Lead-Related Superior Vena Cava Syndrome Resulting in Downhill Esophageal Varices: Resolution Following Pacemaker Lead Removal

Lead-Related Superior Vena Cava Syndrome Resulting in Downhill Esophageal Varices: Resolution Following Pacemaker Lead Removal | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 3 August 2025 V1 Latest version Share on Lead-Related Superior Vena Cava Syndrome Resulting in Downhill Esophageal Varices: Resolution Following Pacemaker Lead Removal Authors : Linfeng Freeman Peng 0009-0000-3337-9684 [email protected] , Dandan Yang , and Xuebin Li Authors Info & Affiliations https://doi.org/10.22541/au.175420091.18513542/v1 195 views 131 downloads Contents Abstract Introduction Case Presentation Discussion Conclusion Figure and Figure Legends Supplementary Material References Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Abstract Introduction : Superior vena cava (SVC) syndrome, traditionally linked to malignancy, is increasingly caused by indwelling pacemaker leads and may lead to downhill esophageal varices. The pathophysiology involves a combination of endothelial injury, thrombosis, and fibrosis. Methods and Results : A 68-year-old man with an 18-year-old dual-chamber pacemaker presented with facial swelling and varices. Intracardiac echocardiography and venography confirmed severe lead-related SVC stenosis. We performed laser-assisted lead extraction, balloon angioplasty, and leadless pacemaker implantation, achieving immediate symptom resolution and sustained relief at eight months. Conclusion : Combining lead extraction, angioplasty, and leadless pacemaker implantation is a safe, effective definitive treatment for pacemaker-induced SVC syndrome. Intracardiac echocardiography (ICE) is an invaluable tool for precise diagnosis and procedural planning. Key Words : superior vena cava syndrome, esophageal varices, pacemaker, lead extraction, intracardiac echocardiography, case report DD MMMM YYYY \acceptedDD MMMM YYYY Introduction Superior vena cava (SVC) syndrome encompasses a group of signs and symptoms caused by the obstruction of blood flow through the SVC (Wilson, 2007). The classic clinical presentation includes facial and neck edema, dyspnea, and the development of dilated collateral veins on the chest wall (Rice, 2006). Historically, malignancy, particularly bronchogenic carcinoma and lymphoma, has been the predominant cause, accounting for the majority of cases (Rice, 2006; Yellin, 1990). However, the etiologic landscape of SVC syndrome has evolved over the past few decades (Straka, 2016). There is a rising incidence of benign, or non-malignant, causes, which are now responsible for a substantial proportion of cases (Rizvi, 2008; Kalra, 2003). This shift is largely attributed to the widespread use of intravascular devices, such as central venous catheters for hemodialysis and, notably, transvenous cardiac implantable electronic device (CIED) leads (Rice, 2006; Barakat, 2000). Pacemaker-induced SVC syndrome, though considered a rare complication, is a well-documented phenomenon (Goudevenos, 1989; Fu, 2014). The pathophysiology is multifactorial, involving chronic endothelial trauma from the indwelling leads, which incites an inflammatory response, subsequent fibrosis, and often superimposed thrombosis, ultimately leading to venous stenosis or occlusion (Kokotsakis, 2014; Dimitrakakis, 2012). Chronic SVC obstruction forces venous return from the upper body to find alternative routes to the right atrium. This leads to the formation of extensive collateral pathways, which can manifest in unusual ways. One such rare manifestation is the development of ”downhill” esophageal varices. Unlike the more common ”uphill” varices associated with portal hypertension, downhill varices are located in the proximal to mid-esophagus and result from retrograde blood flow from the obstructed SVC through the azygos and esophageal venous plexuses towards the portal system (Lopes, 2023; Hein, 2022). While bleeding from downhill varices is uncommon, it can be a life-threatening event (Tavakkoli, 2006; Pashankar, 1999). The management of lead-related SVC syndrome is complex and lacks a standardized protocol (Yu, 2008). Treatment strategies have evolved from conservative medical management to more definitive endovascular and surgical interventions (Straka, 2016). In patients with CIED-induced SVC syndrome, addressing the underlying cause—the leads themselves—is paramount. In this paper, we present a case of a 68-year-old male with severe, symptomatic SVC syndrome and downhill esophageal varices caused by pacemaker leads implanted 18 years prior. We describe a successful, definitive treatment strategy involving complete transvenous lead extraction, balloon angioplasty for SVC reconstruction, and implantation of a leadless pacemaker. We also highlight the crucial role of intracardiac echocardiography (ICE) in diagnosing and guiding the management of this complex condition. DD MMMM YYYY \acceptedDD MMMM YYYY Case Presentation A 68-year-old male was referred to the gastroenterology clinic for the evaluation of abdominal varices that had been incidentally noted on imaging two months prior. A subsequent gastroscopy confirmed the presence of prominent downhill esophageal varices (Panel A) . The patient also reported a nine-month history of progressively worsening facial swelling and a sensation of fullness in the head, particularly upon exertion. This was accompanied by a gradual decline in his hearing. His past medical history was significant for a high-grade atrioventricular block, for which a permanent dual-chamber pacemaker had been implanted via the left subclavian vein 18 years earlier. The pulse generator had been replaced six years ago. He had no known history of malignancy, prior thoracic