Cardioembolic Stroke in Patients with Patent Foramen Ovale and Implanted Cardiac Leads
Article first published online: 18 OCT 2012
©2012, The Authors. Journal compilation ©2012 Wiley Periodicals, Inc.
Pacing and Clinical Electrophysiology
Volume 36, Issue 1, pages 50–54, January 2013
How to Cite
DESIMONE, C. V., DESIMONE, D. C., HAGLER, D. J., FRIEDMAN, P. A. and ASIRVATHAM, S. J. (2013), Cardioembolic Stroke in Patients with Patent Foramen Ovale and Implanted Cardiac Leads. Pacing and Clinical Electrophysiology, 36: 50–54. doi: 10.1111/pace.12014
- Issue published online: 9 JAN 2013
- Article first published online: 18 OCT 2012
- Manuscript Accepted: 14 AUG 2012
- Manuscript Revised: 26 JUL 2012
- Manuscript Received: 21 MAY 2012
- patent foramen ovale;
Implanted cardiac devices, including pacemakers, defibrillators, and resynchronization devices, are known to develop thrombus on their intravascular leads. Patent foramen ovale (PFO) occurs in approximately one-quarter of the adult population. It is unclear whether paradoxical cardioembolism and clinically relevant stroke occur in patients with implanted cardiac leads and PFO. We present a case series of four patients with cardioembolic stroke, presumed to arise from intravascular cardiac leads and associated PFO that required device closure of the PFO.
(PACE 2013; 36:50–54)
Cardiac devices, including pacemakers, defibrillators, and resynchronization devices, are frequently implanted in patients with cardiac rhythm disorders.[1, 2] Thrombus and debris are known to occur along the intravascular portion of these leads.[3, 4] Because the leads associated with these devices are generally placed in the right-sided circulation (right atrium, right ventricle, and coronary sinus), the risk of cardioembolic stroke from thrombi on these leads is thought to be low.
Patent foramen ovale (PFO) occurs in an estimated 25% of the adult population and is often undetected. Although an increased risk of stroke in patients with PFO and an increased incidence of PFO in stroke patients was shown in initial case-controlled studies, these results have not been confirmed in other studies. In patients with known cardiac shunts, intravascular hardware is avoided because of the presumed increased risk of thromboembolic stroke and epicardial leads preferred in such patients.[6-8] Whether or not cardioembolic stroke occurs in patients with implanted leads and known or undetected PFO is unknown, and some minor central nervous system events may go undetected. The attendant thrombi and possible vegetations on implanted leads have increasingly required extraction. We present a case series of four patients with cardioembolic stroke, presumably a consequence of a PFO and indwelling or recently extracted right-sided cardiac devices.
A 74-year-old woman with known coronary artery disease, congestive heart failure, and prior out-of-hospital cardiac arrest had an implantable cardioverter-defibrillator (ICD) with right atrial and ventricular endocardial leads placed 14 years before evaluation. She was hospitalized for a group A beta hemolytic streptococcal urinary tract infection. A transesophageal echocardiogram (TEE) performed indicated no evidence of valvular endocarditis but noted a mobile thrombus on the atrial portion of the ventricular lead (Fig. 1B). A PFO with right-to-left shunting on Doppler imaging was noted (Fig. 1A). Although lead extraction was discussed, because lead thrombi are a common finding on chronic leads it was decided to manage conservatively with intravenous antibiotics; she was discharged on chronic warfarin anticoagulation and antibiotics.
She returned to the hospital one month after discharge with fever, confusion, abdominal pain, and aphasia. Emergency computed tomography (CT) scan of the abdomen showed a hypodensity in the spleen, and CT scan of the head revealed an acute right parietal lesion, findings consistent with embolic infarction. Repeat TEE found only a sleeve of thrombus on the lead, with the mobile component no longer present. It was determined that the patient had paradoxical cardiac thromboembolism and was managed with anticoagulation and PFO closure (Fig. 1C) to prevent further paradoxical embolization. The patient has done well since PFO closure and has been maintained on warfarin.
