Ann Thorac Surg 2001;72:614-615
© 2001 The Society of Thoracic Surgeons
Case report
Dissection of the ascending aorta due to metastatic carcinoma
Baran S. Ugurlu, MDa,
Eyüp Hazan, MDa,
Özer Badak, MDb,
Kutsal Yörükoglu, MDc,
Öztekin Oto, MDa
a Department of Thoracic and Cardiovascular Surgery, Dokuz Eylul University Medical School, Balcova, Izmir, Turkey
b Department of Cardiology, Dokuz Eylul University Medical School, Balcova, Izmir, Turkey
c Department of Pathology, Dokuz Eylul University Medical School, Balcova, Izmir, Turkey
Accepted for publication July 21, 2000.
Address reprint requests to Dr Ugurlu, Dokuz Eylul Universitesi Tip Fakultesi, Gogus Kalp ve Damar Cerrahisi Anabilim Dali, Balcova, 35340 Izmir, Turkey
e-mail: ugurlub{at}yahoo.com
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Abstract
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The association of aortic dissection with a malignancy is a rare finding and previous reports are usually those of primary aortic sarcomas. In this report we present a case with typical ascending aorta dissection associated with metastatic carcinoma originating from the lungs. The metastatic infiltration of the vasovasorum of the aorta by carcinoma cells may have caused aortic dissection by decreasing medial strength and integrity. This is a mechanism of aortic dissection that we have not encountered in previous reports.
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Introduction
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Dissection of the ascending aorta is a relatively common aortic catastrophe that usually begins with a tear in the aortic intima that exposes the underlying media layer directly to blood flow at arterial pressures. Medial degeneration is the chief predisposing factor in most nontraumatic cases of aortic dissection [1]. Medial degeneration can be caused by hereditary defects of the connective tissue such as Marfan and Ehlers-Danlos syndrome; in most cases the cause remains unclear [2]. Aortic malignancies may also affect the integrity of the medial layer, and primary aortic tumors have previously been associated with aortic dissection [3–5]. In this report we describe a patient with aortic dissection caused by metastatic carcinomatous invasion of the aortic vasovasorum.
A 64-year-old man with a history of hypertension, 60 pack/year cigarette smoking, and chronic obstructive lung disease presented with recent-onset shortness of breath. His blood pressure was 90/65 mm Hg in both arms, pulse was 120/min, and respiratory rate was 30/min. He was orthopneic and had jugular venous distention. A chest roentgenogram showed enlargement of the cardiac silhouette. Echocardiography revealed pericardial effusion measuring 27 mm at the lateral border causing tamponade. Hemorrhagic effusion of 900 mL was tapped with a catheter. The patient’s symptoms were relieved but hemorrhagic drainage from the pericardial drain continued the next day. The thorax computed tomogram showed a dilated ascending aorta measuring 5 cm in diameter. A transesophageal echocardiogram was performed that revealed dissection of the ascending aorta starting just above the aortic cusps. The right sinus of Valsalva was obstructed by an intramural hematoma and the ascending aorta was divided into true and false lumens by the dissection (Fig 1). The coronary angiogram showed obstruction of the right coronary artery by the intramural thrombosis.
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Fig 1. Transesophageal echocardiogram (short axis view) showing true and false lumens separated by an intimal flap at the level of supracoronary ascending aorta. (FL = false lumen, TL = true lumen.)
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Surgery was performed through a median sternotomy. The pericardial cavity was filled with defibrinated blood and fibrin. The ascending aorta was dilated and measured 6 cm at its widest diameter just above the coronary ostea. The aorta immediately below the brachiocephalic artery was narrow and appeared normal. The right femoral artery and superior and inferior vena cava were cannulated. The aorta was clamped below the brachiocephalic artery and was opened under cardiopulmonary bypass. There was a semicircular intimal tear, 2 cm above the coronary ostea. The dissection extended for 5 cm. The ascending aorta was replaced with a 30-mm gelatin-coated woven polyester graft (Vascutek, Sulzermedica, Inchinnan, Scotland). A saphenous vein graft was anastomosed to the right coronary artery. The patient had a relatively normal postoperative course that was complicated only by several bouts of bronchospasm.
Histologic examination of the aorta revealed diffuse infiltration of the adventitial vasovasorum with tumor cells (Fig 2). These cells had pleomorphic, hyperchromatic nuclei with eosinophilic cytoplasms (Fig 3). There were localized areas of necrosis. The malignancy was identified as metastatic carcinoma of unknown type, possibly originating from either the lungs or the bladder.
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Fig 2. Microscopic view of the aortic specimen adjacent to the dissected area showing diffuse malignant infiltration of the vasovasorum (thin arrow). The thick arrow points to the intimal side (hematoxylin and eosin, x40).
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Fig 3. High-power view showing carcinoma cells with pleomorphic, hyperchromatic nuclei and eosinophilic cytoplasms in the vasovasorum (hematoxylin and eosin, x200).
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The patient was studied extensively to localize the origin of the malignancy. Tumor cells were identified in the bronchoscopic lavage fluid. The patient was diagnosed as having diffuse lung cancer with lymphangitic spread. Further treatment was deferred because of his health status. He died of respiratory failure, 2 months after being discharged. Autopsy was not performed.
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Comment
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The association of aortic dissection with a malignancy is rare. Previous cases involve primary aortic tumors that are intraluminal, mural, or adventitial [3–5]. The histologic types of these tumors are diverse and include fibrosarcomas, leiomyosarcomas, undifferentiated sarcomas, histiocytomas, and myxomas [3–5]. The use of Dacron prostheses was also associated with some of these tumors [6].
Any disease process that undermines the integrity of the elastic or muscular components of the media layer predisposes to aortic dissection [2]. Malignant infiltration of the aorta may disrupt medial integrity directly by its mechanical effect. It may also cause ischemic degeneration of the aorta by obstructing the vasovasorum. Our patient had diffuse infiltration of the aortic wall by carcinoma cells that were located primarily in the vasovasorum. This may have led to aortic dissection by both mechanical and ischemic mechanisms.
The association of tumoral infiltration of the aorta with dissection may have been incidental in this case. The patient was already at risk for aortic dissection because of hypertension, advanced age, and chronic obstructive lung disease. However, the presence of a dense layer of carcinomatous cells in the media, undermining its integrity, may indicate a causal relationship instead of an incidental one. Furthermore, limitation of the dissection to only a short segment of the ascending aorta with carcinomatous infiltration and not spreading further to uninvolved areas, supports our view.
This case report describes a mechanism of typical type A dissection limited to the ascending aorta. We have not encountered previous reports of this type of dissection with carcinoma metastasis, and could find no reference to it in a computer search using MEDLINE.
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References
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Abstract
Introduction
