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Sinus Arrest Following Angioplasty and Stenting for Superior Vena Cava Syndrome

Michael Tempelhof, MD1,2, Joseph Campbell, MD2, Leonard Ilkhanoff, MD, MS,1,2,3

Michael Tempelhof, MD1,2, Joseph Campbell, MD2, Leonard Ilkhanoff, MD, MS,1,2,3

ABSTRACT: Superior vena cava (SVC) syndrome is a complication resulting from long-term residence of leads or in-dwelling catheters at the SVC to right atrial (RA) junction. SVC syndrome management is complicated by variable responses to anticoagulation therapies and technically challenging interventional procedures, such as balloon dilatation or stent placement at the SVC-RA junction to relieve blood-flow obstruction. Potential complications resulting from angioplasty/stenting for SVC syndrome are serious and include stent migration, major bleeding, and embolism.  Bradyarrhythmias have not been reported.

We describe a case of balloon angioplasty and stenting for SVC syndrome in a dialysis patient that resulted in sinus arrest. The complication developed within hours of angioplasty/stenting of her chronic, non-thrombotic SVC obstruction. We highlight the management approach to this patient and discuss potential mechanisms underlying the complication.

J INVASIVE CARDIOL 2014;26(2):E21-E23

Key words: bradycardia, sinus arrest, superior vena cava (SVC) syndrome, stenting

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Superior vena cava (SVC) syndrome is a complication resulting from long-term residence of leads or in-dwelling catheters at the SVC to right atrial (RA) junction.1 Through an inflammatory process, in-dwelling catheters cause vascular narrowing and obstruction of blood flow, resulting in venous engorgement, extremity swelling, plethora, and in rare cases, death.2 SVC syndrome management is complicated by variable responses to anticoagulation therapies and technically challenging interventional procedures, such as balloon dilatation or stent placement at the SVC-RA junction to relieve blood-flow obstruction.3 Potential complications resulting from angioplasty/stenting for SVC syndrome are serious and include stent migration, major bleeding, and embolism.4 Bradyarrhythmias have not been reported.

We describe a case of balloon angioplasty and stenting for SVC syndrome in a dialysis patient that resulted in sinus arrest. The complication developed within hours of angioplasty/stenting of her chronic, non-thrombotic SVC obstruction. We highlight the management approach to this patient and discuss potential mechanisms underlying the complication.

Case Report

An 80-year-old female presented for evaluation of progressive, extensive, right-upper extremity swelling and facial plethora. The patient’s medical history was notable for end-stage renal disease on hemodialysis, hypertension, non-obstructive coronary artery disease, and a chronic total occlusion of the left internal jugular and left brachiocephalic veins from prior in-dwelling lines related to dialysis. Admission electrocardiogram (ECG) demonstrated normal sinus rhythm with first-degree atrioventricular delay (PR 210 msec) and non-specific intraventricular conduction delay (Figure 1).

Due to the patient’s presenting symptoms and the clinical concern for SVC syndrome, contrast-enhanced computed tomography (CT) was performed, revealing a non-thrombotic occlusion of the SVC near the RA junction with prominent chest wall and abdominal venous collateralization. Despite chronic anticoagulation therapy, right-upper extremity swelling progressed. Therefore, SVC angioplasty and stenting were recommended and successfully performed with 2 overlapping 20 mm Z stents (Cook Medical) deployed at the SVC-RA junction, with postdilatation to 16 mm (Figure 2). After initial dilatation of the angioplasty balloon, sinus arrest was noted transiently, but resolved after balloon relaxation.  Atropine was initially given when sinus arrest was noted with maintenance of sinus rhythm. No vessel dissection or injury was noted.

Within several hours of the procedure, however, the patient developed sinus arrest with junctional bradycardia at 45 bpm, with hemodynamic compromise. Several doses of atropine failed to enhance sinus node activity; therefore, a dopamine infusion was initiated with improvement of blood pressure and an increase in the junctional rate. Cardiac monitoring while on dopamine infusion showed persistent junctional bradycardia, with heart rates of 50-55 bpm and no ECG evidence of myocardial ischemia. Transthoracic echocardiogram demonstrated an ejection fraction of 65% with normal left ventricular wall motion, right ventricular function, and no evidence of pericardial effusion. No acute evidence of bleeding was noted. No pulmonary embolism was detected after CT scan was performed. Laboratory findings, including white blood cell count, hemoglobin, electrolytes and cardiac enzymes (troponin T and creatine kinase/CK-MB), were normal. Sedation had resolved.

