Plaque disruption the healing process

The great majority of episodes of plaque disruption do not cause a major event such as infarction or death. Minor episodes of erosion or disruption are often clinically silent but do contribute to the episodic progression of coronary artery disease seen on sequential angiography.

Thrombus will be removed by natural lysis to some extent and is also associated with "passi-

Plaques at risk of future thrombotic events are characterised by:

• Large lipid cores (> 50% overall plaque volume)

• High densities of macrophages and high levels of expression of tissue factor and metalloproteinases

• Low densities of smooth muscle cells fication", a term implying that the exposed collagen becomes less active in causing platelet adhesion probably due to being coated by natural heparinoids. Any residual thrombus which is still present after 36 hours will provoke smooth muscle cell migration into the area, with the production of new connective tissue which smooths out the surface and restores plaque integrity. The final result will be a stable lesion which may cause anything from chronic total occlusion to only a minor increase from the pre-existing degree of stenosis. The process, however, takes weeks and residual thrombi in the base of the exposed lipid core act as a nidus for a further thrombotic event at the same site for up to six months.

The risk of progressing to complete occlusion on angiography within a year of an episode of unstable angina, or after lysis for acute myo-cardial infarction, is far higher if the culprit lesion has an irregular outline on the initial angiogram taken immediately after the acute event.15

Mechanisms of myocardial ischaemia in non-occluding coronary thrombosis

• Distal embolisation of aggregates of platelets

• Intermittent total occlusion

• Spasm at thrombus site than individual risk. One explanation is that the subjects with the highest concentrations of C reactive protein have the largest plaque mass. The link between systemic markers of chronic inflammation and acute coronary events may, however, be more complex. There is experimental evidence that upregulation of systemic inflammation will have a secondary affect of enhancing inflammatory activity in the plaque.17 18 On this basis any factor which increases systemic inflammation would potentially trigger plaque instability and increase the risk of unstable angina. Causes of such systemic low grade inflammation include infection by chlamydia or helicobacter, diseases such as rheumatoid arthritis, and chronic dental sepsis.

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