Lead failures are classified as either structural lead failu
Lead failures are classified as either structural lead failures or electrical lead failures, and failures of 8F single coil leads are more frequently reported. Structural failures occur with a reported incidence of 14–34% and are evident as cable exteriorization in fluoroscopy studies [6,7]. Electrical failure is seen in 2–6% of leads with structural failure . Electrical failures may present as a sudden rise in capture threshold, a change in impedance, over-sensing due to noise, inappropriate shocks, failure to deliver defibrillation therapy, or a decrease in R wave amplitude. Inappropriate shocks occur in 15–24% of leads with electrical failures [3,5,8].
An unusual feature in the present case is that the occurrence of noise after the first high voltage shock resulted in multiple shocks mimicking an electrical storm that was nearly fatal. Fluoroscopy revealed a structurally abnormal lead with conductor exteriorization. There was no change in electrical parameters. The exact mechanism by which a high voltage shock led to an electrical failure in an aging lead with stable electrical parameters is unknown. A case in which noise followed a high-energy shock during defibrillation testing in a patient with a Riata lead has been described earlier . This event was attributed to a complete breakdown of the hbv virus tetrafluoroethylene coating around the conductor, induced by a high voltage shock, due to partial abrasions in the coating. It is possible that the high voltage shock precipitated an electrical failure in our patient by a similar mechanism in a lead with a preexisting asymptomatic mechanical failure (conductor exteriorization).
Conflict of interest
Case presentation A 79-year-old man with a history of ventricular septal defect underwent catheter ablation of drug refractory paroxysmal atrial flutter (AFL). The 12-lead electrocardiogram during tachycardia showed a biphasic, predominantly positive flutter wave with an initial negative component in leads II, III, and aVF, and positive flutter waves in leads V1 through V6 (Fig. 1, A), consistent with typical counterclockwise (CCW) AFL . A decapolar catheter was advanced with its ♯17 and ♯18 poles in the proximal coronary sinus (CS), and a deflectable duodecapolar Halo catheter was placed parallel to the tricuspid annulus (TA), across the inferior vena cava (IVC)-TA isthmus, with its tip at the CS ostium (Fig. 1, B and C). Although we did not perform contrast CS venography to confirm the location of the CS ostium, we believe that the CS ostium is located near the 5 o׳clock position of the mitral annulus as estimated by the shape of the CS catheter projected in the left anterior oblique fluoroscopic view, consistent with the location of the ♯17 and ♯18 poles of the CS catheter. The atrial activation sequence along the TA during ongoing tachycardia, combined with entrainment pacing at the IVC-TA isthmus, and 10 o׳clock and 2 o׳clock positions of the TA with a pacing cycle length of 220ms confirmed the diagnosis of typical CCW AFL. We did not perform entrainment pacing from the CS. During entrainment pacing from any site along the TA, all atrial deflections in CS recordings immediately after the last pacing stimulus were captured with the activation sequence similar to that during the AFL and a spike-atrial interval shorter than AFL cycle length, consistent with an orthodromic capture. A line of radiofrequency energy delivery blocked conduction across the IVC-TA isthmus, terminated AFL, and restored sinus rhythm. Differential pacing from the low septal and lateral right atrial (RA) region confirmed the successful creation of bidirectional isthmus block. It is noteworthy that, during ongoing AFL before ablation, (1) a latency of low RA conduction, consistent with conduction across the septal isthmus, was observed along the distal Halo catheter (Fig. 1, D), and (2) recording of atrial activation along the CS, instead of being proximal to distal, was centrifugal from CS poles 9 to 10 (Fig. 1, D). What is the underlying electrophysiological mechanism of atypical atrial activation during typical CCW AFL?