External atherosclerosis pathology
Lesions are localized in the endothelium; the endothelium is moderately thickened. The characteristic cells contain adipocytes (foam cells). The middle layer and outer coat are normal.
Atherosclerosis is a very common anatomic injury to the artery wall.
The definition of atherosclerosis is the anatomical definition: it is the alteration of the endothelium of the arteries with large and medium aperture, including the local formation of lipids, glucide complexes, blood and blood products, fibrous deposits and calcifications. All these factors will then alter the midsole (OMS, 1958).
There are many risk factors for atherosclerosis. Atherosclerosis is a serious medical phenomenon because it causes many complications.
The basic treatment is internal medicine. Get surgical treatment for complications.
It is necessary to know the structure of normal artery walls and atherosclerosis:
The structure and physiology of the artery wall are normal
Arterial wall consists of 3 layers from inside to outside: the endothelium, the middle layer and the outer layer (the outer layer).
The endothelium (intima)
Consists of endothelial and sub-endothelial cells. Between the endothelium and the middle layer there is also an elastic leaf. The endothelium has 2 basic functions:
Endothelial cells come into direct contact with the circulating blood stream and prevent blood clots from forming. Endothelial cells play a fundamental role in the regulation of coagulation - haemostasis and thrombosis (it synthesizes 2 of the 3 components of factor VIII), it captures circulating heparin and maintains an electrical negative potential are required on the surface to prevent thrombosis.
Prevent large molecules and blood cells from seeping through.
Middle coat (media)
The middle layer ensures the arterial function of the arteries. Consists of concentric smooth muscle fibre layers.
The smooth muscle cells of the midsection have two main functions:
In addition to the spasmodic effect, it also ensures vasomotor and arterial tone.
It synthesizes the components of the midsole fibre frame.
Mainly connective tissue made up of fibroblasts, fat cells, collagen fibres and mucopolysaccharides. This layer is nourished by the vasodilator vessel (vasa vasorum).
Morphology of atherosclerotic lesions
The primary and primary atherosclerosis is pathology of the arterial endothelium.
Lipid streaks and fat streaks:
General: These are lesions that take the form of white or yellow streaks and form closed folds in the artery lumen. The size of these streaks varies, but with the naked eye, the vein is still smooth.
Micro: Localized lesions in the endothelium, the endothelium is moderately thickened. The characteristic cells contain adipocytes (foam cells). The middle layer and outer coat are normal.
Uncomplicated atheroma plaques: These plaques are easy to see with the naked eye, white or slightly Gray in colour.
Microscopically we can see two parts of a plaque: the fibrous organization, forming a boundary between the plaque and the middle layer. Composed of collagen, mucopolysaccharide, elastin and fibrin arrays. There is a fat organization in the centre. The fat tissue just below the atheroma is thinning. Whether the outer coat has been changed or not.
The progression of atheroma can be: Calcification, stenosis, ulcers, thrombosis and haemorrhage and this is a major part of the clinical manifestations.
All atheroma is always calcified. The calcium deposits are deposited in the fibrous organization of the plaque and partly in the centre of the plaque. It is necessary to distinguish calcification of atheroma from calcification of the inner and middle elastic layers.
Atherosclerosis is usually narrowing of the lumen caused by the plaques of atheroma. Stenosis can decrease blood flow and create an artery flow disorder. Complete stenosis can be caused by an atheroma or, more commonly, by a blood clot forming on the plaque.
This is the rupture of atherosclerotic plaques with a breakdown of the endothelium, the central part of the plaque opening to the lumen, causing the blood flow to come into direct contact with the lower endothelium and cause thrombosis. Breaking up atheroma can cause atheroma or embolism of cholesterol crystals.
Thrombosis usually forms at an ulcer of atheroma, because the lower endothelium (which has platelet binding properties) comes into contact with the blood stream. Initially white thrombosis (due to platelet adhesion), later covered by fibrin to form a layer of red blood cells (mixed thrombosis or red thrombosis). Thrombosis may progress to.
Classification of atheroma lesions
Atheroma lesions are categorized in several ways, here we classify them according to the American Heart Association.
Board. Classification of atheroma lesions.
Lipids are deposited in the endothelium, in the centre of single foam cells (macrophages).
Lots of foam cells accumulate in the endothelium (macrophages and muscle cells).