radiation, or conditions associated with fibrosing mediastinitis. He was on rivaroxaban for atrial fibrillation, but this had not alleviated his symptoms. On physical examination, the patient exhibited marked erythema and non-pitting edema of the face, neck, and upper chest. There were diffuse, serpentine varicosities visible across his anterior chest and upper abdomen, consistent with extensive venous collateralization (Panel B) . His jugular veins were significantly distended. Given the clinical picture of severe SVC obstruction, a diagnostic workup was initiated. Phlebography performed via bilateral upper extremity access revealed severe stenosis extending from the left brachiocephalic vein through the SVC to the cavoatrial junction. The imaging demonstrated an extensive network of collateral veins in the neck and superior mediastinum, which drained inferiorly via the azygos and internal mammary systems (Panel C) . A pullback pressure measurement from the SVC to the right atrium (RA) was performed, revealing a significant mean pressure gradient of approximately 20 mmHg, confirming severe hemodynamic obstruction (Panel D) . After a multidisciplinary team discussion involving electrophysiology, interventional cardiology, and cardiothoracic surgery, a comprehensive treatment plan was formulated. The strategy aimed to address both the obstruction and the ongoing need for cardiac pacing. The plan included: (1) laser-assisted transvenous extraction of the chronic pacemaker leads, (2) reconstruction of the SVC with balloon angioplasty, and (3) implantation of a leadless pacemaker to avoid future lead-related complications. During the procedure, intracardiac echocardiography (ICE) was utilized to guide the intervention. The ICE probe, positioned in the right atrium, provided exceptional visualization of the cavoatrial junction. It revealed dense, hyperechoic tissue proliferation encapsulating the pacemaker leads within the SVC segment, resulting in severe luminal stenosis (Panels E and F, arrow) . Color Doppler imaging across the stenotic segment showed a high-velocity, turbulent jet, appearing as a color mosaic pattern, which further confirmed the severity of the obstruction (Panel E) . Following the successful laser-assisted extraction of both the atrial and ventricular leads, balloon angioplasty of the stenotic SVC and brachiocephalic vein was performed, which successfully restored luminal diameter. A VVI leadless pacemaker was then implanted in the right ventricle without complication. The patient experienced a dramatic and immediate improvement in his symptoms. The facial swelling and erythema resolved completely within 24 hours of the procedure. At an 8-month follow-up visit, he remained entirely symptom-free, with no recurrence of facial edema or other signs of venous congestion. Discussion This case highlights a rare but severe complication of a common medical device: pacemaker-induced SVC syndrome presenting with downhill esophageal varices. The successful outcome underscores the efficacy of a modern, multidisciplinary approach that prioritizes definitive treatment of the underlying cause. Several aspects of this case merit further discussion in the context of the existing literature. Pathophysiology and Clinical Spectrum of Lead-Induced SVC Syndrome The presence of transvenous leads in the central veins is not benign. The leads act as a foreign body, inducing a chronic inflammatory response and endothelial injury that can lead to fibrosis, thrombosis, or both (Kokotsakis, 2014). The risk of venous obstruction is influenced by factors such as the number of leads, lead diameter, history of infection, and the duration of implantation (Goudevenos, 1989). In our patient, the 18-year duration of the leads was likely the primary contributor to the development of extensive fibrosis. The clinical presentation of lead-related SVC syndrome can range from asymptomatic venous stenosis, found incidentally on imaging, to the severe, debilitating symptoms seen in our patient (Rice, 2006). A particularly unusual manifestation of this condition is the development of downhill esophageal varices, as seen in our case. These varices form as a major collateral pathway to bypass the obstructed SVC, shunting venous blood from the head, neck, and upper extremities caudally through the esophageal plexus into the azygos system and eventually the inferior vena cava (Greenwell, 2007). While they bleed less frequently than uphill varices from portal hypertension, the risk is not negligible and can lead to significant gastrointestinal hemorrhage (Lopes, 2023). The presence of these varices in our patient underscores the severity and chronicity of his SVC obstruction. Diagnostic Evaluation: The Role of Intracardiac Echocardiography The diagnosis of SVC syndrome is typically confirmed with imaging. While contrast venography remains the gold standard for delineating the anatomy of the obstruction and collateral pathways, as performed in our case, other modalities are also crucial (Goudevenos, 1989). Computed tomography (CT) provides excellent anatomical detail of the mediastinum and can help rule out extrinsic compression from malignancy (Wilson, 2007). This case particularly highlights the value of intracardiac echocardiography (ICE). While not traditionally a first-line diagnostic tool for SVC syndrome, its use during the interventional procedure was invaluable. ICE provided real-time, high-resolution images of the lead-endothelium interface, clearly demonstrating that the obstruction was caused by dense, organized fibrotic tissue encapsulating the leads rather than a simple thrombus. This level of detail is superior to that provided by fluoroscopy alone and was critical for planning the extraction and angioplasty strategy. The ability