What Is Atherosclerotic Plaque?

It refers to the deposition of blood components such as lipids on the intima of the artery, the proliferation of smooth muscle cells, and the increase in collagen fibers, forming atheroma-like lipid-containing necrotic lesions and vascular sclerosis. The formation of atherosclerosis includes three steps: proliferation of smooth muscle cells and monocytes (possibly including lymphocytes); smooth muscle cells synthesize and secrete connective tissue components, including elastin, collagen fibrin, and proteoglycans; Lipid is mainly the accumulation of free cholesterol and cholesterol ester.

It refers to the deposition of blood components such as lipids on the intima of the artery, the proliferation of smooth muscle cells, and the increase in collagen fibers, forming atheroma-like lipid-containing necrotic lesions and vascular sclerosis. The formation of atherosclerosis includes three steps: proliferation of smooth muscle cells and monocytes (possibly including lymphocytes); smooth muscle cells synthesize and secrete connective tissue components, including elastin, collagen fibrin, and proteoglycans; Lipid is mainly the accumulation of free cholesterol and cholesterol ester.

Chinese name

Atherosclerosis

Foreign name

atherosclerosis

Atherosclerosis I. Overview

The basic pathological change is the formation of plaques on the intimal surface of the artery, with lipid streaks, fibrous plaques, and atheromatous plaques. Continued aggravation of the lesion may lead to secondary lesions such as calcification, atherosclerosis, thrombosis, and intraplaque hemorrhage. Especially the latter two secondary lesions are prone to adverse consequences. Because the lesions easily involve large elastic arteries, such as the aorta and its grade branches, medium-muscle arteries, such as coronary arteries, cerebral arteries, renal arteries, and large branches of limb arteries. In particular, the narrowing or even occlusion of the muscular arteries can cause ischemic changes in tissues or organs. Myocardial infarction caused by coronary atherosclerosis and cerebral infarction caused by cerebral atherosclerosis are the most harmful to human beings and are the cardiovascular diseases with the highest mortality rate. Regarding the nature of atherosclerotic lesions, it is now thought that the endothelial cells and smooth muscle cells of the arterial wall are overreacted after damage, and their properties are similar to inflammation.

Atherosclerosis II. Etiology and common diseases

Its etiology and pathogenesis are complex and have not yet been fully elucidated. The main risk factors are hyperlipidemia, hypertension and heavy smoking, as well as diabetes, obesity, immune damage and genetic factors.

Atherosclerosis III. Differential diagnosis

Atherosclerosis is more common in large, middle arteries, and is characterized by the formation of fibrous lipid plaques on the intima of the arteries that thicken the walls and narrow the lumen.

Atherosclerosis

Atherosclerosis mainly involves the large and middle arteries.

Atherosclerotic angiopathy

Taking aortic atherosclerosis as an example, the process of disease development can be divided into three stages:

1. The striated stage is the early pathological change of atherosclerosis in the blood vessels. Large needle spots on the intima of the artery and yellow stripe lesions of 1 to 2 mm in length and length are seen. The stripes run parallel to the long axis of the artery. See a large number of foam cells aggregated at the intima of the lesion.

2. During the period of fibrous plaque, the lipid deposits increased at the inner membrane, causing the intimal fibrous tissue to proliferate and undergo glass-like degeneration, forming a gray-white plaque protruding from the surface of the inner membrane, with a slight luster and wax-like shape. Thick fibrous tissue is called a fibrous cap.

3. Atherosclerotic plaque period, also known as atheroma, is the formation and degeneration of fibrous plaque fibrous tissue, necrosis, mixed with lipids. At this time, the lesions became larger and merged with each other, more prominently on the endometrial surface. Under the microscope, thin fibrous connective tissue was still seen on the surface of the lesion; cholesterol was crystallized and red-stained necrotic substance was deep; hyperplastic bud tissue and a small amount of foam cells were found on the basal and marginal parts.

4. Secondary changes in atheroma

(1) Plaque emergence is caused by rupture of blood vessels at the bottom and edges of the plaque. Can make the plaque process enlarge rapidly, leading to acute obstruction of the lumen.

(2) The atheroma in the ulcer-forming plaque ruptures towards the intimal surface, forming a rough and uneven ulcer.

(3) Thrombosis is caused by rough and uneven intima. Can exacerbate stenosis of the lumen and cause blockage of the arterial lumen.

