What is atherosclerotic plaque in the aorta?

What is Atherosclerotic Plaque in the Aorta?

Atherosclerotic plaque in the aorta is a pathological intimal lesion characterized by lipid accumulation, inflammatory cells, and connective tissue that protrudes into the arterial lumen, weakens the underlying media, and is often associated with calcification. 1

Pathologic Definition and Composition

Atherosclerosis is characterized by intimal lesions called atheromata, atheromatous plaques, or fibrofatty plaques that fundamentally alter the vessel wall architecture. 1 These lesions represent:

• Accumulation of lipids, inflammatory cells, and connective tissue within the arterial wall leading to plaque formation 1
• Intimal thickening with massive fibrosis and calcification that compromises nutrient supply to the media 2, 3
• Progressive lipid deposition in the intimal-medial layer with secondary inflammation and repetitive fibrous tissue deposition 4

Disease Progression and Plaque Evolution

The natural history follows a predictable pattern:

• Early lesions begin with lipid accumulation and inflammatory cell infiltration, particularly macrophages that consume excess lipids and transform into foam cells 5
• With aging, risk factors, and genetic predisposition, plaques progress to complicated lesions with surface defects, hemorrhage, and/or thrombosis 1
• Advanced plaques demonstrate either fibrous morphology (dense collagen matrix dominated by smooth muscle cells) or lipid-rich morphology (large necrotic core with thin fibrous cap infiltrated by inflammatory cells) 6
• Plaque morphology is modulated by inflammatory mechanisms that promote either synthesis or lysis of the fibrous cap, making fibrous and atheromatous lesions essentially interchangeable 6

Clinical Significance in the Aorta

Thoracic aortic atherosclerosis is less common than abdominal aortic atherosclerosis, but carries substantial clinical importance. 1

Embolic Risk

Aortic plaques pose significant thromboembolic risk:

• Complex aortic plaque (≥4 mm thickness, mobile thrombi, or ulcerations) substantially increases embolic complications 1
• Aortic arch plaques independently predict new ischemic stroke with relative risk of 3.8 (95% CI 1.8-7.8), independent of carotid stenosis or atrial fibrillation 1
• Plaques generate two types of emboli: thromboemboli (occlude medium-to-large arteries causing strokes) and cholesterol crystal emboli (occlude small arteries causing blue toe syndrome, renal insufficiency) 4

Structural Complications

• Atherosclerotic changes affect over 90% of aortic aneurysm surfaces, with severe atherosclerosis involving more than 70% of the aortic surface in patients with aneurysms 7, 2
• Atherosclerotic plaques can ulcerate and penetrate the internal elastic lamina, creating penetrating aortic ulcers with rupture risk as high as 33-75% when complicated by intramural hematoma 2
• Plaque formation weakens the underlying media, predisposing to aneurysm development and dissection 1

Plaque Vulnerability Features

Vulnerable plaques prone to rupture demonstrate specific characteristics:

• Large acellular lipid-rich necrotic core with overlying thin fibrous cap infiltrated by inflammatory cells 8
• Noncalcified plaques carry higher risk for recurrent vascular events compared to calcified plaques 1
• Plaques with larger lipid core, predominance of macrophages, thin fibrous cap, and lack of calcification are more vulnerable to disruption 1
• Calcified plaques are more stable and less likely to result in embolic syndromes 1

Risk Factors

The development of aortic atheroma is driven by:

• Age, male sex, hypertension (present in 85% of patients with ruptured aneurysms), diabetes mellitus, hyperlipidemia, smoking, and sedentary lifestyle 1, 7
• Elevated inflammatory markers (C-reactive protein), homocysteine, or lipoprotein levels 1
• Endothelial dysfunction and genetic predisposition 1

Diagnostic Imaging

Transesophageal echocardiography (TEE) remains the gold standard for visualization of aortic plaques in the thoracic aorta, providing information on plaque mobility, ulceration, composition, and anatomic relationship to great vessels with excellent reliability. 1 However, a small portion of the ascending aorta near the innominate artery origin is masked by the tracheal air column, potentially missing approximately 2% of plaques. 1

CT angiography reveals calcification and atherosclerotic changes effectively, though MRI may underestimate plaque thickness compared to other modalities. 1

Common Pitfall

Do not assume all aortic plaques carry equal risk. Complex plaques (≥4 mm thickness with mobile components or ulcerations) require more aggressive management than simple, calcified plaques, as they carry substantially higher embolic risk. 1 Additionally, while general atherosclerosis management strategies are recommended, no proven therapies exist specifically for aortic embolism prevention. 4