widespread recalls continue and doctors (as shown by these two perspectives) remain eager to participate in the process.

-Wes

More Troubles for St. Jude's Riata Defibrillator Leads?

From the Minneapolis Star Tribune:

Researchers in Ireland have discovered a possible problem with a heart defibrillator component made by St. Jude Medical Inc. in which wires that run from the device to the heart may poke through the outer coating of their cable.

The study looked at 212 patients in Ireland who received St. Jude's Riata defibrillator lead and found that 15 percent had suffered such an "insulation breach," which could interfere with the device's life-saving therapy. Normal screening of the device or even X-rays may not pick up the breach, and patients would have no outward clue that their lead wire may be compromised.

It should be noted that the "study" referenced in this artice was actually an abstract published in the European Heart Journal's September supplement edition. I could not find it online yet, but a copy of the source abstract can be found on CafePharma, the medical device / pharmaceutical industry representative's anonymous messaging board.

-Wes

Thin Defibrillator Leads from St. Jude Questioned

Area of a circle equals pi (3.14159...) times the radius squared. I remember that equation from geometry class.

Now, all kinds of engineers are rethinking this equation, too. As are doctors.

Since Medtronic had their recent thin Sprint Fidelis lead (6.6Fr) recalled due to an elevated rate of fractures, new scrutiny is being placed on St. Jude's even thinner (6.3Fr) Riata® ST defibrillator lead. But the concern in this case is less about fractures, but rather heart perforations.

This morning the Wall Street Journal reports that St. Jude's Riata ST lead is being evaluated for an increased cardiac perforation rate compared to conventional thicker defibrillator leads. Cardiac perforations are not new to defibrillator or pacemaker implantations. An example of this can be found on a dramatic case recently published in Circulation (reference below) where a pacemaker lead had punctured a patient's heart and had eroded through his 7th rib. But with the recent FDA hypersensitivity and the concerns about thin defibrillator leads, it is not surprising that such concerns have been raised.

You see in cross section, the thinner a lead becomes, the more force from the lead pressing against heart muscle is concentrated over a smaller area. And unfortunately, as the radius of leads are downsized, the force applied over that area increases geometrically (radius squared, remember?). An example of the difference that surface area makes on pressure to tissues can be felt when you apply the same amount of pressure from a pencil's erasure over your hand versus its sharpened tip.

So when a thin lead has a narrowed diameter, it might be more likely to perforate. And given the concerns aired in the Wall Street Journal article, I bet implanting electrophysiologists will be slow to rush these leads until the dust settles a bit more. After all, we've become a bit sensitized to these issues.

-Wes

References:

Wall Street Journal.

Singhal S, Cooper JM, Cheung AT, Acker MA. "Rib Perforation From a Right Ventricular Pacemaker Lead." Circulation; 115: e391-392.

Update 21:49 CST - The PACE articles with the studies regarding the Riata lead issues are now up. Dr Steven V. Vlay of Stony Brook University, New York in his accompanying editorial states:

"What is particularly troublesome about this lead is not only the perforation but its late presentation. Sometimes the lead perforation does not come to clinical attention until it is well beyond the right ventricular free wall. Furthermore with the Riata, the movement continues until it protrudes out several cm into adjacent tissue. This factor seems to distinguish it from a small perforation in which only the tip of the lead penetrates the right ventricular wall. It could result in ventricular asystole if a patient is pacemaker dependent or in failure to successfully defibrillate, both resulting in sudden death. If perforation does not occur in the first three months, can we stop worrying? We do not yet know the answer to this question.

Here's the references from this issue of PACE:

1. Krivan L, oz M, Viasinova J, Sepšsi M. Right ventricular perforation with an ICD defibrillation lead managed by surgical revision and epicardial leads.

2. Fisher JD, Fox M, Kim SG, Goldstein D, Haramati LB. Asymptomatic anterior perforation of an ICD lead into subcutaneous tissues.

3. Satpathy R, Hee T, Esterbroooks D, Mohiuddin S. Delayed defibrillator lead perforation: An increasing phenomenon.