Overview
Arteriosclerosis is an artery condition that occurs when an artery's wall gets thick and loses elasticity. Oxygenated blood with nutrition flows through arteries from the heart to organs and tissues in the body. If an artery wall gets thick, it will restrict the blood supply to other organs. Eventually, this leads to many severe conditions.
Symptoms of arteriosclerosis
Usually, there are no symptoms. This is why regular checkup is necessary. When the artery progress to its severe condition by a clot, it may show the following symptoms of heart attack and stroke
- Angina (chest pain)
- High blood pressure
- Loss of vision
- Difficulty in speaking
- Dangle facial muscle
- Kidney failure
Types of arteriosclerosis
- Atherosclerosis
- Arteriolosclerosis
- Monckeberg medial calcific sclerosis
1. Atherosclerosis
An artery's wall is made up of three layers, intima (inner layer), media (middle layer, and adventitia (outermost layer). Atherosclerosis is a degenerative disease of large and medium-sized arteries characterized by forming a plaque in the intima. Intima is the layer on top of the basement membrane within the endothelial. This intimal plaque mostly consists of a necrotic lipid core (the key product would be cholesterol). This plaque has a fibromuscular cap overlaying the necrotic lipid core and it is not common for atherosclerosis to be calcified.
Arteries involved in atherosclerosis
- Large arteries
- Aorta (especially the abdominal artery)
- Aorta's large branches (iliac artery, and internal carotid artery)
- Medium-sized arteries
- Coronary arteries
- Cerebral arteries
- Renal arteries
Risk factors of atherosclerosis
Divided into modifiable, nonmodifiable, and additional risk factors.
Modifiable risk factors
- Hyperlipidemia (Usually diet-dependent but may also occur as a result of some forms of familial hyperlipidemia. This is the major risk factor for atherosclerosis, HDL decreases the risk and LDL increases the risk of hyperlipidemia. HDL is believed to mobilize cholesterol from an existing atheroma and transport it to the liver for excretion in the bile)
- Hypertension (Hypertension is another major risk factor for the development of atherosclerosis, the risk is diminished when the blood pressure is controlled by drugs)
- Smoking (Damage to the endothelium, the mechanism is unclear, such as Carbon monoxide)
- Diabetes mellitus (those who have had Diabetes Mellitus for more than 10 years are likely to have atherosclerosis)
Good cholesterol foods
Nonmodifiable factors
- Age (severity of atherosclerosis increase with age)
- Gender (males and postmenopausal females have increased risk. premenopausal women are relatively protected against atherosclerosis compared with age-matched men because of estrogen)
- Genetics (most familial risk is related to polygenic traits)
Other risk factors
- Inflammation
- Metabolic syndrome
Atherosclerotic risk factors
Pathogenesis of atherosclerosis
The endothelium is sitting on top of the membrane. if there is damage to the endothelium within the intima, lipid molecules will enter into the intima then lipids will be oxidized. Once it gets oxidized it will be taken up by macrophages so there will be a collection of macrophages with lipids within them. That forms the initial lesion of atherosclerosis which is called fatty streaks. Nowadays there will be yellow fatty streaks that are running along the large blood vessels of teenagers, they arise early in life. Eventually, if a patient gets inflammation and healing and increased deposition of lipids within the intima, that is going to result in the thickening of this lipid layer within the necrotic lipid core and the formation of the fibromuscular cap. The fibromuscular cap is due to the inflammation and healing which leads to the deposition of extracellular matrix and proliferation of smooth muscle and in the end, it is going to create an atherosclerotic plaque that will occlude the blood flow.
Morphology of atherosclerosis
The key processes are intimal thickening and lipid accumulation
- Fatty streak
- Atherosclerotic plaque
- Complicated plaques
Fatty streak
Grossly multiple yellow flat spots and streaks, slightly raised above the intimal surface. There will be no disturbance of blood flow. Can appear in the aortas of infants younger than 1 year of age and are present in virtually all children older than 10 years. Although they may develop precursors of plaques it is uncertain.
Atherosclerotic plaque (atheroma)
Grossly, white to yellow, and raised focal lesion. Impinge on the lumen of the artery. These lesions are more prominent around the origins of major branches.
Microscopically, the superficial fibrous cap is consist of dense collagen, scattered smooth muscle cells, and macrophages. the deep fibrous cap will have a necrotic core, foam cells extracellular lipids, cholesterol crystals, debris, and fibrin.
