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.