Appearance of Lipids in extracellular matrix
This is considered to be the first progressive lesion; lipid concentrates in the intracellular region
Mature atheroma (atheroma + atheroma)
Atheroma rupture, thrombosis formation or internal haemorrhage => thrombosis / embolism
Distribution of atherosclerotic lesions on the arterial system
Atherosclerosis can affect anywhere on the artery system with a large to medium aperture. The most common sites, however, are the branching sites, the bifurcation sites, the curved branches and the artery stenosis.
The single cause for atherosclerosis probably doesn't exist, but a lot of risk factors can be found.
The danger elements
Constant (irreversible) risk factors
Age: Atherosclerotic lesions appear very early and increase with age; Age reflects how long an individual is exposed to other risk factors.
Gender: Men have a higher risk of atherosclerosis than women (male / female = 5/1).
Genetic traits: A family history of cardiovascular disease (parent-father) is also a high-risk factor.
The risk factors are modifiable
Lifestyle risk factors:
Tobacco: In addition to the overall risk of causing cancer, it also causes atherosclerosis. The risk is associated with the number of packages of cigarettes per year.
Diet: A diet high in saturated fatty acids causes high atherosclerosis by increasing the ratio of LDL - Cholesterol.
Drinking alcohol: Alcohol increases blood pressure and triglycerides.
Obesity: Assessment based on body mass index (BMI = Body mass index).
Normal BMI is 20-25 in men and 19-24 in women. Pathological obesity when BMI> 40. Male obesity (waist circumference> 102 cm in men and> 88 cm in women) is at highest risk.
How It Works: Regular bodily activity alters risk factors (maintaining a normal weight, reducing smoking and making dietary changes). Activity also reduces LDL - Cholesterol.
Spiritual - social factors.
Diabetes: Type I and II diabetes are both associated with an increased cardiovascular risk. For type I diabetes, risk appears before age 30. While type II diabetes is often accompanied by other risk factors (hypertension, dyslipidaemia, obesity).
The increase in LDL - Cholesterol and triglycerides are very dangerous. The increase in HDL- Cholesterol has a protective effect.
Hypertension: The most important cardiovascular effects of hypertension are cerebral vessels
New risk factors
Increased blood homocysteine.
Increased fibrinolytic blood count.
Increased C Reactive protein (CRP).
Pathogenesis of atheroma
The physiological mechanism of the disease is still unknown. However, there are risk factors that contribute to atheroma:
Altering endothelial cells.
Increases the production of smooth muscle cells, endothelium.
Changes in metabolism in smooth muscle cells (lipid accumulation, increase LDL - cholesterol ...) (H. 14.2, 5, 6 and diagram 14.1).
This is an early cell that is influential in the pathogenesis of atherosclerosis.
The first step is to adhere to the endothelium, then to penetrate the endothelium.
These cells can transform into cellule spumeuse, which are fat droplets after LDL binding.
Smooth muscle fibre (FML)
Is the second most important factor.
It is able to move, multiply, and synthesize elements of the extracellular framework. This contributes to the formation of the fibrous part of the plaque.
The role of smooth muscle fibres appears to be important in the process of stenosis following vascular formation.
This is the barrier that works between the blood flow and the artery wall.
All the mechanical or mechanical changes of the endothelial cell increase the formation of atheroma, which facilitates platelet aggregation.
Platelets can not only facilitate artery occlusion, but also participate in atheroma formation due to growth factor synthesis (PDGF).
The alteration of endothelial cells facilitates adhesion of mononuclear cells and penetration of lipid molecules.
There are many factors in this group, including growth factors, cytokines, etc. and especially LDL. LDLs undergo oxidation inside artery walls, causing foam cells to form. In fact, only the modified or oxidized LDL is captured by the macrophages.
Spread of the injury
Along with the endothelial cell changes are nicotine, LDL, increased blood pressure, various injuries.
Facilitates adhesion, followed by infiltration of mononuclear cells (it turns into macrophages) and invasion of LDL.
In addition, the endothelial alteration facilitates platelet adhesion, it secretes growth factor, which stimulates the proliferation of smooth muscle fibres. Smooth muscle fibres synthesize the extracellular matrix and can be converted into foam cells.
Vascular diseases caused by atherosclerosis
Lower extremity artery disease caused by atherosclerosis
Atherosclerosis or atherosclerotic arteritis is the most common cause of lower limb artery diseases with a frequency of about 1% in the population.
The male to female ratio # 3/1 and age of onset usually starts at 40 years, while the onset of females is usually about 10 years later.
In lower extremity arteritis, lesions can be found simultaneously in all locations: from the aorta in the lower kidney to the arteries in the lower legs. However, the pelvic and superficial arteries are the most commonly damaged sites.