Complicated plaques
- Thrombus formation at the plaque (the most feared complication. there will be a rupture and ulceration on the surface of the plaque. Loss of endothelial integrity and exposure to thrombogenic substances lead to thrombus formation)
- Hemorrhage into the plaque (due to rupture of fibrous cap and capillaries. Hemorrhage may acutely narrow the arterial lumen)
- Calcification (dystrophic calcification will increase the rigidity of the wall)
- Aneurysms (localized dilation of blood vessels)
Complications of atherosclerosis
Account for more than half of diseases in the western world
- Stenosis of medium-sized vessels (usually major organs in the body are getting blood through medium-sized vessels. if one of those arteries is blocked by atherosclerosis, that is going to cause stenosis of that blood vessel. Hence this can result in various signs and symptoms. This can occur in the coronary artery resulting in episodic chest pain or angina. if the popliteal artery is blocked by atherosclerosis, it will result in peripheral vascular disease. it also can occur in mesenteric arteries which could create ischemic bowel disease. Usually, patients don't get symptoms until they have greater than 70% stenosis.
- Rupture of plaque with stenosis (usually, the neck of intimal plaque will get ruptured which will then expose all that necrotic lipid core and the tissue underneath the necrotic lipid core will be exposed and that is going to result in activation of the coagulation cascade and so rapidly that will develop a thrombus which could then occlude the vessel and create infarction in that organ. This is how myocardial infarction occurs. If this occurs in the coronary artery resulting in myocardial infarction and this could also occur in the middle cerebral artery and lead to developing a stroke)
- Plaque rupture with embolization ( it is possible for a plaque to break off and then part of that plaque could embolize and go through the blood supply and then lodge in a distance site. Which is called embolization)
- The blood vessel wall gets weak (the vessel wall contains intima, media, and adventitia. Blood vessel walls require oxygen to maintain themselves. Usually, the oxygen from the blood feeds the entire vessel wall. However, if an artery gets atherosclerosis which means the inner layer or intima becomes thick and creates a diffusion barrier, as a result of this oxygen can not feed the vessel wall then the vessel wall becomes weak and atrophic. As the wall is weakened it is going to increase the risk of ballooning of the wall because now it is a weak wall with a lot of stress. So the complication would be it could develop something called an aneurysm which is balloon-like dilatation of the blood vessel wall.
2. Arteriolosclerosis
Arteriolosclerosis means the thickening of a small blood vessel wall which then narrows the small blood wall and then creates complications downstream. Arteriolosclerosis is divided into hyaline arteriolosclerosis and hyperplastic arteriolosclerosis.
Hyaline arterioloscerosis
Proteins will leak into the small blood vessel wall. This produces vascular thickening and microscopically, there will be a pink hyaline appearance within the blood vessel. It arises due to two conditions the first one is benign hypertension (because high blood pressure forces the protein into the blood vessel wall) and the second condition is Diabetes (patients who have diabetes, have non-enzymatic glycosylation of the basement membrane which then makes the blood vessel wall leaky and then protein begins to leak in)
A consequence of hyaline arteriolosclerosis is reduced vessel caliber which is going to result in end-organ ischemia. This can occur throughout the body but it classically occurs within the kidney producing glomerular scarring (if the afferent arteriole of the glomerular gets hyaline arteriolosclerosis it will decrease the blood flow to the glomerulus. The glomerulus will then scar which is called glomerular scarring) so this is the key consequence of hyaline arteriolosclerosis.
This is the reason why patients with diabetes and patients with high blood pressure get chronic renal failure because over time it develops this glomerulus scarring (arteriolonephrosclerosis) due to hyaline arteriolosclerosis.
Hyperplastic arteriolosclerosis
In this case, instead of wall thickening due to protein leak, there will be hyperplasia of smooth muscle which then results in something called onion-skin thickening. This reduces the luminal caliber which then decreases the blood flow to the organ.
Hyperplastic arteriolosclerosis is the consequence of malignant hypertension. When there is very high blood pressure, the smooth muscle of the vessel wall begins to respond by hyperplasia, which is called hyperplastic arteriolosclerosis. The luminal narrowing is going to result in reduced vessel caliber so it leads to end-organ ischemia.
High blood pressure can also result in fibrinoid necrosis. The classical finding is an acute renal failure with a flea-bitten appearance.
3. Monckeberg medial calcific sclerosis
It doesn't alter the luminal caliber, therefore it doesn't affect the blood flow and which is not clinically significant. It can show up on x-rays in particular on mammography. Mammography is classically used to find out calcification as a sign of cancer.
