Di cư trong buồng tim của stent TIPS gây nhịp nhanh thất

Abstract

Intracardiac migration of a transjugular intrahepatic portosystemic shunt (TIPS) stent is a rare but potentially life-threatening complication. A 52-year-old man developed asymptomatic nonsustained ventricular tachycardia within 24 hours of elective TIPS creation. Echocardiography demonstrated a migrated TIPS bare-metal stent segment protruding into the right ventricle and interacting with the tricuspid valve. The stent was retrieved endovascularly using balloon and snare techniques via dual venous access under echocardiographic and fluoroscopic guidance. Arrhythmias resolved after stent removal. This case highlights the importance of early post-TIPS monitoring and prompt endovascular intervention for intracardiac stent migration presenting with ventricular arrhythmias.

Background

Transjugular intrahepatic portosystemic shunt (TIPS) is a well-established therapy for complications of portal hypertension, including refractory variceal bleeding and recurrent ascites 1. Although generally safe, complications include vascular injury, hemorrhage, biliary trauma, hepatic encephalopathy, and shunt dysfunction 2, 3.

Stent migration is rare but clinically significant. Cranial migration into the inferior vena cava, right atrium, or right ventricle may lead to arrhythmias; valvular injury, such as tricuspid leaflet or chordal damage with regurgitation; myocardial perforation with tamponade; intracardiac thrombosis with potential pulmonary embolism; and hemodynamic compromise. In rare cases, it may serve as a nidus for infection leading to endocarditis or sepsis 2, 4. Management includes observation, endovascular retrieval, or surgery depending on presentation 5.

We report a case of right ventricular migration of a TIPS stent causing nonsustained ventricular tachycardia requiring urgent endovascular retrieval.

Case Report

A 52-year-old man with alcoholic cirrhosis complicated by portal hypertension and esophageal varices presented for elective transjugular intrahepatic portosystemic shunt (TIPS) creation for refractory large-volume ascites requiring monthly paracentesis, with recent outputs approaching 20 L per session. He did not report recent jaundice, abdominal pain, fever, altered mental status, decreased urine output, or positional dyspnea. Physical examination revealed a tense and distended abdomen with dullness to percussion.

Preprocedural right upper quadrant ultrasound showed cirrhotic liver morphology with coarse echotexture, surface nodularity, and large-volume ascites that limited evaluation. Cirrhosis was established based on alcohol use and imaging, and a liver biopsy was never performed. Cytologic analysis of ascitic fluid from prior paracenteses was negative for malignancy. Initial vital signs were temperature, 98.1°F (36.7°C); heart rate, 77 beats/min; respiratory rate, 18 breaths/min; blood pressure, 99/56 mm Hg; and oxygen saturation, 96% on room air. Hypotension was attributed to cirrhosis-associated vasodilatory physiology and the patient received 25 g of intravenous 25% albumin with midodrine, 5 mg for hemodynamic support before the procedure.

Laboratory results were pertinent for a hemoglobin level of 11.2 g/dL (reference range, 13.5–17.5), platelet count of 102 × 10³/µL (reference range, 150–450), albumin level of 2.6 g/dL (reference range, 3.5–5.0), total bilirubin level of 3.4 mg/dL (reference range, 0.1–1.2), direct bilirubin level of 0.77 mg/dL (reference range, 0.0–0.3), alkaline phosphatase level of 59 U/L (reference range, 40–129), aspartate aminotransferase level of 53 U/L (reference range, 10–40), alanine aminotransferase level of 34 U/L (reference range, 7–56), international normalized ratio of 1.7 (reference range, 0.8–1.2), partial thromboplastin time of 43.5 seconds (reference range, 25–35), sodium level of 132 mmol/L (reference range, 135–145), and creatinine level of 0.7 mg/dL (reference range, 0.6–1.3). Prior viral hepatitis serologies and autoimmune markers—including antinuclear antibody, anti–smooth-muscle antibody, anti–liver kidney microsomal antibody, and antimitochondrial antibody—were noncontributory. The patient’s Model for End-Stage Liver Disease–Sodium (MELD-Na) score at the time of TIPS creation was 22.

A reflux carbon dioxide venogram was performed, and a right hepatic vein to right portal vein TIPS was created using a 10-mm × 8-cm Gore Viatorr stent. Two additional Medtronic Protégé GPS 10-mm × 4-cm bare-metal stents were deployed in an overlapping fashion to lengthen the shunt and extend it superiorly to the hepatocaval junction. All stents were postdilated using a 10-mm balloon. Completion venography confirmed brisk flow through the portal venous system and the newly created shunt (Figure 1).