to visualize the stenosis and assess the hemodynamic consequences with color Doppler in real-time makes ICE a powerful tool for managing complex lead-related venous obstructions. Management Strategy: Lead Extraction, Angioplasty, and Leadless Pacing The management of symptomatic, benign SVC syndrome has shifted towards endovascular intervention (Rizvi, 2008). In cases caused by CIED leads, the optimal strategy involves addressing the source of the problem. We strongly advocate for the complete removal of the offending transvenous leads as the cornerstone of therapy. Modern transvenous lead extraction techniques, including the use of laser sheaths, have made the removal of even old, heavily fibrosed leads a safe and feasible procedure when performed by experienced operators with surgical backup (Fu, 2014). Following lead extraction, the residual fibrotic stenosis must be addressed. The two main options are balloon angioplasty and stent placement. While many reports advocate for primary stenting as a durable solution (Kee, 1998; Lanciego, 2001), our case demonstrates that after the removal of the chronic nidus of inflammation (the leads), simple balloon angioplasty can be sufficient to achieve an excellent and durable result. This approach avoids implanting a permanent metal stent, which can have its own long-term complications, such as fracture, migration, or in-stent restenosis. The decision to stent should be reserved for cases with significant elastic recoil or residual obstruction after angioplasty. Finally, the advent of leadless pacemaker technology represents a paradigm shift for patients requiring pacing after the extraction of a conventional system (Tan, 2023). By implanting a leadless device, we provided our patient with reliable pacing while completely eliminating the risk of recurrent lead-related venous obstruction (Ekizler, 2018). This ”leave nothing behind” strategy in the central veins is the most logical approach to prevent future complications in this patient population. Conclusion Pacemaker-induced superior vena cava syndrome is a rare but serious condition that can lead to debilitating symptoms and unusual manifestations such as downhill esophageal varices. This case illustrates that a definitive and curative approach is not only possible but should be the goal of therapy. A multidisciplinary strategy combining advanced diagnostic imaging like intracardiac echocardiography with a therapeutic intervention centered on complete transvenous lead extraction, balloon angioplasty, and subsequent implantation of a leadless pacemaker offers a safe, effective, and durable solution. This approach directly addresses the pathophysiology of the disease and prevents recurrence, providing patients with complete and lasting symptom relief. Early recognition and referral to a specialized center with expertise in complex lead management are critical for achieving optimal outcomes. Figure and Figure Legends Panel A: Gastroscopy image showing large, tortuous ”downhill” varices in the proximal esophagus. Panel B: Clinical photograph of the patient’s chest and abdomen, demonstrating extensive and dilated superficial collateral veins. Panel C: Digital subtraction venogram showing severe stenosis of the superior vena cava with extensive collateral vessel formation in the superior mediastinum. Panel D: Hemodynamic pressure tracing obtained during catheter pullback from the superior vena cava to the right atrium, demonstrating a mean pressure gradient of approximately 20 mmHg across the stenosis. Panel E: Intracardiac echocardiography (ICE) image with color Doppler, showing the stenotic superior vena cava lumen. The color mosaic pattern indicates high-velocity, turbulent blood flow through the narrowed segment caused by fibrotic tissue surrounding the pacemaker leads. Panel F: Two-dimensional intracardiac echocardiography (ICE) image showing the chronic pacemaker leads encased in dense, fibrotic tissue, causing severe narrowing of the superior vena cava at the junction with the right atrium. Supplementary Material File (image5.emf) Download 14.17 MB References 1. Wilson, L, Detterbeck, F, & Yahalom, J (2007). Superior Vena Cava Syndrome with Malignant Causes. New England Journal of Medicine , 356 (18), 1862-1869. https://doi.org/10.1056/nejmcp067190 Crossref Google Scholar 2. Rice, T, Rodriguez, R, & Light, R (2006). The Superior Vena Cava Syndrome. Medicine , 85 (1), 37-42. https://doi.org/10.1097/01.md.0000198474.99876.f0 Crossref Google Scholar 3. 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Journal of Innovations in Cardiac Rhythm Management , 10 (9), 3312-3314. https://doi.org/10.19102/icrm.2018.090902 Crossref Google Scholar Information & Authors Information Version history V1 Version 1 03 August 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords clinical: cardiac mapping – intracardiac echo clinical: implantable devices – biventricular pacing/defibrillation clinical: implantable devices – lead implantation/extraction Authors Affiliations Linfeng Freeman Peng 0009-0000-3337-9684 [email protected] Peking University Health Science Center View all articles by this author Dandan Yang Peking University People's Hospital View all articles by this author Xuebin Li Peking University People's Hospital View all articles by this author Metrics & Citations Metrics Article Usage 195 views 131 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Linfeng Freeman Peng, Dandan Yang, Xuebin Li. Lead-Related Superior Vena Cava Syndrome Resulting in Downhill Esophageal Varices: Resolution Following Pacemaker Lead Removal. Authorea . 03 August 2025. DOI: https://doi.org/10.22541/au.175420091.18513542/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu . 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