Atherosclerotic  Diseases of the Aorta

The Common Vein Copyright 2007

Ashley Davidoff MD

The most common disease of the aorta is atherosclerosis, a process in which lipid material, fibrous tissue, and calcium form deposits, called plaques, within the inner layer of the aortic wall (the intima). The earliest signs of atherosclerotic change are yellow fatty streaks in the intima Although it is an area not prone to atherosclerosis, these fatty streaks are first observed in the descending thoracic aorta adjacent to the departure of intercostal arteries (1) After age 20 years, atherosclerotic plaques are more extensive in the abdominal aorta than in any other area Aortic (true) aneurysms are thought to be caused by a variety of factors including atherosclerosis; the vast majority of aortic aneurysms are found in the infrarenal abdominal aorta (2) The ascending thoracic aorta is the area least prone to atherosclerosis Aortic dissections occur as a result of hypertension, and are formed after the intima of the aorta ruptures, leading to entry of blood into the aortic wall Initiating tears are most frequent in the ascending aorta, though the ascending aorta is not the most commonly involved portion of the aorta regarding dissecting aneurysms The proximal portion of the descending thoracic aorta is the second most common location of a primary intimal tear, but because most ascending aortic dissections extend to involve the descending portion, and because few primary tears in the descending aorta extend retrograde to the ascending aorta, the descending aorta is the most commonly involved portion of the aorta with dissecting aneurysms (3)

Pathogenesis

Atherosclerosis is a degenerative disorder of the intima of arteries. (occasionally affecting other structures in the cardiovascular system) chatracterised by accumulation of fatty and fibrous elements within the intima of the vessel wall. The multifactorial causes of atherosclerosis include age, sex, genetics, lifestyle and dietary factors. among many other unfolding factors. The recognizable “phases” of atherosclerosis include ; 1) breach of the endothelium (33792d) 2) migration of lipoproteins from the lumen into the intima. (33792d) 3) Formation of a lipoprotein-proteoglycan complex that traps the lipoprotein in the intima (33792e) 4) Migration of leukocytes from the lumen into the intima. (33792g) 5) Transformation of the monocytes into macrophages and phagocytosis of the fat complexes to form fat laden foamy macrophages. (33792h) 6) Migration of smooth muscle cells from the media into the intima and transformation into fibrocytes. A fibrous capsule around the fatty complex is formed. (33792i, 33801b) 7) Cell death and destruction with associated formation of dystrophic calcification. 8) Growth of the atheromatous complex with impingement on the lumen. (33801b) 9) Potential of the complex to rupture. (33801d) The progressive impingement on the lumen causes reduction of blood flow, usually manifesting clinically with angina when the lumen is reduced by 70% of its original size. Acute rupture of a plaque predisposes to superadded thrombosis and occlusion of the lumen. Acute myocardial infarction and death are complications of this event. The initial phase of endothelial injury has multifactorial contributing factors including hypertension, hemodynamic factors, hyperlipidemia, homocysteine, smoking, toxins, immune reactions, and viral disease. The result is a breach in the intima and migration of lipoproteins into the subendothelial layer. The lipoproteins and proteoglycans form a complex compound that traps the fat complex in the subepithelial layer. The next phase heralds the migration of leukocytes and platelets into the subendothelial layer. The monocytes, phagocytose the lipoprotein-proteoglycan complex forming the lipid laden foamy histiocytes. These macrophages can apparently repllicate. At this stage the macroscopic appearance is the well known “fatty streak”. The next phase of atherosclerosis occurs following smooth muscle proliferation and migration from the media into the evolving plaque. Smooth muscle also undergoes apoptosis and death. The vascular smooth muscle produces the extracellular matrix has major contribution to the atheromatous lesion. Interstitial collagens (types I and III) and proteoglycans such and elastin fibers also accumulate in atherosclerotic plaques. Accumulation of cholesterol and cholesterol esters occur. Smooth muscle migrates from the media into the intima and transform into fibrous elements both within the lesion as well superficial to the lesion forming a fibrous plaque. The monocytes and macrophages ingest the fat and foamy fat laden macrophages result. An inflammatory reaction evolves. Continued accumulation of lipid, macrophages, foamy cells, extracellular matrix result in a fibrofatty complex that grows in size over time. As it enlarges it bulges and thins the intima and eventually erodes the surface. As the disease progresses, cell death within the plaque results, and dystrophic calcification follows.

 

Why is it Important to Understand

 

Stenotic Disease

 

The Fear  – The Vulnerable Plaque

The Cutting Edge and the Holy Grail

Evaluating the Chemical Makeup of the Wall of the Arteries

Wall

Links and References

Acute Aortic Syndrome

Atherosclerosis Pathogenesis

Ulcerated Plaque

Atherosclerosis of the Aortic Wall

13316 13314 13313 aorta aortic wall elastic layer intima plaque complex lesion atherosclerosis atheroma complex lesion histopathlogy Courtesy Dr Isabelle Joris

 

Normal and Severe Atherosclerosis

18485c01 aorta artery hepatic artery renal artery splenic artery superior mesenteric artery SMA kidney severe atheroscleroris atheroma occluded renal artery spleen liver normal anatomy angiogram angiography Davidoff MD

Pathogenesis of Penetrating Diseases of the Aorta and Acute Aortic Syndrome

42409c01.800 aorta artery atherosclerosis atheroma acute aortic syndrome a aortic ulcer b = acute mural hematoma c = acute mural hematoma large d = focal dissection e penetrating ulcer f rupture histology histopathology Davidoff art pathogenesis Courtesy Ashley Davidoff MD

 

Growth Rate

This seriesof images spans the follow up of an infrarenal AAA first evaluated in February in 204 by US, (a,b,c) and CT (d,e,f) followed by a repeat US in September 2004 – 6 months later. The rapidity of growth from a transverse diameter of 4.8cms (a) to 5.3 cms (d) suggest rapid growth of the saccular aneurysm and in and of itself would warrant repair. In addition the presence of advancing hydronephrosis (c,i) would raise the possibility of perianeurysmal fibrosis with secondary obstruction probaly requiring surgical release and preferable treatment with open repair. Courtesy Ashley Davidoff MD 37245c code CVS aorta abdomen AAA infrarenal saccular hydronephrosis

Aneurysm of the Abdominal Aorta

This angiogram of the abdominal aorta shows a widened infrarenal aorta. At first glance the lumen of the aorta appears normal, but a faint curvilinar calcification of the true wall can be seen to the patients left in the first image. The second image (b) reveals the true size of the aneurysm. Courtesy Ashley Davidoff MD 22734 cW02 codeCVS aorta artery abdomen aneurysm AAA

Penetrating Ulcer with Rupture

17529c01 artery descending thoracic aorta abdominal aorta dx rupture pseudoaneumysm ulcerating plaque mural hematoma ruptured through aortic wall hemorrhage hematoma retroperitoneum CTscan Courtesy Ashley DAvidoff MD Ashley Davidoff MD

 

Atherosclerotic Occlusion of the Aorta

14646.803 aorta kidney size hypertrophy atrophy artery superior mesenteric artery arc of Drummond IMA inferior mesenteric artery collaterals renovascular disease occluded aorta internal iliac artery fx occluded occlusion small compensatory hypertrophy collaterals MRA MRIscan Davidoff MD

 

Links and References

Acute Aortic Syndrome

Atherosclerosis Pathogenesis

Ulcerated Plaque