Atherosclerosis/CVD is the leading cause of death world-wide.
Location and lifestyle plays a huge part in MI
1.1 Risk factors
Genetics: Most important risk (family history). But it is a small percentage.
Age: MI increases fivefold between ages 40 to 60.
Gender: Premenopausal females are less likely to have MI, but the ones post menopausal have higher risk than males
Almost the same as the one for forming a clot.
Except it forms a chronic inflammatory response and stance towards it.
Lesion progression involves interaction of modified lipoproteins, monocyte-derived macrophages, T Lymphocytes and the cellular constituents.
It results from the following pathogenic events:
Accumulation of lipoproteins
Monocyte adhesion to the endothelium and differentiation into macrophages and foam cells.
Smooth muscle cell recruitments due to the factors realised
Smooth muscle cell proliferation and ECM production.
Fatty streaks coalesce into elongated lesions. Composed of lipid-filled foamy macrophages are minimally raised.
3.1 Atherosclerotic Plaque
3 principal components:
1. Cells incl smooth muscle, macrophages and T Cells
3. Extracellular Matrix: Includes collagen, elastic fibbers and proteoglycans
3. Intracellular and extracellular lipid:
3.2 Acute Plaque Changes
Stable vs Unstable plaques.
Stable plaques tend to have a smaller lipid core, a thicker fibrous cap.
Unstable plaques on the other hand have lpids in the core, thin fibrous cap and more macrophages and T cells.
May induce thrombus formation. may lead to tissue ischaemia. It may organise and incorporate into growing plaque.
3.2.3 Haemorrhage into atheroma
Rupture plaque could discharge debris into blood.
Pressure may also cause ischaemic atrophy of underlying media, with loss of elastic tissue and cause structural weakening to dilate and rupture.