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Year : 2003  |  Volume : 13  |  Issue : 2  |  Page : 191-194
Penetrating atherosclerotic ulcer of aorta - a case report


Dept. of Radiodiagnosis, K.G. Hospital and Postgraduate Medical Institute, Arts College Road, Coimbatore-641018, Tamil Nadu, India

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Keywords: Atherosclerosis, Aorta

How to cite this article:
Karthikeyan D, Vijay S, Kumar T. Penetrating atherosclerotic ulcer of aorta - a case report. Indian J Radiol Imaging 2003;13:191-4

How to cite this URL:
Karthikeyan D, Vijay S, Kumar T. Penetrating atherosclerotic ulcer of aorta - a case report. Indian J Radiol Imaging [serial online] 2003 [cited 2019 Jul 18];13:191-4. Available from: http://www.ijri.org/text.asp?2003/13/2/191/28658

   Introduction Top


The term 'penetrating atherosclerotic aortic ulcer' describes the condition in which ulceration of an aortic atherosclerotic lesion penetrates the internal elastic lamina into the media. This lesion may precipitate intramural haemorrhage. In most patients this intramural (intramedial) haematoma is localised, but occasionally it can involve the entire descending thoracic aorta. These ulcers may be complicated by aneurysm formation, by breaking through into the adventitia to form a pseudoaneurysm, by rupturing completely (transmural rupture) into the mediastinum or the right and left hemithorax, and even by precipitating an aortic dissection. The diagnosis of these ulcers is made on CT scan, MR imaging, and transoesophageal echocardiography (TOE) by demonstration of an outpouching of the aortic wall with jagged edges, usually in the presence of extensive aortic atheroma.

We present a patient, in whom the diagnosis of penetrating atherosclerotic aortic ulcer was made on CT with a review of the natural history, imaging diagnosis and management of the condition.


   Clinical presentation Top


A 62-year-old man with a history of hypertension presented to the emergency room with sudden onset of severe chest pain radiating to the back. The physical examination on admission was unremarkable, and a chest radiograph (not shown) revealed a tortuous thoracic aorta. CT thorax was done (CTe, GE, Milwaukee, USA. Helical acquisistion with 100 ml of intravenous contrast medium) to rule out aortic dissection or aneurysm.

Axial CECT section at the level of the aortic arch shows an ulcer with overhanging margins on the anterolateral wall of the aorta (white arrow in [Figure - 1]). Diffuse aortic wall thickening is also seen. Coronal reconstruction shows the ulcer as a crater-like filling defect (white arrow in [Figure - 2]). Oblique sagittal reconstruction shows a tortuous thoracic aorta with diffuse wall thickening and the ulcer defect in the anterior arch of the aorta (white arrow in [Figure - 3]).


   Discussion Top


Current concepts in aortic pathology present a new cardiovascular syndrome called Acute aortic syndrome (AAS). AAS embraces a heterogenous group of patients with similar clinical profile, but entirely different precipitating pathophysiological mechanisms. AAS includes penetrating atherosclerotic aortic ulcer (PAU), aortic intramural haematoma (IMH) and classical aortic dissection. All these conditions are characterised clinically by a severely intense, acute, searing or tearing, throbbing and migratory chest pain, referred to as "aortic pain" in patients with coexisting history of hypertension. Occasionally some patients exhibit several or all of these lesions, demonstrating the existence of a link between them. In such cases it is difficult to know which was the initiating event. The clinical progress of these patients is unpredictable and, in many cases, unfavourable. Therefore, an early diagnosis is essential.

Penetrating atherosclerotic aortic ulcer, one of the conditions included under AAS, was first described as a distinct clinical and pathological entity by Stanson et al in 1986. The condition refers to an ulcerating atherosclerotic lesion that penetrates the elastic lamina and is associated with haematoma formation within the aortic wall. PAU is typically seen in elderly individuals with hypertension and atherosclerosis and usually involves the descending thoracic aorta. The patients are also usually active smokers.

Atheromatous ulcers develop in patients with advanced atherosclerosis. In the initial stages, the lesions are usually asymptomatic and confined to the intimal layer. These lesions can progress to a deep atheromatous ulcer that penetrates through the elastic lamina and into the media. PAU ulcer can lead to IMH, aortic dissection, aortic aneurysm, or rupture [Figure - 4].

