The process for the development of arteriosclerosis, as put forward by Duguid, is that repetitive stress to the arterial wall produces damage which is patched by a microthrombus. This then covers with epithelium and organises in to what is essentially a scar used to strengthen the arterial wall exactly where this is needed.
Here are a few micropgraphs of Duguid's showing microthrombus on the arterial wall, again taken from his monograph The Dynamics of Arteriosclerosis.
These require frozen sections, formalin fixing and paraffin wax embedding will tend to lose microthrombi or convert them to "gunk" in the lumen of the artery.
Willis used ascorbate deficiency in Guinea Pigs to produce pressure induced trauma (unfortunately without histopathology) and Coulson and Carnes (thanks Stephan) used copper deficiency to produce elastosis lesions, both probably allowing easy intimal damage and subsequent need for repair. In fact the frank adventitial haemorrhage of copper deficiency looks to be a rather extreme model of what actually occurs in apparently normal humans. But the elastosis is there at the start...
Now the processing of thrombus to collagen is just that, a process. It doesn't simply "happen". So the very obvious question is what happens when the process goes wrong?
Unhappily there are a number of mucopolysaccharide storage diseases which result from the inability to degrade proteoglycans. If you cannot degrade proteoglycans but continue to produce the microthrombi, as suggested by Duguid, you might expect some accumulation of mucopolysaccharide in the walls of stressed arteries.
Here is a nice picture (part B) from this paper of the coronary artery of a young child who died of complications of this genetic defect. You might accept that there is some narrowing of the lumen.
There are a number of factors under our control which seem to influence our ability to obstruct our arteries with the sequelae of microthrombi, some of which I'll get to eventually. I happened on this fascinating acount of sudden death in young fit adults.
This condition is usually associated with abnormal cardiac rhythm, particularly sudden onset ventricular fibrillation. Obviously making your salad dressing with sunflower oil is probably your best risk factor for throwing serious cardiac rhythm abnormalities, but developing an ischaemic atrioventricular node seems to be an excellent trigger for local hypoxia to start the fibrillation. Stenosis of the micro artery to the AV node appears to be a feature of sudden death in young males.
I don't have access to the full text so I don't know what the histology pictures look like. I'm a bit suspicious that the changes will turn out to be merely those which any numpty with internet access can down load from Pubmed, in papers going back 60 years.
The terms in the abstract are "dysplasia" and "nonatherosclerotic" and "mucopolysaccharide deposition". Hmmmmmmmmm........
It really brings home the utter ignorance of cardiologists working under the cholesterol paradigm. BTW, does anyone have access to the pictures? It would be nice to have them here... Assuming they look as I think they do!
EDIT: The pics are here, thanks Anna.