Associated with these conditions there is low grade inflammation in the lining of the blood vessel wall, with a build up of cells that are associated with, initially, the laying down of soft inflammatory tissue, then collagen, a substance found in scars, and finally calcium. This 'plaque' slowly builds up over time and gradually pushes into the lining of the vessel causing a narrowing that restricts blood flow to the organ. When this involves the heart the term we use to describe this is ischaemic heart disease, when it involves the leg blood vessels it is peripheral vascular disease and when it involves the the brain vessels, it is called cerebrovascular disease.
At the same time as this is occurring, and driving on the inflammation, cholesterol can build up in the lining of the blood vessels. This occurs when the supply exceeds the body’s natural disposal system and the cholesterol is taken up by scavenger cells in the endothelium. A pool of liquid cholesterol develops in the lining of a vessel, and if a break occurs in the lining of the vessel then the cholesterol pool oozes out and, on contact with blood causes the blood to clot, which reduces blood flow down the artery. This causes an acute coronary syndrome if the heart is involved (otherwise known as unstable angina or a heart attack) or an acute cerebral syndrome (or stroke / transient ischaemic attack).
We cannot completely prevent atherosclerosis or 'hardening of the arteries'. However we can minimise the chance of developing it through lifestyle choices, such as eating healthily, exercising regularly - this does not have to be extreme exercise, but we should aim to do 30 minutes of moderate exercise five times per week, quitting smoking cigarettes and keeping one's weight down.
Through medication: (which is essential if atherosclerosis is shown to have developed)
One of the markers of inflammation in the body is called C reactive protein. (CRP). This is elevated in a whole host of conditions including infection, malignancy (cancer) and organ specific inflammatory diseases (eg Crohn’s disease of the bowel, rheumatoid arthritis). In the absence of these conditions the CRP should be normal (below 3). Even in the range below 3 there is still variation, measured by the high sensitivity CRP (hsCRP). Data is becoming increasingly available that shows that mild elevation of the hsCRP is associated with arteriovascular events, even in the face of a relatively normal cholesterol. This has the implication that the test, in health, assesses the total inflammatory load of the vascular tree. We know that interventions to reduce vascular risk lower hsCRP, suggesting that part of the benefit is through reducing inflammation at the endothelial cell level, and that after a vascular event persistent elevation of the hsCRP is linked to a higher risk of recurrent vascular events.