In diabetic atherosclerosis, the pathogenesis is completely different from the pathogenesis of patients without diabetes. Very little calcified blood vessels are, atherosclerosis lesions are often peripheral and can affect small blood vessels, especially arteries in the legs.
Patients with atherosclerotic obstruction of the lower extremities often have combined damage in many arteries in different locations: the risk of damage to coronary arteries in 5 years is 40-50%, damage to brain blood vessels, carotid circuit in 15 - 20% of cases.
Clinical examination of 1 patient with obstructive lower limb artery caused by atherosclerosis to:
Determine the extent of vascular damage.
Determine the degree of anaemia of the limbs, locate the damage in the lower extremities.
Determine the stage of the disease according to Leriche - Fontain.
Select appropriate subclinical investigations, determine treatment options.
Atherosclerosis of the artery trunks in the aortic arch and the arteries reaching the brain
Circulation for the brain is ensured by two carotid arteries, the vertebrae, and these two systems are connected by Willis polygons.
Atherosclerosis is often characterized by fibrous-endothelial plaques and increases in size over time. Progressive injury gradually causes tight narrowing and thrombosis.
Clinically Possible: Asymptomatic (detected by a blowing in the carotid artery just below the jaw angle or detected by asymmetrical biceps), or clinical symptoms (transient ischemia, stroke due to carotid stenosis, cerebrovascular accident due to stenosis of the vertebral artery - basal body).
Marseille classification in cerebrovascular pathology (1984):
Stage 0: The disease has no symptoms.
Stage I: Transient cerebral anaemia.
Ia: Short time.
Stage II: Progressive stroke.
IIa: The disease improves.
IIb: Progressive disease.
Stage III: Stable stroke.
IIIa: Leaving mild sequelae.
IIIb: Leaving severe sequelae.
Diagnosis is based on clinical and subclinical investigations (Doppler ultrasound, CT Scan, carotid artery scan, vertebrae - basal body). Depending on the degree of narrowing of the artery and each clinical situation, medical or surgical treatment is indicated.
Pathology of the digestive arteries
Gastrointestinal arteries include the visceral trunk artery, the mesenteric artery, the lower mesenteric artery. The most common atherosclerotic lesion is the narrowing or complete obstruction of these arteries and the clinical appearance of acute or chronic intestinal anaemia. Some fewer common cases are lesions of the aneurysm (accounting for about 1 / 10,000 cases of autopsy). It is important to identify the aneurysm injury before its complications (rupture, thrombosis - embolism).
Stenosis / occlusion of the gastrointestinal artery is relatively rare. The disease often appears in obese people and is often combined with other vascular diseases (coronary artery, carotid artery disease, chronic lower limb vascular disease ...). Clinically suggests when there are three controls: abdominal pain after eating (20-30 minutes), weight loss, and hearing blowing in the epigastric region.
The diagnosis is usually made by a selective gastrointestinal angiogram.
Treatment is mainly surgery. The most commonly used methods are to remove the endothelium, the aortic bridge - downstream or upstream digestion, and percutaneous angioplasty.
Renal atherosclerosis pathology
Atherosclerotic renal artery stenosis is the most common cause of renal artery stenosis (70-80%). The damage is usually found in the renal artery or around the renal artery hole (80% of cases).
In 75% of cases, the kidney artery was damaged in both sides. There is no specific clinical sign of renal artery stenosis, but the frequency is very high in newly emerging severe hypertension cases and a murmur in the renal artery is often detected. Diagnosis is based on Doppler ultrasound, renal artery scan, CT Scan. Treatment is mainly surgery, or intervention through the intravascular route
Treatment of major risk factors: dyslipidaemia, tobacco addiction, diabetes, hypertension ...
Treatment of complications of atherosclerosis by preventing primary or secondary.
Treatment of vascular lesions in specific vascular pathologies.
Prevent risk factors
Primary prevention (level 1)
Is the prevention of risk factors in the absence of atherosclerosis.
Treatment of hypertension: Treatment decisions depend on the degree of hypertension, the characteristics of hypertension, and the combined risk factors.
Diabetes: Must maintain a stable blood sugar, guide patients to use a reasonable diet and have regular monitoring regimen.
Lipid disorders: risk assessment based on LDL - Cholesterol fraction
Obesity: Must use a low-calorie and fat-poor diet, and coordinate with regular physical activity.
Secondary prevention (level 2)
Means to prevent when the symptoms of the vascular disease appear. Treatment includes the prevention of general risk factors (as above), anti-platelet aggregation therapy and the indication of case-based surgery.