Most cases of PAU occur in the mid to distal portion of the descending thoracic aorta. The ulcers are locally confined and not known for propagation, branch vessel compromise and therefore not accompanied by valvular, pericardial or neurovascular complications. Complications of PAU ulcers are IMH, aortic dissection, aortic aneurysm and aortic rupture.

Haematoma formation may extend along the media, resulting in either 'double-barreled' or 'thrombosed' aortic dissection. Double-barreled aortic dissection shows communication between the true and false lumen, whereas thrombosed aortic dissection shows no opacification of the false lumen. Thrombosed aortic dissection is probably more common than double-barreled aortic dissection because severe atherosclerosis is believed to prevent the extension of hematoma and the creation of reentry. In contrast to classic dissection, dissection secondary to an aortic ulcer is shorter in extension, away from classic entrance tears, and has a thicker, calcified and static flap. This type of dissection, in an area of gross atherosclerosis, is usually limited by neighbouring fibrosis and calcification.

In some cases, hematoma extension causes stretching of the weakened aortic wall, leading to the formation of a saccular aortic aneurysm. The aortic aneurysm and dissection may eventually rupture. Spontaneous rupture of the thoracic descending aorta is a rare condition that occurs in the absence of a true aneurysm. Most cases involve predisposing conditions such as hypertension and atherosclerosis. Though the precise mechanism of spontaneous rupture is not well understood, it is speculated that there may be pressure atrophy of the media due to overlying intimal atherosclerotic plaque with localized ballooning of the aortic wall prior to perforation. Most spontaneous aortic ruptures are believed to be associated with perforation through the atheromatous plaque.

Imaging Appearances

Since PAU, IMH, classic aortic dissection, and aortic rupture have similar clinical manifestations, they must be distinguished radiologically. CT, MR and TOE have largely replaced angiography, which was previously considered the standard of reference for the diagnosis of many aortic diseases.

Essentially, all these modalities reveal an out pouching of the aortic wall with jagged edges, usually in the presence of extensive aortic atheroma. Plain chest radiographs could reveal an abnormality in the size or contour of the thoracic aorta. Angiography shows features of associated atherosclerotic disease and clear ulceration extending beyond the intimal border, often with the nipple-like projection and with subjacent haematoma formation.

CECT images in patients with penetrating aortic ulcer reveal focal involvement with adjacent subintimal haematoma located beneath the frequently calcified and inwardly displaced intima in the middle or distal third of the thoracic aorta. Rarely, the abdominal aorta could instead be involved where it is severely atherosclerotic. There is no evidence of any intimal tear or circumferential haemorrhage into the media. Therefore, they are characterized by focal contrast enhancement (or filling defect) beyond the confines of the aortic lumen, but communicating with it. The ulcer is often associated with thickening or enhancement of the aortic wall. CT could also identify the complications of penetrating ulcers.

Shorter examination times and high-quality two- and three-dimensional image reconstructions are possible with the use of helical CT. CT may not depict small, penetrating atherosclerotic ulcers because of its lower spatial resolution compared with conventional angiography. However, CT angiography can demonstrate complex spatial relationships, mural abnormalities, and extraluminal pathologic conditions, which may offset this weakness.

MRI has been shown to be superior to CT in differentiating IMH from atherosclerotic plaque and chronic intraluminal thrombus. MR has the additional advantage of allowing multiplanar imaging without the use of contrast material.

TOE is also reported to be highly sensitive and specific for the characterization of aortic disease. TOE shows PAU as a crater-like or focal out pouching in the atherosclerotic wall that occurs in the middle or distal portions of the descending thoracic aorta.

Differential Diagnosis

PAU has to be differentiated from other causes of AAS. The absence of an ulcer crater distinguishes IMH from PAU. Aortic ulcers are usually focal lesions most frequently located in the descending thoracic aorta. IMH and classic aortic dissection are more extensive lesions. Aortic intramural haematoma (IMH) has been recognized as a distinct pathologic entity since 1920 usually associated with pre-existent disorders of connective tissue. Haemorrhage occurs within the wall of the aorta, despite a non-atheromatous intact intima. IMH can also result in an intimal tear with subsequent aortic dissection, laceration occurring at points of greatest hydraulic stress. On imaging, there is no ulcer crater and lesions are more extensive. In some cases, there could be eccentric thickening of one wall of the aorta due to the haematoma. In contrast to IMH, aortic ulcers are characterized by focal contrast enhancement (or filling defects) beyond the confines of the aortic lumen but communicating with the aortic lumen. Most often cases of IMH are not diagnosed by aortography as there is no disruption of the luminal surface of the aorta.

