Atheroma & Thrombi: Causes & Effects

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SUMMARY

Atheromas form primarily due to the accumulation of low-density lipoproteins (LDLs) and macrophages beneath the endothelium, rather than from an initial thrombus formation. This process involves macrophages entering the endothelium, leading to inflammation and thickening of the vessel wall, which narrows the blood vessel. The instability of atheromas can result in plaque rupture, exposing tissue factor (TF) that triggers coagulation and thrombus formation. Understanding these mechanisms is crucial for addressing cardiovascular diseases.

PREREQUISITES
  • Understanding of atheroma formation and its relationship with LDLs and macrophages
  • Knowledge of endothelial cell function and vascular biology
  • Familiarity with the coagulation cascade and the role of tissue factor (TF)
  • Basic concepts of inflammation and its effects on vascular health
NEXT STEPS
  • Research the mechanisms of LDL accumulation and its impact on endothelial health
  • Study the role of macrophages in atheroma development and inflammation
  • Explore the coagulation cascade and the significance of tissue factor (TF) in thrombus formation
  • Investigate treatment options for unstable plaques and their implications for cardiovascular health
USEFUL FOR

Cardiologists, vascular biologists, medical students, and healthcare professionals interested in understanding the pathophysiology of atherosclerosis and thrombotic events.

Cheman
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Atheroma and thrombi...

I have read that atheromas usually result when a tear occurs in the endothelium occurs which allows phagocytes and LDL's to enter, etc.
Why does this occur rather than a thrombus form first? Afterall, clots form when we cut ourselves as a result of the blood being exposed to collegen - surely this would be exposed when a tear occurs in the endothelium?

Also, I have read that atheromas, as they are rigid, can break and this leads to formation of thrombi - is this because collegen in vessal walls is exposed, or something inside the atheroma?

Thanks in advance. :smile:
 
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Cheman said:
I have read that atheromas usually result when a tear occurs in the endothelium occurs which allows phagocytes and LDL's to enter, etc.
Actually the LDL accumulates underneath the endothelium without there being a tear. Also, macrophages can enter the endothelium by squeezing themselves so there is no tear.

So, what happens is that LDL accumulates, macrophages are attracted that try to eat the LDL, the macrophages overeat and die, more macrophages get attracted due to an inflammation response, endothelial cells start to replicate, this thickening of endothelium leads to a narrowing of the bloodvessel. The narrowing of the bloodvessel can be dangerous when it leads to an obstruction, but it is more dangerous to have an unstable plaque which can tear. You are correct that this leads to thrombi formation, because a chemical that is called TF (tissue factor) is released from the inner part of the vessel wall that activates coagulation.
 

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