Author + information
- aCardiovascular Division, Washington University School of Medicine, Saint Louis, Missouri
- bDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
- cDepartment of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota
- ↵∗Address for correspondence:
Dr. Samuel J. Asirvatham, Department of Cardiovascular Medicine, Mayo Clinic, 200 1st Street Southwest, Mary Brigh 4-523, Rochester, Minnesota 55905.
- cardiac implantable electronic device
- chronic thromboembolic pulmonary hypertension
- paradoxical embolism
In this issue of JACC: Clinical Electrophysiology, Nayak et al. (1) report on the presence of cardiac implantable electronic devices (CIED) in a large, single-center cohort of patients who underwent pulmonary thromboendarterectomy (PTE) for chronic thromboembolic pulmonary hypertension (CTEPH). This is a significant and critically important addition to the published reports, especially because the group at the University of California-San Diego is indisputably the pre-eminent center for PTE in the United States and has established PTE as effective treatment for CTEPH. The investigators describe their experience in a cohort of 982 patients who had undergone PTE and compared patients with CIED with patients without CIED.
This large body of work brings forth several important findings. In their cohort, 17 patients had CIED at time of PTE (14 pacemakers, 3 defibrillators), which is a CIED prevalence of 1.7%. Another significant finding presented in this work includes the management of CIED in the presence of CTEPH at the time of PTE, which is both informative and thought-provoking. Intraoperatively, 6 patients had CIED extracted. Epicardial systems were placed in 5 of these patients and 1 patient had a new endocardial pacemaker system implanted. The remaining patients retained their intracardiac devices. Interestingly, CTEPH patients undergoing PTE who had a CIED were much less likely to have a history of venous thromboembolism (50% vs. 78.6%). A very intriguing finding was that the embolus burden in these patients was more likely to be located in the distal pulmonary circulation in patients with CIED (70.6% vs. 25.8%), and Nayak et al. (1) speculate that this may be reflective of micro-emboli from the leads.
What Is Known About CIED-Related Thromboembolism?
It is well established that transvenous intracardiac CIED leads are a nidus for thrombus formation (2–4). Furthermore, a large proportion of patients with CIED likely have subclinical pulmonary emboli, which causes an increase in pulmonary artery pressure, though there is no definite evidence for increase in clinical pulmonary embolic events (5–7). Prior work has suggested that in the presence of a patent foramen ovale (PFO), CIED patients have a signal for and increased risk of stroke or transient ischemic attack from systemic embolism (8,9). However, current clinical practice does not include prophylactic anticoagulation or PFO closure, merely due to presence of CIED.
CTEPH, PTE, and CIED
A majority of patients with CTEPH have documented venous thromboembolic events, though in a sizable minority the cause for CTEPH may be unknown. However, because it is well known that CIED leads are a nidus for thrombi, these may serve as a potential contributor to the pathogenesis of CTEPH from recurrent subclinical showering of microemboli to the pulmonary circulation, especially in the absence of peripheral deep venous thrombosis. Patients with CIED, however, may have associated cardiovascular disease including left heart failure that may be falsely attributed as the cause for pulmonary hypertension and thus lead to underdiagnosis of CTEPH. Importantly, on the account of comorbidity, patients with CIED may be less likely to be referred for PTE.
What Is This Study Unable to Reveal?
Even though this study is a welcome addition to medical publications, it is limited in scope. We are unable to infer the epidemiologic role of CIED in the pathogenesis of pulmonary hypertension in patients with endocardially placed CIED leads.
This study provides support for strongly considering chronic thromboembolism in the differential diagnosis of pulmonary hypertension, especially in the absence of other risk factors for pulmonary embolism, in patients with CIED. The pictures demonstrating the visual similarity of chronic thrombotic material adhered to the extracted device leads and the surgically removed pulmonary emboli add further support to the possibility of a mechanistic link between CIED lead-related thrombi and CTEPH. The presence of more distal than proximal embolic burden in the pulmonary circulation is also consistent with the smaller size of lead-related thrombi that can embolize to these regions. Additionally, this study shows the feasibility of the PTE in CIED patients, and it is reassuring that the clinical response was comparable to other patients despite the technical difficulty in removing more distal thrombi.
This study provides the landscape for further research to explore epidemiologic studies to examine the link between CIED leads and complications from chronic microembolism. As with all good studies, this investigation leaves us with several unanswered questions and provides an area ripe for further investigation. Should we consider extraction of intracardiac hardware in those patients who develop pulmonary hypertension? Is systemic anticoagulation alone sufficient treatment? Though not commented on in the paper by Nayak et al. (1), it would be interesting to know whether patients who were transitioned to epicardial devices still continue to have pulmonary emboli and pulmonary hypertension.
This study should also cause us to pause and reflect on ramifications beyond the comorbidity of CTEPH. Not only does this study add to the growing evidence concerning right-sided intracardiac device leads (4,5,7–9) and increased pulmonary pressures, but it should also cause us to re-examine the situation of CIED in the presence of an intracardiac shunt such as a PFO. Just as we search for deep vein thrombus in the leg for lung emboli, is it really a surprise that close juxtaposition of CIED leads extremely close to a PFO poses risk for stroke/transient ischemic attack, even with transient changes in shunt from right to left? In addition, chronic showering of microemboli has the potential to cause an increase in pulmonary pressures and tip the scales in favor of a right to left gradient across the PFO. In the presence of CIED leads with thrombus burden, this poses the threat of microemboli to the systemic circulation and thus can potentially increase the risk for stroke/transient ischemic attack. These issues underscore the importance of this study and, furthermore, the importance of further study in this area to guide our clinical management. Such considerations make technological developments such as subcutaneous defibrillators and leadless pacemakers favorable in such patients, especially with features that prompt extraction of a thrombus-burdened CIED lead and need for reimplantation. Such a step would be the first toward ameliorating the morbidity associated with transvenous intracardiac CIED leads. In addition, other innovative avenues are being pursued such as percutaneously placed epicardial pacing and defibrillation devices, offering the merits of both a nonsurgical approach and extracardiac placement of chronic leads that can pace and defibrillate (10,11).
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- 2018 American College of Cardiology Foundation
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