Shown is an adult aorta that is as normal as possible. The intimal surface is quite smooth, with only occasional small, pale yellow, fatty lipid streaks visible. Such fatty streaks may initially appear in the aortas of children. (The faint reddish staining in this autopsy specimen comes from hemoglobin that leaked from red blood cells after death.) With a healthy lifestyle and without additional risk factors, these intimal fatty lesions are unlikely to progress. The lipid streaks can serve as precursors for atheroma formation. Major risk factors advancing atheroma formation include increased serum LDL cholesterol, decreased HDL cholesterol, hypertriglyceridemia, diabetes mellitus, hypertension, and smoking.
This coronary artery opened longitudinally shows yellowish atheromatous plaques over much of its intimal surface. There is focal hemorrhage into a plaque, a complication of atherosclerosis that can acutely narrow the lumen. Endothelial dysfunction that impairs vasoreactivity or induces a thrombogenic surface or abnormally adhesive surface to inﬂammatory cells may initiate thrombus formation, atherosclerosis, and the vascular lesions of hypertension. Advanced atheromas can be complicated by erosion, ulceration, rupture, hemorrhage, aneurysmal dilation, calcifcation, and thrombosis. Arterial narrowing may lead to tissue ischemia, and marked or prolonged loss of blood supply may lead to infarction. This may lead to acute coronary syndromes involving the heart.
Severe aortic atherosclerosis involving nearly the entire intimal surface is shown, with ulceration of the atheromatous plaques along with formation of overlying mural thrombus. This degree of atherosclerosis may develop when atherogenesis proceeds over many years or with signifcant risk factors driving more accelerated atherosclerosis, such as hyperlipidemia, diabetes mellitus, smoking, hypertension, and obesity. Mitigating these risk factors through adoption of a healthy lifestyle with increased exercise and reduced caloric intake can halt the progression of atherosclerosis, and atheromas can even regress over time, with reduced likelihood of complications.
This cross-section of aorta shows a large overlying advanced atheroma containing numerous cholesterol clefts, resulting from breakdown of lipid imbibed into foam cells. The luminal surface at the far left shows ulceration of its fbrous cap with hemorrhage. Despite this ulceration, which predisposes to mural thrombus formation, atheromatous emboli are rare (or at least, clinically signifcant complications from them are infrequent). The thick medial layer is intact, and the adventitia appears normal at the right. As atheromas become larger, they can be complicated by ulceration, which promotes overlying thrombosis. Organization of the thrombus further increases the size of the plaque.
This high-magnifiation view of the necrotic center of an aortic atheroma shows foam cells and cholesterol clefts. In the process of atheroma formation, endothelial injury leads to increased permeability, leukocyte adhesion, and release of cytokines that attract blood monocytes, which become macrophages that accumulate lipids, becoming foam cells. Macrophages readily ingest oxidized LDL cholesterol through their scavenger receptors. Macrophages also generate cytokines driving cellular recruitment. An increased serum LDL level increases the amount of oxidized LDL, promoting this process. In contrast, HDL cholesterol tends to promote mobilization of lipid in an atheroma and transport to the liver.
This coronary artery cross-section shows severe occlusive atherosclerosis. The atheromatous plaque is circumferential and markedly narrows the remaining lumen. Note the prominent cholesterol clefts within this atheroma. This advanced atheromatous process involves the arterial media and the overlying intima with numerous cholesterol clefts. The remaining lumen has become occluded by a recent thrombus that fils it. Thrombosis is often the basis for acute coronary syndromes, including unstable angina, sudden death, and acute myocardial infarction.
This coronary artery cross-section shows residual smooth muscle in the media with overlying atheroma composed of extensive lipid deposition in lipophages and a cholesterol cleft from breakdown of those cells. Such plaques are prone to rupture, hemorrhage, and thrombosis. Platelets become activated and adhere to sites of endothelial injury, then release cytokines such as platelet-derived growth factor that promote smooth muscle proliferation, and the adherent platelet mass increases the size of the plaque while narrowing the residual arterial lumen. Use of antiplatelet agents such as aspirin helps reduce platelet “stickiness” and slows platelet participation in atheroma formation. Daily exercise is even better.
Aortic aneurysm, gross
Atherosclerosis involving the intima and media may focally weaken the wall of the aorta so that it bulges out to form an aneurysm. A classic atherosclerotic aortic aneurysm typically occurs in the abdominal portion distal to the renal arteries, as shown here. Aortic aneurysms tend to enlarge over time, and those with a diameter greater than 5 to 7 cm are more likely to rupture. Aneurysms may also form in the larger arterial branches of the aorta, most often the iliac arteries. On physical examination, there may be a palpable pulsatile abdominal mass with an atherosclerotic aortic aneurysm. Increased expression of matrix metalloproteinases that degrade extracellular matrix components such as collagen is observed in aortic aneurysms.
Aortic aneurysm, gross
This aorta has been sectioned longitudinally to reveal a large abdominal atherosclerotic aortic aneurysm distal to the renal arteries (at the right) and proximal to the iliac bifurcation (at the left). This bulging aneurysm, 6 cm in diameter, is filed with abundant layered mural thrombus. Note the rough atheromatous surface of the aortic lumen.
Hyaline arteriolosclerosis, microscopic
Another form of arteriosclerosis (hardening of the arteries) in addition to atherosclerosis is hyaline arteriolosclerosis, typically seen in kidneys and brain. It is shown here involving the markedly thickened arteriole at the lower right of this glomerulus with PAS stain. This change often accompanies benign nephrosclerosis, leading to progressive loss of nephrons and eventual renal atrophy. Hyaline arteriolosclerosis is also seen in elderly individuals, who are often normotensive. More advanced arteriosclerotic lesions may occur in persons with diabetes mellitus or hypertension.
Medial calcific sclerosis, microscopic
Mönckeberg medial calcifi sclerosis is the most insignifiant form of arteriosclerosis (atherosclerosis and arteriolosclerosis are signifiant because of arterial luminal narrowing). It is more common in the elderly. Note the purplish blue calcifiations involving only the media; the lumen appears unaffected by this process. No signifiant clinical consequences occur in most patients, and it is usually an incidental fiding. Recall this process when you see calcifid muscular arteries on a radiograph of the pelvic region, although other regions such as the neck or breast may also be involved.
Aortic dissection, microscopic
The tear in this aorta extends through the media, but blood also dissects along the media. Medical management can be undertaken; but with leakage or rupture, surgical repair of the dissection can be performed with closure of the tear and placement of a synthetic graft or endovascular stent.
Aortic dissection, gross
This aorta opened longitudinally shows an area in the thoracic portion of limited dissection that is organizing within the media. The red-brown thrombus can be seen on both sides of the section as it extends around the aorta. The intimal tear would have been at the left. This creates a “double lumen” to the aorta. This aorta shows severe atherosclerosis, which was the major risk factor for dissection in this patient.