Atherosclerosis

Atherosclerosis is the settling of the so-called atherosclerotic plaque (also atheroma) below the inner surface of the vessel wall, thereby ultimately causing their narrowing and obstruction. The name does not originate from the word artery, but in ancient Greek it means something like hardening of oatmeal. This refers to the nature of the atheroma mass and the fact that in the advanced phase with the help of calcium the surface of the atheroma hardens (calcifies).

The simplified process works as follows:

• normally, cholesterol-transporting lipoproteins (LDL) circulate in the body through the vessels, and are absorbed in target tissues (which actually need cholesterol) or in the liver. The correct pathway is mediated by the LDL receptor.
• worse, LDL penetrates the interior of the vessel (where blood flows) just below the surface of the vessel wall
• LDL oxidizes in the vessel wall, making it a target for immune system (scavenger receptor – inflammatory process)
• a monocyte (white blood cell) arrives beneath the vessel wall, forming a macrophage (a cell that has the task of destroying pathogens) and starts to eat oxidized LDL until it becomes full (it becomes a foam cell)
• Instead of being decomposed with undesirable contents (which is its normal function), the macrophage remains in place until it “dies” and discharges its contents into the space in the vessel wall. This creates a “mash” predominantly consisting of dead macrophages and cholesterol, which further stimulates inflammation.
• a protective fibrous envelope is formed around the mash that separates it from the inside of the vessel, where blood flows
• The volume of the mash in the vessel wall (atheroma) increases over the course of decades. The vessel is not narrowing yet, it bulges out instead and the flow remains the same. Therefore, it is virtually impossible to directly diagnose it using available methods (stress test, angiography, ultrasound, CT, MRI) and a person still feels OK.
• at a later stage, the cover of the atheroma (the partition between the settled slurry and the flowing blood) starts to harden (using calcium) and sometimes becomes thin, making it fragile and prone to break
• especially at higher blood pressure, this bar breaks and the slurry (plaque) is thrown into the vessel through the newly formed crack. Blood clots arise immediately:
  • around the crack, which immediately obstructs the blood vessel, or the vessel remains tapered after the crack has been healed up (this is a moment when this condition finally can be diagnosed)
  • around the ejected mass, which can also block the vessel, either straight in place, or downstream when the clot enters the capillary

Risk factors and mechanisms for the prevention of atherosclerosis are very similar to those of type 2 diabetes, and both are part of the metabolic syndrome.
The mechanism of some risk factors is as follows:

• factors increasing oxidative stress (smoking, alcoholism, polluted environment, trans fats, lack of vitamins and antioxidants):
  • the effect of free radicals worsens the quality of the tissue inside the vessel, which is then more prone to LDL penetration
  • promoting LDL oxidation below the vessel surface
  • at a later stage, promoting the inflammatory process
• traditional “western” diet, overeating:
  • it’s involved in increasing oxidative stress (see above)
  • forms dyslipidemia (especially increase in relative LDL concentration, resulting in more cases of LDL penetration into the vessel wall)
  • inhibits (suppresses) LDL receptor function (more LDL particles remain unabsorbed and thus potentially risky)
• excessive consumption of carbohydrates (fast carbohydrates, refined carbohydrates, added sugar, especially added fructose):
  • it forms a specific dyslipidemia, which involves the reduction of HDL and the increased formation of small LDL particles (sdLDL), and these are capable of penetrating inside the vessel walls
• stress
  • increases blood pressure (hypertension), which strains the vessel wall that so it becomes more permeable to LDL
  • at a later stage, the internal wall of the vessel is more prone to fractures due to hypertension
  • increases LDL concentration
• saturated fats
  • debatable (under certain circumstances)

The mechanism of some prevention factors:

• balanced ω-3:ω-6 ratio in tissues (ie emphasis on ω-3)
  • counteracts chronic inflammation (and thus suppresses atheroma spreading)
  • corrects the lipid profile (especially lowers the level of triglyceride and small sdLDL particles)
  • it also acts antithrombotically (and thus reduces the risk of blood vessel clogging in the event of atheroma rupture)

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