Plaque vulnerability, arterial remodelling and age-related risk
THE CONTEXT
Plaque composition and mechanical stress influence rupture, while arterial remodelling changes the effect of atheroma on the lumen. Age and sex also influence disease risk.
Vulnerable and stable plaques
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Plaque number and complexity increase with age and risk factors, but individual plaques progress at variable rates.
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Vulnerable plaques have a lipid-rich core, a thin fibrocellular cap, speckled calcification and increased inflammatory cells that release matrix-degrading enzymes.
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Stable plaques have a small lipid pool, a thick fibrous cap, heavy calcification and plentiful collagenous cross-links.
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Fissuring and rupture tend to occur where mechanical stress is greatest, especially at the margins of an eccentric plaque. A surge in blood pressure during exercise or emotional stress may trigger an event.
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Most plaque events are subclinical and heal spontaneously. Incorporation of thrombus into the lesion can nevertheless enlarge the plaque and further obstruct flow.
Arterial remodelling
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Atherosclerosis can alter the arterial media and produce remodelling.
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Negative remodelling is slow constriction of an arterial segment; positive remodelling is gradual enlargement.
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These changes may amplify or minimise the extent to which atheroma encroaches on the arterial lumen.
Age, sex and unexplained risk
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Age is the most powerful independent risk factor for atherosclerosis.
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Pre-menopausal women have lower disease rates than men. The sex difference disappears after menopause, and women develop the same degree of coronary artery disease about 10 years later than men.
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Hormone replacement therapy does not prevent coronary artery disease and is associated with increased cardiovascular events in post-menopausal women.
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Unknown factors account for up to 40% of variation in atherosclerotic risk between individuals.