|
|
CASE REPORT |
|
Year : 2018 | Volume
: 6
| Issue : 4 | Page : 153-155 |
|
Pacemaker lead fracture as a cause of pacing failure
Vikas Gupta, Akshyaya K Pradhan, Ravninder Singh Kuka, Rishi Sethi
Department of Cardiology, King George Medical University, Lucknow, Uttar Pradesh, India
Date of Web Publication | 17-Dec-2018 |
Correspondence Address: Dr. Akshyaya K Pradhan Department of Cardiology, King George Medical University, Lucknow - 226 003, Uttar Pradesh India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/heartindia.heartindia_23_18
Cardiac pacing is a rapidly advancing technique. There are many potential complications of pacemaker implantation. In view of increasing implantations of pacemakers, we must have some insight of possible complications. We describe here a case of pacing lead fracture which was managed by new lead implantation.
Keywords: Lead fracture, lead impedance, pacemaker, pacing failure, pacing threshold
How to cite this article: Gupta V, Pradhan AK, Kuka RS, Sethi R. Pacemaker lead fracture as a cause of pacing failure. Heart India 2018;6:153-5 |
Introduction | |  |
Permanent pacemakers have been used to manage bradycardia and atrioventricular block since the 1960s. Increasing number of implants and complexity of both the mechanical and software features such as complex algorithms has created a potential for increased component or software malfunction. We report a case of pacing failure due to lead fracture which was managed by implantation of a new lead.
Case Report | |  |
A 74-year-old male, hypertensive patient presented with recurrent episodes of syncope for the past 2 days. Three years earlier, he had been implanted a permanent pacemaker (ventricle paced, ventricle sensed, pacing inhibited if beat sensed, rate responsive, St. Jude Medical Inc., Minnesota) for complete heart block. Right ventricular outflow tract (RVOT) active fixation (screw-in) type of lead was placed. These episodes had no relation to his level of activity (rest or exertion) or his position (upright or supine). No symptoms of nausea, shortness of breath, diaphoresis, or visual disturbances accompanied these episodes, and they resolved spontaneously over the course of a few minutes. The patient stated that the symptoms were similar to those he had experienced before his pacemaker placement 3 years ago for syncope and complete heart block.
The patient's vital signs were normal without any evidence of orthostatic hypotension.
His complete blood count, basic biochemistry, and thyroid-stimulating hormone levels were normal. His 12-lead electrocardiogram showed complete loss of pacing with underlying complete heart block with left bundle branch block escape [Figure 1]. | Figure 1: The 12-lead electrocardiogram at the time of presentation showing AV dissociation without any pacing artifacts suggestive of failure to capture
Click here to view |
The patient was examined under fluoroscopy for lead malposition, but lead appeared to be in the correct position in RVOT. However, on magnified view, lead disruption was noticed in the infraclavicular region [Figure 2]. Hence, the diagnosis of lead fracture was established.
On interrogation of the device, pacing threshold of device was found to be 4.0 V, and lead impedance was >2000ohms (out of range), further confirming the diagnosis [Figure 3].
Subsequently, a temporary transvenous pacing was done via right femoral access, and a lead (St. Jude Medical Inc., Minnesota) was placed in the RV apex with complete relief of patient's symptoms.
The next day, the patient underwent pacemaker extraction from the left subclavian pocket, followed by a new active lead implantation via the right subclavian access at the RV apex. The fractured lead could not be extracted and was left in situ.
The patient was discharged 2 days later in satisfactory condition. The pacing parameters on discharge were as follows threshold 0.7 V and lead impedance 680 ohms. He was asymptomatic at 3-month follow-up.
Discussion | |  |
Pacemaker system malfunction can be secondary to pacemaker circuitry failure or to lead dysfunction.[1] Major electrocardiographic abnormalities of pacemaker system malfunction are broadly categorized into the following: failure to capture, failure to output, undersensing, and oversensing.[1] [Table 1] describes the various causes of pacing failure and changes in pacing thresholds and impedance with these malfunctions. | Table 1: Differenital diagnosis of common pacing malfunctions based of alteration in pacing threshold and impedance
Click here to view |
Pacemaker lead fracture is an uncommon cause of pacemaker failure. The incidence of lead fractures in pacemakers is about 1%–4%.[2],[3] Transvenous implantation of permanent pacemakers is most commonly carried out via a subclavian vein puncture. Subclavian placement of the pacemaker lead can put the lead at risk for “subclavian crush syndrome,” wherein it is damaged overtime by direct friction of the lead against the clavicle and first rib or by compression of the lead between the soft tissues contained within this very narrow space.[4] Other lead-related complications include dislodgment, Twiddler's syndrome, header-connector pin problems, or insulation break.[4],[6],[7]
Early lead fractures lead to elevated pacing thresholds and impedances associated with failure to capture, oversensing, and undersensing.[4] With early lead problems, the malfunction is typically intermittent and may be exacerbated by certain body positions or motions; in later stages, the combination of oversensing, undersensing, and failure to capture is almost always diagnostic of a lead-related problem. Programming to an asynchronous mode may temporarily control the problem while awaiting lead replacement, which should be carried out as soon as possible.[4],[5]
The risk of fracture is higher in patients under the age of 50 years, those who perform an intense physical activity, women, and patients with greater left ventricular ejection fraction.[6],[7]
The treatment for lead fracture is usually to implant in a new lead, with or without extracting the old one. In view of the potential complications of lead removal such as cardiac perforation or vascular tear, lead abandonment with placement of a new lead may be performed.[8]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Hongo RH, Goldschlager N. Conduction disorders and cardiac pacing. In: Crawford MH, editor. Current Diagnosis & Treatment Cardiology. 3 rd ed. New Delhi: McGraw-Hill; 2009. p. 293-6. |
2. | Alt E, Völker R, Blömer H. Lead fracture in pacemaker patients. Thorac Cardiovasc Surg 1987;35:101-4. |
3. | Magney JE, Flynn DM, Parsons JA, Staplin DH, Chin-Purcell MV, Milstein S, et al. Anatomical mechanisms explaining damage to pacemaker leads, defibrillator leads, and failure of central venous catheters adjacent to the sternoclavicular joint. Pacing Clin Electrophysiol 1993;16:445-57. |
4. | Ellenbogen KA, Kaszala, editors. Cardiac Pacing and ICDs. 6 th ed. Massachusetts: Blackwell; 2014. p. 280-4. |
5. | Swerdlow CD, Ellenbogen KA. Implantable cardioverter-defibrillator leads: Design, diagnostics, and management. Circulation 2013;128:2062-71, 1-9. |
6. | Farwell D, Green MS, Lemery R, Gollob MH, Birnie DH. Accelerating risk of fidelis lead fracture. Heart Rhythm 2008;5:1375-9. |
7. | Morrison TB, Rea RF, Hodge DO, Crusan D, Koestler C, Asirvatham SJ, et al. Risk factors for implantable defibrillator lead fracture in a recalled and a nonrecalled lead. J Cardiovasc Electrophysiol 2010;21:671-7. |
8. | Kaseer B, Al Mouslmani MY, Hirsh DS, Hammadah M. A broken pacemaker lead in a 69-year-old woman. Cleve Clin J Med 2017;84:346-7. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1]
|