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36
Progression of
Atherosclerosis
- Fatty Streaks- Fatty streaks are composed of lipid-filled foam cells but are not
significantly raised and thus do not cause any disturbance in blood
flow
- Fatty streaks can appear in the
aortas of infants younger than 1 year and are present in virtually all
children older than 10 years, regardless of geography, race, sex, or
environment.
- The relationship of fatty streaks
to atherosclerotic plaques is uncertain; although they may evolve into
precursors of plaques, not all fatty streaks are destined to become
advanced atherosclerotic lesions.
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Progression of
Atherosclerosis
Atherosclerotic
Plaque-The key processes in atherosclerosis
are intimal thickening and lipid accumulation Atheromatous plaques (also
called fibrous or fibro fatty plaques) impinge on the lumen of the artery
and grossly appear white to yellow
Plaques vary
from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses.
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Components of
Atherosclerotic plaque
- Atherosclerotic plaques have three principal components:
- Cells, including SMCs, macrophages, and T cells
- ECM, including collagen, elastic fibers, and proteoglycans
and
- Intracellular and extracellular lipid
- These components occur in varying proportions and
configurations in different lesions.
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Changes in Atherosclerotic
Plaque
Atherosclerotic
plaques are susceptible to the following pathologic changes with clinical
significance:
- Rupture, ulceration, or erosion
- Hemorrhage
- Atheroembolism
- Aneurysm formation
- Atherosclerosis is a slowly evolving lesion usually
requiring many decades to become significant.
- However, acute plaque changes (e.g., rupture, thrombosis,
or hematoma formation) can rapidly precipitate clinical sequelae (the so-called
"clinical horizon“)
40
Progression of
Atherosclerosis
41
Atherosclerosis-
Symptoms
- Symptomatic atherosclerotic disease most often involves
the arteries supplying the heart, brain,
kidneys, and lower extremities.
- Myocardial infarction (heart attack), cerebral infarction (stroke), aortic aneurysms, and peripheral vascular disease (gangrene of
the legs) are the major consequences of atherosclerosis.
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Prevention of
Atherosclerotic Vascular Disease
Primary prevention aims at either delaying atheroma formation or encouraging regression
of established lesions in persons who have not yet suffered a serious
complication of atherosclerosis
Secondary prevention is intended to prevent recurrence of events such as myocardial
infarction or stroke in symptomatic patients
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Prevention of
Atherosclerotic Vascular Disease
Primary prevention
of atherosclerosis
- Cessation of cigarette smoking
- Control of hypertension
- Weight loss
- Exercise, and lowering total and LDL blood cholesterol
levels while increasing HDL (e.g., by diet or through statins).
- Statin use may also modulate the inflammatory state
of the vascular wall.
- Risk factor stratification and reduction should even
begin in childhood.
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Prevention of
Atherosclerotic Vascular Disease
Secondary prevention
involves use of –
- Aspirin (anti-platelet agent),
- Statins, and beta blockers (to limit cardiac demand),
- Surgical interventions (e.g., coronary artery bypass
surgery, carotid endarterectomy).
- These can successfully reduce recurrent myocardial
or cerebral events.
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Summary
- Atherosclerosis is an intima-based lesion organized
into a fibrous cap and an atheromatous (gruel-like) core and composed
of SMCs, ECM, inflammatory cells, lipids, and necrotic debris.
- Atherogenesis is driven by an interplay of inflammation
and injury to vessel wall cells.
- Atherosclerotic plaques accrue slowly over decades
but may acutely cause symptoms due to rupture, thrombosis, hemorrhage,
or embolization.
- Risk factor recognition and reduction can reduce the
incidence and severity of atherosclerosis-related disease.
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