Dr David McGrath

Spine Physician

MB BS (Hons) FAFOM, RACP, FAFMM
Master of Pain Medicine

Atheromatous Artery Disease
(atherosclerosis)

There are several striking facts, giving some clue to this devastating disease:

1. It affects arteries not veins
2. It occurs at certain locations more frequently (eg bifurcations)

This suggests
1. Haemodynamic inputs (pressure, turbulence )
2. Strong local Influences

There may be other inputs such as:
1. Vascular Fragility
2. Blood Viscosity
3. Repair Processes

This appears to be the case, with upstream inputs to 1-3
1. Inflammation (blood proteins such as fibrinogen)
2. Metabolic disturbance (hyper-homocysteine)
3. Oxidative stress (poor anti-oxidant reserve)

There may be further upstream inputs to those factors:
1. Carbohydrate excess, with high levels of Insulin
2. Low levels of Fat soluble Vitamins
3. Low levels of B group vitamins
4. Inadequate vitamin C
5. Infection
6. High blood pressure
7. Genetic predisposition
8. Trace element deficiency (eg copper)

Thus the speed of development of this disorder might be slowed or arrested, by influencing these upsteam convergent inputs.

In addition to the disease itself, the plaques can be either:

1. Stable. (vitamin C production of collagen, pivotal factor)

2. Unstable

Atheroma can dislodge, or fissue exposing the vascular bed to haemorhage. Inadequate clotting mechanism, can lead to vessal occlusion and infarction (death) of the downstream tissue. (eg heart attack or stroke ). Dislodged atheroma or clot can be swept downstream to block the artery at a distal site. (embolus)

Factors may influence both:
1.Clotting repair to damaged plaque
2.The stability of the original plaque.

Futher complications include
1. Dissection of damaged artery, with occlusive thrombosis
2. Tortuous expansion/elongation of the artery.
3. Aneurism or vessal wall prolapse
4. Rupture, with catastrophic consequences.

Theories
1. Vascular vulnerability (low NO at regions of low shear stress-low levels of adhesive endothelial proteins-vascular permeability high-poor antioxidant capacity-unsaturated fatty acids oxidised+oxidised cholesterol uptake-fatty streak-plaque

2. Damage to the vasa-vasorum by antigen/lipoprotein complexes in areas of high interstitial tissue pressure,with leakage of complexes into endthelial and myometrium space

3. Antibodies to lipoprotein complexes eg ag-LDL complex

4. Failure to clear overloaded foam cells from endothelial space. Insufficient HDL

4.

(to be continued)