Cardiac perforations by pacemaker and defibrillator leads: rare complications with severe implications

This editorial refers to ‘Iatrogenic cardiac perforation due to pacemaker and defibrillator leads, a contemporary multicentre experience’, by P. H. Waddingham et al., on pages 1824–1833.

Cardiac perforations caused by pacemaker or defibrillator leads are potentially fatal complications to cardiac implantable electronic device (CIED) therapy. They are reported to occur in 0.1–0.7% of patients,^1,2 but are sometimes difficult to diagnose; clinical presentation is highly variable; symptoms may be absent, lead parameters sometimes remain stable, and perforations may present late after implantation, occasionally with year-long delays. Moreover, there is no guideline support for diagnosing or managing lead-related cardiac perforations. As indications for CIED therapy broaden, the absolute burden of these rare and severe complications increases. To counter this, we rely on high-quality, contemporary data to guide prevention and optimize management.

In this issue of Europace, Waddingham and colleagues³ report on iatrogenic cardiac perforations due to pacemaker and defibrillator leads in a contemporary multicentre UK cohort. Adhering to the 2017 HRS consensus statement for lead extractions,⁴ clinically significant cardiac perforations were considered present in case symptoms consistent with a cardiac perforation were accompanied by significant pericardial effusion or lead parameter changes with definite perforation on imaging or in case of right ventricular (RV) non-capture associated with diaphragmatic or chest wall stimulation during bipolar pacing. Subclinical perforations were not assessed. Among more than 10 000 lead interventions, the authors identified 70 (0.5%) patients with acute-, subacute-, or chronic cardiac perforations. A rather high proportion occurred late after implantation; 35 (50%) within 1–30 days, and 19 (27%) patients were diagnosed later than >30 days after implantation. The study is the largest and most comprehensive on this topic to date and provides detailed descriptions of clinical presentations, lead characteristics, and outcomes after transvenous lead extraction (TLE). For this contribution, the authors are to be commended. Their study confirms previous findings that lead parameter changes are present in most patients and should lead to suspicion of perforation regardless of timing since implantation, especially when accompanied by symptoms suggestive of cardiac perforation.

Although cases were identified from a complete sample of lead interventions conducted at three tertiary UK centres, baseline characteristics were only presented for confirmed cases, and no information was provided about loss to follow-up, emigration, or mortality in the source population. As per usual in retrospective research, there is vulnerability to misclassification, and restriction to tertiary centres might also lead to selection of more severe cases, such as those with a stronger indication for TLE. Thus, some degree of uncertainty with regard to both the numerator and denominator persists in their estimates of (period) prevalence, and about the characteristics of the population from which these cases arose. The authors report that anticoagulation was positively associated with pericardial effusion with tamponade in patients diagnosed with clinically significant perforations. However, to inform the clinician, there is greater value in knowing predictors of perforation and tamponade in the population, rather than to condition this information on an event unknown to the physician at time of implantation. Whether (and to what extent) anticoagulation predicts perforation with tamponade in patients undergoing CIED implantations pends further investigation, although it is a plausible association; anticoagulation has been associated with higher risk of tamponade in patients undergoing catheter ablation, and a previous study identified treatment with antiplatelet agents as a risk factor for pericardial effusion.⁵ Even so, the potential impact of this analysis on current clinical practice is minimal as is.

Accurate diagnosis of cardiac perforations by CIED leads is often a challenge to obtain. In the study by Waddingham et al.,³ the perforating lead was successfully identified in 95% of cases. Computed tomography (CT) imaging was performed in 36 of 70 patients (51%) and concluded to be diagnostic in 97% (35 of 36 patients). However, for the majority of patients in whom the tip of the perforated CIED lead is not visible outside the silhouette of the heart on X-ray or fluoroscopy, no golden standard for diagnosing cardiac perforations has been established. Although other studies also indicate that CT may be superior to alternative imaging modalities,⁶ the true sensitivity of CT imaging in diagnosing lead-related cardiac perforations is not clear. Artefacts due to pacing leads can complicate interpretation, possibly leading to overestimation,⁷ and CT has been shown to increase risk of incidental findings of micro-perforations⁸ whose clinical significance is uncertain.

Currently, lead management in cardiac perforations is not subject to guideline recommendations, but TLE is preferred in most cases and is generally associated with favourable outcomes.^7,9 Conservative management may be considered in selected asymptomatic patients with preserved lead parameters and no or minimal pericardial effusion,⁴ but risk of symptom recurrence and progression with development of tamponade must be considered,¹⁰ especially in patients treated with anticoagulants and/or antiplatelet agents. Waddingham et al. made restriction to symptomatic perforations, and TLE was performed in all cases; 40% by lead reposition, 59% by lead replacement, and a single patient required a surgical cardiac intervention. Despite the relatively short dwell time of these leads, five patients (7%) experienced significant complications to TLE; one lead complication, one device infection, one pneumothorax, one experienced worsening of pericardial effusion, and one patient died. Two additional patients died from pneumonia within 30 days of the procedure. This data highlight the severity of these complications and their treatment in a patient group that is predominated by elderly and frail patients.^1,7 Unfortunately, the issue of subclinical and asymptomatic perforations could not be addressed by this study, although these may be candidates for conservative management strategies.

Consistent with previous reports,⁹ the majority of perforations in the study by Waddingham et al. were caused by RV lead perforation of the apex (65%) or the RV free wall (24%). Avoiding cardiac perforations was addressed in a recent EHRA consensus paper, and certain anatomical considerations are generally advised: (i) to use fluoroscopic markers to confirm lead deployment and prevent over-rotation (for active-fixation leads), (ii) to aim for a mid-septal RV lead position, and (iii) to avoid placing the RA lead in the lateral RA appendage, where areas of the RA wall can be particularly thin¹ (Figure 1). However, as highlighted by the high proportion of RV free-wall perforations in this and other studies, intraoperative assessment of lead placement using fluoroscopy is difficult—and often deceiving. Nonetheless, these findings emphasize the higher perforation risk associated with non-septal RV lead positions.

Figure 1

(A) Areas between the pectinate muscles of the right atrial (RA) appendage are extremely thin walled, especially in the lateral RA appendage. (B) The free right ventricular (RV) wall is significantly thinner and more easily perforated than the interventricular septum. IVC, inferior vena cava; LV, left ventricle; TV, tricuspid valve.

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The present study provides important descriptive data about lead-related cardiac perforations, but adds little to change current clinical practice. It confirms previous findings that perforations are not restricted to the immediate peri-procedural period, that lead parameter changes are almost always present with clinically significant cardiac perforations, that RV leads in the free wall or apex are the major culprits, and that TLE is feasible in most patients but not without risk of new complications. Several questions are left unanswered: what are the clinical implications of subclinical lead perforations in the short- and long-term? When, how, and in whom is a conservative management strategy feasible and safe? And when is lead revision sufficient as opposed to lead replacement? Such questions are more appropriately addressed in a prospective study; ideally in a randomized controlled trial, but for the study of rare, adverse events, we must often rely on large-scale observational registries and clinical quality databases for answers.

Funding

M.H.J.P.F. is supported by a grant from the Karen Elise Jensen Foundation.

Data availability

No new data were generated or analysed in support of this research.

References

Author notes