A 43-year-old woman with prior history of left main coronary artery dissection, emergency coronary artery bypass grafting, ventricular tachycardia, and dual chamber ICD placement seven years prior was evaluated for recurrent ventricular tachycardia. She had a history of transient ischemic attacks (TIAs) with visual symptoms despite chronic adequate warfarin therapy. She underwent a TEE that revealed a PFO with intermittent spontaneous right-to-left shunting on Doppler imaging (Fig. 2A). No lead-related or other intracardiac thrombi or masses were noted. She was scheduled for device upgrade to a biventricular ICD in two weeks, and warfarin was held four days before the procedure. An intraprocedural TEE showed small linear mobile densities attached to the endocardial atrial portion of the ICD lead (Fig. 2B). In addition, a small echo dense clump was attached to the ventricular lead at the level of the tricuspid annulus. Smaller mobile densities were seen at the right atrial-superior vena cava junction on both leads. The coronary sinus left ventricular lead was implanted, and the patient was dismissed home on warfarin. Four days after the procedure, she developed slurred speech, facial drooping, and left-sided weakness. An outside echocardiogram confirmed a clot on the right-sided leads, and because of concern of paradoxical embolization causing recurrent stroke syndrome, she underwent PFO closure (Fig. 2C) and was continued on warfarin. With two-year follow-up after the procedure, she has had no TIA or strokes.
A 71-year-old woman with chronic kidney and liver disease presented with worsening dyspnea. Four years ago she had had sick sinus syndrome and dual chamber pacemaker implantation, and subsequently developed sepsis requiring device explantation and subsequent reimplantation. With her current illness, blood cultures revealed methicillin-resistant Staphylococcus Aureus (MRSA) bacteremia, and she was started on vancomycin therapy. TEE demonstrated a lobulated mobile mass 2.5 × 0.5 cm within the right atrium attached to the ventricular pacemaker lead (Fig. 3B). No valvular masses were noted. The right atrial lead tip was cultured but did not grow MRSA, but did grow a gram-negative bacillus which was felt to be a contaminant. An atrial septal aneurysm with a 4-mm PFO and bidirectional shunting was present on Doppler flow imaging (Fig. 3A). She underwent device explantation with insertion of a temporary pacemaker.
Four days following extraction, the patient developed a right-sided hemiplegia. A CT scan of the head showed a focal zone of decreased attenuation involving the cortex and adjacent subcortical white matter consistent with acute cardioembolic infarction. Neurological evaluation revealed dense hemiparesis, and she was diagnosed with paradoxical embolization and stroke through her PFO. To prevent future episodes, given the presence of a PFO with right-to-left shunting and need for reimplantation of endocardial leads, she underwent closure of the PFO (Fig. 3C). The patient had no further episodes of TIA or stroke, but passed away from complications related to decompensated cirrhosis and renal failure.
A 28-year-old man with a history of long QT syndrome presented with symptoms of right-sided leg and arm weakness. He had an ICD placed 5 years prior because of a strong family history of sudden cardiac death (SCD). Neurologic evaluation determined this weakness was consistent with a TIA. TEE showed the right ventricular lead with a 1.2-cm elongated, thin, and mobile strand present as it traversed the right atrium. Agitated saline was performed and showed a PFO with right-to-left shunting. He was started on heparin anticoagulation and was bridged with Coumadin. Because of the young age of the patient, concern of stroke recurrence, and the need for continued ICD for SCD prophylaxis, it was determined that extraction of the lead in addition to PFO closure by a minimally invasive surgical approach would be the best course of action. He was discharged on Coumadin and scheduled to return in three months for surgical intervention.
A minimally invasive video-assisted thoracoscopic surgery procedure was performed and an intraoperative TEE showed a PFO, along with a 0.5-cm linear strand attached to the lead as it coursed the right atrium. The thrombus was debrided from the ICD lead, and the lead was not extracted. He also had primary closure of the PFO with a patch repair. Repeat TEE showed an intact septum with no agitated saline crossing into the left atrium and no thrombus on lead. He was discharged on Coumadin and was later transitioned to aspirin 10 months later. He continued to do well and has been free of any neurovascular events.
