Fracture of Epicardial Resynchronization Lead Caused by Deceleration Injury
Angel L Fernández-González, MD,
José B García Bengochea, MD,
Joaquín Cortés Laíño, MD1,
Amparo Martínez Monzonis, MD2,
Sonia Veiras del Río, MD1,
Julian Alvarez Escudero, MD1
Division of Cardiac Surgery
1 Division of Anesthesiology
2 Division of Cardiology, University Hospital, University of Santiago de Compostela, Santiago de Compostela, Spain
Angel L Fernández-González, MD, Tel: +34 981 950212, Fax: +34 981 950227, Email: alfg{at}secardiologia.es, Division of Cardiac Surgery, University Hospital, Ave. Choupana, s/n, 15706 Santiago de Compostela, Spain.
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ABSTRACT
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A 50-year-old man with heart failure, systolic dysfunction, and abnormal septal motion underwent ventricular resynchronization. Postoperative clinical and echocardiographic improvement was observed. Several months later, he complained of worsening functional class after a traffic accident. Pacing lead fracture was diagnosed. After replacing the lead, improvement of clinical condition and ventricular parameters was achieved. The role of seat belts in causing dysfunction of pacemakers and resynchronization devices after deceleration injury is discussed.
Key Words: Accidents • Traffic • Defibrillators • Implantable
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INTRODUCTION
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Pacing lead fracture has been described after physical exertion, thoracic trauma, and acute arm stretching.1–3 The role of a seat belt in lead fracture due to motor vehicle accidents is unclear. We report the case of a seat belt user who presented with an epicardial lead fracture after deceleration injury in a car crash.
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CASE REPORT
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A 50-year-old man was referred to our hospital because of shortness of breath. An electrocardiogram demonstrated atrial fibrillation at a rate of 95 beats·min–1 and left bundle branch block with a QRS duration of 196 ms. Doppler echocardiography showed severe dilation of the left ventricle with an ejection fraction of 24% and paradoxical septal motion. Digoxin, angiotensin-converting enzyme inhibitors, diuretics, and oral anticoagulants were prescribed, and the patient was discharged. After 13 months of follow-up, the clinical status of the patient had not improved, so ventricular resynchronization was indicated. Two sutureless epicardial electrodes (ELC 54-UP; Biotronik, Germany) were implanted in the diaphragmatic surface of the left and right ventricles through an anterior extrapleural left subcostal approach. The electrodes were connected to a bipolar Y-adaptor (A1-CS; Biotronik) that was placed at the level of the left lower costal margin, and attached to a pulse generator (Kairos SR; Biotronik) in bipolar VVI mode. No sutures were inserted around the lead. The generator was placed in a pocket posterior to the muscle in the left rectus sheath, and programmed to a rate of 65 beats·min–1. Postoperative Doppler echocardiography showed disappearance of the paradoxical septal motion and a left ventricular ejection fraction of 32%. New York Heart Association functional class after the operation was I–II. Four months later, the patient was involved in a high-speed car crash while wearing a seat belt. He was referred to the casualty department. Skin abrasion was observed along the path of the seat belt, crossing from the right shoulder down to the abdomen. Chest radiography revealed fractures of the 4th and 5th left ribs. Electrocardiography showed atrial fibrillation at 58 beats·min–1 without pacemaker capture.
The patient refused hospital admission for further evaluation. Five weeks later, he returned to our hospital because of heart failure. His electrocardiogram showed absence of electrical stimulation despite magnet application and reprogramming to a higher pulse width and amplitude. A Doppler echocardiogram showed paradoxical septal motion and a left ventricular ejection fraction of 20%. A radiograph of the chest and upper abdomen showed the position of the leads and the generator (Figure 1A
). An amplified chest radiograph revealed a fracture in the lead at the level of the Y-adaptor (Figure 1B). The adaptor was surgically removed and replaced, confirming lead fracture without damage to the insulation of the lead (Figure 1C). The patient was discharged in a satisfactory clinical condition with optimal electrical stimulation after 3 days. A repeat Doppler echocardiogram demonstrated adequate ventricular resynchronization.
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Figure 1. (A) Plain radiograph of the chest and upper abdomen. The Y-adaptor is positioned at the level of the left lower costal margin (arrow). Arrowhead indicate previous rib fractures; (B) Oblique chest radiograph revealing a fracture of the pacing lead adaptor (arrow), which is more apparent when the image is enlarged; (C) The bipolar Y-adaptor after being removed, showing a fracture (arrow) that is more apparent when the image is enlarged.
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DISCUSSION
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Acute pacemaker dysfunction has been related to blunt thoracic trauma, car accidents being the most common cause compared to other forms of transportation. Pacing lead fracture or dislodgement and generator failure are possible mechanisms of pacing dysfunction after blunt injury.1,4 Our patient was found to have a heart rate of 58 beats·min–1 immediately after the accident. As he refused further examination, stimulation failure was not diagnosed at this time because he was not rate-dependent and chest radiography did not visualize the fractured lead.
The role of wearing seat belt on pacemaker pocket injury during traffic accidents has been widely documented.5 However, the effect of a seat belt on lead fracture after a deceleration injury has not been described. Although it is not possible to definitively ascertain the mechanism of the lead fracture in this case, compression by the seat belt on the left subcostal space generated by sudden deceleration appears to have been the cause.
In view of the large number of patients requiring cardiac stimulation either for pacing or resynchronization, awareness of the possibility of trauma-related malfunction is necessary when caring for chest trauma patients with this sort of device.
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REFERENCES
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- Grieco JG, Scanlon PJ, Pifarré R. Pacing lead fracture after a deceleration injury. Ann Thorac Surg 1989;47:453–4.[Abstract/Free Full Text]
- Sakakibara Y. Delayed pinpoint exposure of a pacemaker following seat belt trauma. Pacing Clin Electrophysiol 1997;20:370–1.[Medline]
- Saha A, Tan J, Prendergast B. Pacemaker lead fracture. Heart 2003;89:783.[Free Full Text]
- Gould L, Betzu R, Taddeo M, Judge JD, Lee J. Pulse generator failure due to blunt trauma. Clin Cardiol 1988;11:581–2.[Medline]
- Schuger CD, Mittleman R, Habbal B, Wagshal A, Huang SK. Ventricular lead transaction and atrial lead damage in a young softball player shortly after the insertion of a permanent pacemaker. Pacing Clin Electrophysiol 1992;15:1236–9.[Medline]
Asian Cardiovasc Thorac Ann 2010;
18:77-78
© 2010 by SAGE Publications
DOI: 10.1177/0218492309354388
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ABSTRACT
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