Rupture of the fibrous cap on the plaque surface often forms atheromatous ulcers and is complicated by thrombosis. Necrotic atherosclerotic material can be discharged into the bloodstream and cause cholesterol embolism.

Superficial or deep intimal damage caused by plaque rupture exposes collagen in the artery wall, causing platelet aggregation to form thrombus

In severe atherosclerotic plaques, the smooth muscle of the media at the base is compressed and thinned, and its elasticity is weakened. It cannot withstand the pressure of blood flow and causes the artery wall to expand outward and form an aneurysm.

The excessive deposition of salt and calcium in the fibrous cap and atheroma lesions causes the arterial wall to become brittle and hard, making it easy to rupture.

Rupture of new capillaries within the plaque or rupture of the plaque fibrous cap

fiber cap

base

lipid region

It is initially a gray-white plaque raised on the surface of the intima. As the collagen fibers on the surface of the plaque continue to increase and hyalinization occurs, the plaque gradually turns into a porcelain white, like a wax drop.

Foam cell necrosis leads to the formation of extracellular lipids and massive SMC proliferation.

surface

Deep

After foam cells undergo necrosis and collapse, the lipids in their cytoplasm are released and lysosomes are released to promote necrosis and collapse of other cells.

surface

Deep

Fatty streaks on the aorta are commonly found on its posterior wall and branch openings, as spots 1 to 2 mm wide or yellow stripes of varying lengths.

A large number of foam cells accumulate under the endothelial cells in fat streaks. Foam cells are round and large in size, with a large number of small vacuoles in the cytoplasm. Foam cells in fat streaks are more derived from macrophages than SMCs, and a small number of lymphocytes and neutrophils can also be seen.

gender

age

obesity

Infect

Endothelial cell damage and increased blood carbon monoxide concentration and carboxyhemoglobin increase stimulate endothelial cells to release growth factors and promote the migration and proliferation of medial SMC into the intima.

The incidence of AS is high in patients with familial hypercholesterolemia, familial lipoprotein lipase deficiency, etc.

Blood flow exerts strong mechanical pressure and impact on the blood vessel wall

Hypothyroidism and nephrotic syndrome

hyperinsulinemia

diabetes

Abnormally elevated plasma total cholesterol or triacylglycerols

Monocytes adhere to the damaged endothelial surface through adhesive molecules expressed on the surface of endothelial cells, then move into the endothelial cell space and localize in the intima, transforming into macrophages. Mediated by the scavenger shoutiW, CD36 receptors and Fc receptors on their surface, macrophages engulf a large number of lipoproteins, mainly ox-LDL, and transform into macrophage-derived foam cells, which are early lesions of AS. The main components of lipopoietinosis

The local accumulation of lipids in the blood vessel wall originates from plasma lipoproteins. Dyslipidemia caused by various mechanisms (TC, TAG, LDL, IDL, sLDL,) is the initiating link in the pathogenesis of AS.

SMC in the arterial media migrate into the intima, proliferate in the intima and synthesize EMC, transforming fat streaks into fibrous plaques and atherosclerotic plaques. Therefore, SMC proliferation is the main link involved in the formation of progressive AS lesions.

The permeability of vascular endothelial cells increases, and chronic or repeated endothelial cell damage is the initial lesion of AS.

Commonly seen in the right main trunk, but also in the left main trunk, left circumflex branch, and posterior descending branch. The left anterior descending coronary artery is the most serious.

The lesions are often segmental and mostly occur on the heart wall side of the blood vessels. The plaques are mostly crescent-shaped, causing eccentric stenosis of the lumen. They are often accompanied by coronary artery spasm, bleeding and thrombosis.

Commonly found in the posterior wall of the aorta and the openings of its branches, with the abdominal aorta the most serious disease

The lumen of blood vessels becomes thinner and is affected by blood pressure, which can easily form aneurysms. The rupture of aneurysms can lead to fatal bleeding.

Commonly occurs in the origin of the internal carotid artery, basilar artery, middle cerebral artery, and circle of WILLIS

Cerebral arteriosclerosis causes brain atrophy

95%, long course, slow progression, more common in middle-aged and elderly people

dysfunctional period

Arteriopathy stage

visceral disease stage

More common in young adults, blood pressure increases significantly, and the disease progresses rapidly

Hyperplastic arteriolar sclerosis, concentric layer thickening of the arterioles, necrotizing arteritis, mainly involving the kidneys

Rapid rise in blood pressure, persistent proteinuria, cerebral hemorrhage, retinal hemorrhage and detachment, heart failure

Hypertension has a clear hereditary tendency

People who are mentally stressed for a long time or repeatedly may easily experience cerebral cortex dysfunction.

It is inversely related to high blood pressure. People who lack physical activity have a higher risk of developing high blood pressure than those who are physically active.

Increased excitability of sympathetic nerve fibers in arterioles is the main neurological factor in the onset of hypertension

Sympathetic nervous system regulation

Regulation of the renin-angiotensin system

Pressor effects of epinephrine and norepinephrine

The role of vasoactive substances produced by vascular endothelium

Sodium and water retention

functional vasoconstriction

structural blood vessel wall thickening