Given the increasing number of patients with implanted cardiac devices, the frequent presence of lead-related thrombus, and the fact that one-quarter of the adult population have a PFO, the possibility that right-sided pacemaker and defibrillator leads increase the risk of cardioembolic stroke in patients with a PFO warrants consideration. In general, the stroke risk in patients with a PFO is probably low, but the exact incidence is unclear. Furthermore, whether closure of the PFO is superior to medical therapy with anticoagulation even in patients with recurrent stroke or TIA and PFO has not been clearly established. PFO closure versus medical management to prevent recurrent stroke was examined by Wahl et al., who found that patients with PFO closure had less risk of developing continued symptoms compared to patients treated with medical therapy. However, in the preliminary report of the CLOSURE1 trial, a randomized study to compare PFO closure to medical management in patients with prior cryptogenic stroke did not show a significant enough difference between these management options.[10, 12] However, the follow-up time was relatively short, averaging 2 years, and there have been some concerns about study patient selection.
We present four patients with a more complex and potentially higher risk situation, in which a PFO was present in the setting of endocardial leads with associated thrombus. Prior literature addressing the risk of endocardial leads in patients with a PFO is scarce. Agnelli et al. reported a case with endocardial pacemaker leads and a neurological event from infected emboli. Their patient also had closure of the PFO and removal of the infected lead. In contrast to our patient (#3) who may have benefited from earlier PFO closure, their earlier intervention of PFO closure along with device extraction likely prevented paradoxic embolization through the PFO. Although we cannot be completely certain as to the mechanism cardioembolism in our patients, the history and profile of the neurological and TEE findings strongly suggest paradoxical lead-related embolization through a PFO. Three of the four patients were on warfarin anticoagulation, had evidence of right-to-left shunting, echo-documented thrombi/debris on the intravascular leads, and clinical sequela consistent with thromboembolism.
Although the incidence of cardioembolic stroke in patients with intravascular leads is unknown, given the frequency with which PFO and lead-related thrombus occur, there is a pressing need for evaluating the exact risk of stroke in such patients. The implications of this possibility are far-reaching. If in fact there is an increased risk of cerebral thromboembolism with right-sided leads in patients with a PFO, then screening for PFO and possibly device closure of PFOs when implanting endovascular leads may be indicated. At present, in patients with known septal defects or other right-to-left shunts, endocardial lead placement is avoided, even when chronic warfarin is used, and an epicardial approach is preferred. In some cases, prior PFO device closure has been advised when the presence of a PFO has been previously documented. Certainly, patients with documented lead thrombus and PFO should have closure of their PFO. Our patients with relatively limited follow-up did well without stroke/TIA syndromes following PFO closure. However, without larger study of patients receiving intravascular leads with documented PFOs to compare intervention with conservative management, the positive effect of interventional PFO closure is unknown.
We present four patients with cerebrovascular embolic syndromes suggestive of intravascular lead thrombi-related paradoxical embolization through a PFO. Further study to evaluate the incidence of stroke in patients with intravascular leads and PFO and the benefit of PFO device closure is needed.
- 1Implantation of cardiac resynchronization devices. In: St. John Sutton M, Bax J, Jessup M, Brugada J, Schalij MJ (eds.): Cardiac Resynchronization Therapy. London, Informa Healthcare, 2007..
- 3Clinical significance of debris on pacemaker leads detected by transesophageal echocardiography (abstract). Europace 2000; 1:D239., et al.
- 9Extraction of implantable cardiac electronic devices. Curr Cardiol Rep 2011; 13:407–414., .
- 10Study design of the CLOSURE I Trial: A prospective, multicenter, randomized, controlled trial to evaluate the safety and efficacy of the STARFlex septal closure system versus best medical therapy in patients with stroke or transient ischemic attack due to presumed paradoxical embolism through a patent foramen ovale. Stroke 2010; 41:2872–2883., , , , , , , et al.