(4) Aneurysm formation Due to the smooth muscle atrophy and thinning at the lesion site, local expansion and bulging are formed under the effect of blood pressure.

(5) Calcium salt deposition in calcified plaque. Reduce the elasticity of the arterial wall and increase the brittleness.

Atherosclerotic heart disease

Coronary atherosclerosis

The most common sites of coronary atherosclerosis are the left anterior descending coronary artery, followed by the right main trunk, and the left circumflex branch and left main trunk again. Vascular vessels can be involved at the same time, and the lesions are multiple and segmental. Coronary atherosclerotic heart disease caused by coronary atherosclerosis, referred to as coronary heart disease. Is one of the types of ischemic cardiomyopathy.

2. Coronary atherosclerotic heart disease

(1) Angina pectoris is a clinical syndrome caused by acute transient myocardial ischemia and hypoxia. It manifests as paroxysmal pain in the anterior region of the heart, which can be accompanied by a sense of urgency, and sometimes radiates to the left shoulder and left arm for several seconds to several minutes. The occurrence of angina pectoris is based on coronary atherosclerosis, transient spasm of blood vessels or sudden increase in myocardial oxygen consumption, myocardial ischemia and hypoxia, and acid metabolites stimulating reflex symptoms produced by sensory nerve endings. There is generally no myocardial histomorphological change.

(2) Myocardial infarction is myocardial necrosis caused by severe and persistent myocardial ischemia and hypoxia. It is common in coronary atherosclerosis with thrombosis, persistent coronary spasm, intraplaque hemorrhage, etc., leading to sudden occlusion of the coronary lumen and myocardial infarction.

Pathological changes Myocardial infarction mostly occurs in the anterior wall of the left ventricle, the apex, and 2/3 anterior to the ventricular septum; followed by the posterior wall of the left ventricle and posterior 1/3 of the ventricular septum; infarctions of the right ventricle and left ventricular sidewall are rare. Its morphological characteristics are similar to anemia infarction. Microscopically: Myocardial fibers show coagulative necrosis. Depending on the infarct time, neutrophil infiltration and granulation tissue growth may occur, and scar tissue is formed after about 5 weeks.

Atherosclerotic brain lesions

Occurrence of cerebral atherosclerosis is the middle cerebral artery and basilar artery. Insufficient long-term blood supply can cause brain tissue atrophy. The patient is mentally retarded. For example, when thrombosis is combined, the brain tissue becomes softened, and the patient shows aphasia, hemiplegia, and even death. Atherosclerosis of the cerebral arteries can sometimes lead to the formation of small aneurysms, such as small ruptures that can cause cerebral hemorrhage.

Atherosclerosis renal atherosclerosis

Renal atherosclerosis is rare in the clinic and can occur in the openings of the renal arteries, interlobe arteries, and arcuate arteries. Due to the narrowing or even obstruction of the diseased arterial lumen, it can cause renal infarction. After the infarct is mechanized, it forms a single or A number of large concave depressions. When there are more scars, the kidney volume becomes smaller. It is called renal atherosclerotic sclerosis. If it occurs in both kidneys, the two kidney lesions may be asymmetric.

Atherosclerosis V. Principles of treatment

Atherosclerosis beta blockers are good for atherosclerosis

Research from Sweden believes that B-blockers can help slow the progression of atherosclerosis.

Lipid-lowering treatment for patients with atherosclerosis and diabetes

A new study finds that correcting dyslipidemia in patients with diabetes can slow the progression of coronary artery disease. The new study, called the Diabetic Atherosclerosis Intervention Study (DAIS), found that fenofibrate can slow the progression of atherosclerosis by about 40%.

Atherosclerosis gene therapy for peripheral vascular disease

Preliminary results from a study in Finland suggest that gene therapy can help treat peripheral vascular disease.

New anticancer drug for atherosclerosis may be beneficial for heart disease treatment

Angiogenesis inhibitors, new drugs that are being tested for cancer treatment, may also have an effect on heart disease.

New drug for atherosclerosis to inhibit cholesterol absorption

It can inhibit the increase of LDL cholesterol levels without affecting HDL or triglyceride levels; if combined with statins, it may have a further effect on reducing LDL levels.

HDL- Atherosclerosis HDL-mimetic

Drugs that mimic high-density lipoprotein (HDL) are now being developed to reverse atherosclerosis by a factor. Animal tests have shown that increasing HDL levels can promote the reversal of atherosclerosis by transferring cholesterol from the arteries.