Asian Cardiovasc Thorac Ann 2008;16:e58-e59
© 2008 Asia Publishing EXchange Ltd
Graft Replacement for Massive Mobile Embolic Source in Brachiocephalic Artery
Yasuhisa Oishi, MD,
Nana Hirahara, MD,
Toru Takaseya, MD,
Takemi Kawara, MD,
Masahiro Yasaka, MD1,
Shigeki Morita, MD
Department of Cardiovascular Surgery
1 Cerebrovascular Center and Clinical Research Institute, National Hospital Organization, Kyushu Medical Center, Fukuoka, Japan
For reprint information contact: Yasuhisa Oishi, MD Tel: 81 92 642 5557 Fax: 81 92 642 5566 Email: yooo{at}heart.med.kyushu-u.ac.jp. Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
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ABSTRACT
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A 76-year-old woman presented with multiple brain infarctions in the right middle cerebral artery and vertebral artery area. Carotid sonography revealed a large mobile pedunculated mass in the brachiocephalic artery, which showed rapid growth despite treatment with heparin and aspirin. Graft replacement of the brachiocephalic artery was performed under selective cerebral perfusion with deep hypothermia. Histology of the resected specimen revealed aortic atherosclerotic plaque.
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INTRODUCTION
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Surgery for a mobile embolic source in the aortic arch is extremely rare. We describe a case of recurrent ischemic stroke caused by atherosclerotic plaque, which was difficult to diagnose preoperatively.
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CASE REPORT
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A 76-year-old woman with history of hypertension, hypercholesterolemia, and brain infarction was admitted on an emergency basis to the Stroke Care Unit in Kyushu Medical Center because of worsening dizziness and vomiting. Brain magnetic resonance imaging (MRI) showed multiple infarctions in the right middle cerebral artery and vertebral artery areas. Transesophageal echocardiography did not demonstrate any embolic source in the heart. Routine carotid sonography indicated only small plaques in the bilateral common carotid arteries, however, a large mobile pedunculated mass at the take-off of the brachiocephalic artery was revealed in the upper sternal window (Figure 1A
). The mass measured 8.5 x 7.6 mm initially, and gradually increased to 17.3 x 7.8 mm despite 3 weeks of anticoagulation therapy with heparin (Figure 1B). Recurrent brain infarctions in the right middle cerebral artery and vertebral artery areas were detected on repeat MRI. Electrocardiography showed normal sinus rhythm. A Holter electrocardiogram determined only premature atrial contractions and monofocal premature ventricular contractions. Calcifications of the aortic arch were noted on chest computed tomography. From these findings, we suspected that the mass was probably a primary tumor. We operated under cardiopulmonary bypass, deep hypothermia, and selective cerebral perfusion with 8-mm woven Dacron grafts, which anastomosed to the axillary arteries bilaterally. The brachiocephalic artery was replaced with a 40-mm length of 10-mm diameter woven Dacron graft, using 5/0 Prolene. Intraoperative inspection revealed an ulcerated atherosclerotic plaque in the brachiocephalic artery (Figure 2). The diagnosis was confirmed by histopathological examination. No thrombus or tumor was found. The patient’s postoperative course was complicated by transient disturbances of consciousness and left hemiplegia, however, she recovered to her preoperative state. Postoperative MRI did not show any new findings compared to the preoperative MRI. Carotid sonography revealed only small plaques in the bilateral common carotid arteries, as seen preoperatively.
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Figure 1. Carotid sonography showing (A) a mobile mass (8.5 x 7.6 mm) in the brachiocephalic artery, and (B) the same mass after 3 weeks of anticoagulant treatment.
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Figure 2. Intraoperative appearance of the brachiocephalic artery; a large fragile atherosclerotic plaque was seen at the take-off of the brachiocephalic artery (black arrow), the white arrow indicates the brachiocephalic vein.
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DISCUSSION
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It was difficult to make an unequivocal diagnosis on the results of preoperative investigations in this case. Considering the clinical course of rapid growth of a large mobile mass despite full anticoagulation therapy, we suspected a tumor rather than a thrombus, but neither was found intraoperatively or by histopathology. Although transesophageal echocardiography, computed tomography, and MRI have been reported as effective diagnostic tools for atherosclerotic lesions in the aortic arch, only carotid sonography was useful in this case.1–4 This may be because examination of the brachiocephalic artery is more difficult than the aortic arch. Severe atherosclerotic lesions of the aortic arch have been reported to be a significant factor in recurrent ischemic stroke, of the same magnitude as carotid artery disease and atrial fibrillation.3 In recurrent stroke, attention must be paid not only to the possibility of an intracardiac thrombus or mass, such as myxoma, but also to atherosclerotic lesions in the aortic arch.
In this case, MRI revealed multiple brain infarctions in the right middle cerebral artery and vertebral artery areas. This is consistent with an aortic plaque as the embolic source in the brachiocephalic artery. The medical management of patients with severe aortic plaque remains controversial. Treatment with anticoagulants and antiplatelet drugs seems suitable for the prevention of systemic embolization.5,6 In this case, there was recurrent stroke due to a rapidly growing mass despite anticoagulant and antiplatelet therapy. Thus we believed that surgery was required. Graft replacement for atherosclerotic plaque in the aortic arch has been reported, but we could not find any report of surgery for plaque presenting only in the brachiocephalic artery.7,8 Although embolism from an atherosclerotic aortic arch is increasingly recognized as a possible cause of recurrent stroke, it is still underestimated. As the safety of aortic arch operations has been established, surgery for atherosclerotic plaques that are sources of systemic embolization may be as widely performed in the near future as carotid endarterectomy.
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REFERENCES
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ABSTRACT
INTRODUCTION
