Postulate: Atherosclerosis is an inflammatory disease, and advanced lesions in the arteries are similar to end-stage inflammatory changes in other tissues (e.g. cirrhosis in liver, glomerulosclerosis in kidney)
Chlamydia pneumoniae has been demonstrated in plaques. Antibiotics against C. pneumoniae have reduced recurrent events in patients with ischemic heart disease.
Certain viruses cause atherosclerotic plaques in chickens.
Some areas of endothelium may generate more superoxide dismutase, accounting in part for the nonrandom localization of atherosclerosis.
Medial smooth muscle may have a heterogeneous embryologic origin & may respond differently, accounting in part for the nonrandom localization of atherosclerosis.
“Inflammatory lesion” is an oversimplification. AS is perhaps better described as an ongoing process of injury and imperfect repair.
Could plaques be benign neoplasia or caused by an oncogenic virus? Unlikely – some plaques probably are monoclonal, but probably just arise from pre-existing developmental clones.
There is evidence that the fine particulate matter (soot) in diesel exhaust may act synergistically with cholesterol to activate genes that cause inflammation of blood vessels (Genome Biology 2007, 8:R149).
Def: An abnormal dilatation or outpouching of a blood vessel, usually the aorta (or even the heart!)
True: Has all layers of vessel wall (c.f. true diverticulum in bowel)
False: Not all layers (pseudoaneurysm – c.f. false diverticulum in bowel)
Most common causes: Atherosclerosis and cystic medial degeneration
An extravascular hematoma or dissection of blood into the media of a vessel are examples of false aneurysms.
Can obstruct ostia of renals, SMA, IMA, vertebrals
Variants are inflammatory and mycotic
AAA’s are usually not initiated by a primary abnormality of the media (although a weaker media may predispose). The media is secondarily weakened by severe atherosclerotic involvement of the intima.
Inflammatory AAA’s feature dense periaortic fibrosis and lymphoplasmacytic inflammation. The cause may be a recently recognized entity, “immunoglobulin G4 (IgG4)-related disease.” This fibrosing, autoimmune disorder can also affect the pancreas, salivary glands and biliary system. It responds to steroid therapy.
A typical AAA can become secondarily infected (mycotic) esp. from Salmonella gastroenteritis – this may lead to rapid dilatation and rupture.
The dreaded complication
4 cm is the “cutoff” for risk of surgery less than risk of rupture (varies a little among institutions)
Newer stent devices now available – can be placed via intravascular route