Sinus node activity recovered about 48 hours after the angioplasty/stenting procedure. The dopamine infusion was weaned and the patient remained in sinus rhythm throughout the hospital stay.  She was discharged several days later without clinical deterioration or complications. Twelve-month follow-up exam and regular rhythm evaluations at hemodialysis continue to demonstrate sinus rhythm.

Discussion

The development of sinus arrest has not been described as a complication of angioplasty and stenting for SVC syndrome.

Potential mechanisms. There are several potential mechanisms worth considering. First, patient characteristics likely contributing to this complication include advanced age, prior instrumentation with resulting SVC stenosis, and underlying comorbidities. Second, the initial sinus arrest noted at the time of the angioplasty balloon dilatation was likely secondary to sinus node stretch or pressure, as immediate restoration of sinus rhythm occurred after balloon relaxation and with administration of atropine. Balloon angioplasty and stenting at the SVC-RA junction creates significant mechanical and radial stress on adjacent tissue and structures, especially in narrow or stenosed vascular beds. Given the proximity of the sinus node to the SVC-RA junction, it seems plausible that the sinoatrial node was adversely affected by the mechanical trauma associated with balloon inflation and subsequent stent placement. We cannot fully explain the delayed sinus arrest noted in this case, as one may have expected the sinus node to be equally vulnerable to mechanical stretch from stent dilatation. However, there may have been a more delayed perturbation to the sinus node following stent positioning. Although not previously reported to occur in the SVC or RA vasculature, perivascular inflammation is known to occur following stent deployment in other vascular beds.5-6 It is possible that the mechanical stress on the sinus node region triggered a similar inflammatory process that ultimately affected sinus node function or its autonomic inputs. Prior reports using magnetic resonance imaging demonstrate that vascular bed inflammation and edema following large vessel stenting manifest several hours post procedure, and subsequently may resolve.5 This transient, inflammatory state of the sinus node region could, in theory, explain the delayed onset and reversible nature of the sinus arrest noted in our patient. Third, the autonomic inputs to the sinus node could be transiently disrupted by the inflammatory state following stent dilatation, which may also have contributed to the bradyarrhythmia noted in our patient.

Potential interventions. Pacemaker implantation for hemodynamically significant bradycardia was considered. However, medical management with dopamine infusion stabilized the patient’s hemodynamic status. The eventual restoration of sinus rhythm highlights an important role for ongoing rhythm monitoring in select angioplasty and stenting cases for SVC syndrome, and the potential for sinus arrest reversibility.  Judicious monitoring and supportive care obviated the need for permanent pacemaker implantation in this case.

An increasing number of patients receive pacemakers, defibrillators, and in-dwelling catheters for a variety of indications. As a result, a greater proportion of patients may be susceptible to SVC syndrome. As interventional therapies to treat SVC syndrome become more prevalent,7 greater recognition of interventional complications related to SVC syndrome is warranted.  SVC stenting with or without predilatation angioplasty is currently recommended as a definitive therapy for SVC syndrome.4  Although periprocedural arrhythmias following SVC stenting have been previously reported,8-12  in our experience, this is the first case report of an association between a high-risk bradyarrhythmia and angioplasty/stenting of the SVC.

Although an uncommon occurrence, sinus arrest with junctional bradycardia following SVC stenting can have dramatic consequences, including hypotension and impaired end-organ perfusion. Currently, there are no recommendations or guidelines outlining the duration of telemetry monitoring of patients following balloon dilation and stenting for SVC syndrome. Although we cannot universally advocate routine cardiac monitoring following such interventions, prudent cardiac monitoring following SVC stenting seems warranted, especially for elderly patients and other high-risk patients, including those who develop intraprocedural bradyarrhythmias. 

References

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From the 1Department of Medicine, 2Division of Cardiology, and 3Section of Electrophysiology, Northwestern Memorial Hospital, Northwestern University, Chicago, Illinois.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted July 5, 2013, provisional acceptance given August 19, 2013, final version accepted August 27, 2013.

Address for correspondence: Leonard Ilkhanoff, MD, MS, Assistant Professor, Northwestern University, 251 East Huron Street, Feinberg 08-503, Chicago, IL 60611. Email: l-Ilkhanoff@northwestern.edu

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