Pure aortic dissection begins in the proximal aorta, a location where atheromatous ulcers are only rarely seen. However, atherosclerosis is frequently associated with aortic dissection, the dissection being limited by the medial atrophy and fibrosis secondary to atherosclerosis.

Atheromatous ulcers that are confined to the intimal layer sometimes appear radiologically similar to penetrating atherosclerotic ulcers. Therefore, care should be taken in making a diagnosis of penetrating atherosclerotic ulcer, particularly if the disease entity is discovered incidentally. Intravascular US, which can help accurately assess the aortic wall layers, may be useful in the evaluation of penetration by atheromatous ulcers.

Prognosis

Little is known about the natural history of penetrating atherosclerotic ulcer. This disease entity has been considered by most authors to have a poorer prognosis than classic aortic dissection. However, Harris et al reported that disease progression is slow, with a low prevalence of acute rupture or other life-threatening complications. Coady et al reported that the risk of aortic rupture was considerably higher among patients with PAU than among patients with type A or type B aortic dissection.

Hayashi et al state that in their experience prevalence of critical cases of symptomatic penetrating atherosclerotic ulcer is higher than that of classic aortic dissection. They occasionally encountered saccular aneurysms, which seemed to be caused by a PAU. Although rupture or other life-threatening complications were rare, they opine that affected patients must be followed up because such complications can progress slowly.

Most authors suggest that surgical intervention with grafting of the affected area is the treatment of choice. In particular, persistent or recurrent pain, hemodynamic instability, and a rapidly expanding aortic diameter have been considered indications for surgical treatment. On the other hand, some authors believe that immediate surgical treatment is not always required because the disease may have a benign course. Hayashi et al concluded that penetrating ulcers of the descending thoracic aorta should initially be treated aggressively and that pertinent clinical and radiologic data should be monitored carefully during the first month after onset. Surgical treatment may become necessary in cases involving evidence of intramural hematoma expansion, signs of impending rupture, inability to control pain, or blood pressure changes.

Conclusion

PAU is typically seen in elderly individuals with hypertension and atherosclerosis and usually involves the descending thoracic aorta. Differentiation of PAU from other causes of Acute Aortic Syndrome such as intramural haematoma, aortic dissection, aortic aneurysm, and spontaneous aortic rupture is difficult or impossible in some cases. Because critical cases of penetrating atherosclerotic ulcer cannot be identified on the basis of initial imaging findings, careful follow-up is needed in affected patients, particularly during the first month after the onset of the disease[5].

 
   References Top

1.H Hayashi, Y Matsuoka, I Sakamoto, E Sueyoshi, T Okimoto, K Hayashi, N Matsunaga. Penetrating Atherosclerotic Ulcer of the Aorta: Imaging Features and Disease Concept. Radiographics. 2000;20:995-1005.  Back to cited text no. 1    
2.Coady MA, Rizzo JA, Hammond GL, et al. Penetrating ulcer of the thoracic aorta: what is it? how do we recognize it? how do we manage it?. J Vasc Surg 1998; 27:1006-1016)  Back to cited text no. 2    
3.Harris JA, Bis KG, Glover JL, et al. Penetrating atherosclerotic ulcers of the aorta. J Vasc Surg 1994; 19:90-99.  Back to cited text no. 3  [PUBMED]  
4.I Vilacosta, JA San Roman. Acute aortic syndrome. Heart 2001;85:365-368.  Back to cited text no. 4    
5.PT O'Gara, RW DeSanctis. Acute Aortic Dissection and Its Variants. Toward a Common Diagnostic and Therapeutic Approach. Circulation. 1995;92:1376-1378.  Back to cited text no. 5    

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Correspondence Address:
D Karthikeyan
Dept. of Radiodiagnosis, K.G. Hospital and Postgraduate Medical Institute, Arts College Road, Coimbatore-641018, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


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    Figures

[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]

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