Corresponding Author

Key Words: cardiac resynchronization therapy, lead fracture, submuscular ICD implants
Lead fracture is one of the most threatening causes of device malfunction in patients with pacemakers (PMs) and implantable cardioverter-defibrillators (ICDs) (1). Considering PMs and ICDs as a unit, the lead is usually its weakest link because of the traction and the friction it continuously undergoes since its insertion in the blood stream and its connection to the header of the device at the time of the implantation.
The case presented by Kumar et al. (2) in this issue of JACC: Case Reports is remarkable because of the multiple hints given to the reader and to the general cardiologist on this topic. It provides simple troubleshooting steps to follow when a cardiac electronic implantable device (CIED) malfunction is suspected and highlights a possible association between submuscular implantation and this cause of lead failure.
It is important to remember that the diagnosis of lead malfunction related to lead fracture is often clinical. In this case, the fracture of the left ventricular lead impeded cardiac resynchronization in the patient, who subsequently developed signs and symptoms of acute systolic heart failure. In other clinical scenarios, lead fracture can cause syncopal events or symptoms related to cerebral hypoperfusion, especially if the involved lead is the right ventricular one, and the patient is pacemaker-dependent. Lead fracture can also present as inappropriate shocks, if the fracture affects a defibrillator lead and causes appearance of the so-called “make-break” noise at the fracture site, which is read by the device as ventricular fibrillation. Although the lead fracture can be also completely asymptomatic, lead fracture is one reason why regular device checks and remote monitoring are necessary in patients with CIEDs.
Clinical evaluation should be performed with an electrocardiogram. This simple tool can give useful information and confirm the clinical suspicion of lead malfunction. In the presented case, lack of pacing artifacts and evidence of left bundle branch block in the patient, who had a cardiac resynchronization device, immediately raised the suspicion of a possible malfunction of the left ventricular lead. At this point, a device check should be encouraged; lead fracture is usually associated with high impedance values of the involved lead, with the presence of make-break noise and an inability to pace the cardiac chambers. In some cases, these features can be absent; therefore, lack of capture, oversensing, and high impedance need to be unmasked by direct manipulation of the device or by movements of adduction and/or abduction of the arm homolateral to the device (please watch the video in Kumar et al. [2] for an example of such a maneuver).
When the suspicion of lead fracture is high, its final diagnosis is made through a chest radiograph with possibility of magnification. The entire lead needs to be inspected with this modality. Most commonly, lead fracture occurs in the vicinity of the header of the device or at the entrance in the circulation, in the area between the first and second rib and the clavicle, where the subclavian vein usually projects into the brachiocephalic vein.
There are multiple risk factors that have been recognized by the scientific literature as possible causes of lead fracture (3); intrathoracic subclavian vascular access, weight-lifting, and chest trauma are the most common problems reported. In the current case report, Kumar et al. (2) wanted to increase awareness of another possible cause of lead fracture―submuscular implantation. Originally implemented to reduce skin necrosis related to the first subcutaneous implantations (the first devices were quite big), submuscular implantation can be reasonably considered a possible cause of lead fracture, especially if the can of the ICD is not anchored to the muscular sleeves of the pectoral major muscle. This muscle has 3 segments: clavicular, sternocostal, and abdominal (4). The pocket of the device is usually located medially to the thoracoacromial artery between the clavicular and the sternocostal segments. Repeated contractions of this muscle sleeve can impinge the lead at the level of the header or at the insertion under the clavicle, causing potential damage of the insulation and eventually fracture of all of the lead.
More data are needed in the future to confirm this possible association. I thank the investigators of the current case report for enriching our knowledge of this complex field. Nevertheless, I can confirm at the moment that, unfortunately, lead fracture cannot be fixed with a cast.
Footnotes
Dr. Sorgente has reported that he has no relationships relevant to the contents of this paper to disclose.
References
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