Thread by @ChrisZhouDO

The other day, I was asked by a med student: "Why do we give some people antiplatelet therapy and other people anticoagulation therapy?"

Time to talk about thrombotic pathophysiology!

#medtwitter #tweetorial @MedTweetorials

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A major hemodynamic difference between arteries and veins:
- Arteries have high pressure > high shear stress.
- Veins have low pressure > low shear stress.

Veins are like washing a plate in the kitchen sink.
Arteries are like power-washing the wall.

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Arterial clots are primarily due to endothelial damage leading to platelet aggregation. The high flow/shear stress prevents coagulation factors from easily attaching; thus, arterial clots are made mostly of platelets.

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Venous clots tend to be due to turbulent flow leading to venous stasis. Low flow environments allow for increased fibrin buildup. Pathologically, these clots are made of red blood cells and fibrin. Because they don't attach as well, they also easily break off into emboli.

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Thus, in patients with high risk for arterial clots, such as in CAD, we preferentially place patients on anti-PLATELET therapy.

In patients w/ venous clots, such as DVT or PE, we place patients on anti-COAGULATION therapy.

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What about A Fib? We treat w/ anticoagulation, but isn't that kinda arterial?

Turbulent flow in the left atrium, made worse w/ poor left atrial contractility in A Fib, markedly reduces flow rates.

ncbi.nlm.nih.gov/pmc/articles/P…

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In summary:

Arteries > high shear stress > platelet-rich clots > antiplatelet therapy

Veins > low shear stress > fibrin/RBC-rich clots > anticoagulation therapy

Figure source: academic.oup.com/eurheartj/arti…

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Thanks for reading first #medtweetorial. 😬

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