London, Aug 26 (Inditop.com) Thick blood is a double edged sword. It can cause heart attacks and strokes, but prevent them as well.
Scientists explained for the first time how this clinical paradox works. Mice with a greater tendency to form blood clots have larger plaques in their vessels, but they are more stable. Thus, there is less risk that these plaques will rupture and obstruct circulation.
In principle, the more blood coagulates, the greater is the risk of vascular obstruction. Anticoagulants protect against these complications.
But clinical studies thus far have not proven that an increased clotting tendency also retards plaque development. Berend Isermann, consultant at Heidelberg University Hospital, internal medicine-I department and clinical chemistry and his team have now found an explanation for this.
They examined mice with elevated blood fat levels and a genetic defect that leads to an increase in blood clotting. The mice developed larger plaques than those without the genetic defect, but the plaques were more stable.
Besides, no vascular obstruction was observed, as the vascular wall expanded to adapt to the new situation. The negative effect of larger plaques on circulation was compensated by the positive effect of stability and a greater vessel opening, said a Heidelberg release.
However, the long-term use of anticoagulants (in this case, heparin) reversed these advantages. The size of the plaques was reduced, but stability was lost, increasing the risk of complications.
“Our findings were made on mice, but they confirm the results of clinical studies on humans,” says Isermann. “In addition, in vitro studies show that human cells react similarly to mouse cells.”
These findings were published in Circulation.
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