During overnight telemetry monitoring, the patient had 5 episodes of non-sustained ventricular tachycardia (NSVT), with the longest run showing 9 beats (Figure 2). Electrocardiography showed normal sinus rhythm with isolated polymorphic premature ventricular contractions. The cardiology team was consulted and a transthoracic echocardiogram revealed a 4.5- × 1.3-cm echobright prosthetic object in the right ventricle adjacent to the tricuspid valve consistent with a migrated Medtronic Protégé GPS bare-metal stent (Figure 3), normal biventricular size and function, and mild tricuspid regurgitation. The patient was transferred to the intensive care unit for closer monitoring and scheduled for urgent retrieval to prevent distal embolization or malignant ventricular arrhythmia.

Under general anesthesia with transesophageal echocardiogram (TEE) monitoring, 10-Fr access was obtained via the right internal jugular and right femoral veins. The TEE revealed the migrated stent extending into the right ventricle with interaction with the tricuspid valve and bidirectional free blood flow through the stent. A guidewire was advanced from the internal jugular access and placed through the stent under fluoroscopy and TEE guidance. A 14-mm high-pressure angioplasty balloon was inflated within the stent to anchor it and the assembly was withdrawn into the superior vena cava. The guidewire was then snared and removed through the femoral access. The stent was navigated into the inferior vena cava and the right external iliac vein using the balloon, which was then deflated and removed. A cloverleaf snare was used to capture the distal end of the stent. During withdrawal through the femoral sheath, the stent fractured and was removed in 2 parts via femoral and internal jugular access. Both fragments were retrieved without surgical cutdown or venotomy enlargement. Completion imaging showed no residual fragments (Figure 4). The patient returned to the intensive care unit and had no further arrhythmias.

Discussion

Several reports describe stent migration into the right atrium or ventricle with variable outcomes, including failed endovascular retrieval, severe tricuspid regurgitation, or asymptomatic retention until transplantation 6–8. Asymptomatic endothelialization of a migrated fractured stent segment into the pulmonary artery has also been reported 9. In our patient, the migrated stent segment directly abutted the right ventricular wall, provoking NSVT and multifocal ectopy, highlighting how mechanical irritation can precipitate arrhythmias.

Extension of the TIPS to the hepatocaval junction is recommended to improve long-term patency 10, though proximity to the cavoatrial junction may complicate future hepatectomy, and optimal positioning is often guided by institutional preference. In our case, use of multiple overlapping bare-metal stents with possible insufficient overlap may have contributed to stent instability and migration 11. Use of a single appropriately sized extension stent with adequate overlap (≥1 cm) can mitigate this risk.

Additional mechanisms of stent dislodgement include increased portal venous flow after TIPS creation generating shear forces on an inadequately anchored stent as well as negative intrathoracic pressure during respiration facilitating cephalad migration into the right atrium or ventricle. Other factors include improper stent sizing, suboptimal deployment, and vascular remodeling, which may predispose to delayed migration.

Management depends on symptom severity and stent location. Asymptomatic patients can be managed conservatively, whereas arrhythmia warrants urgent intervention. Endovascular retrieval is increasingly recognized as safe and effective, avoiding the morbidity of open cardiac surgery (5, 11, 12). In our patient, successful retrieval was achieved using combined balloon and snare techniques through dual venous access under TEE guidance. Compared with snare or forceps retrieval alone, the use of a balloon catheter coaxial with the stent limited exposure of the tricuspid valve leaflets to the edges of the stent, protecting them from trauma during retrieval. Transesophageal echocardiography provided real-time assessment of valve function and guided safe extraction without embolization or surgical intervention. Resolution of arrhythmias following removal supports a causal relationship between the migrated stent and ventricular tachycardia.

Intracardiac migration of a TIPS stent is a rare but potentially life-threatening complication that may present with arrhythmias or remain clinically silent. This case highlights the importance of vigilant postprocedural monitoring, prompt diagnosis with echocardiography, and early multidisciplinary management. When feasible, endovascular retrieval offers a safe and effective alternative to open surgery, and timely intervention is essential to prevent catastrophic outcomes. Careful procedural planning and postprocedural surveillance are critical to ensuring patient safety.