WP 1 - Gaining a better mechanistic understanding of the molecular and cellular events triggering late ST

Currently, three predominant mechanisms are thought to lead to ST (including late ST):

  1. Failure of reendothelialisation or coverage of stent struts with dysfunctional endothelial cells (characterized by impaired thrombo-resistance),
  2. Platelet adhesion and aggregation, as well as
  3. Activation of clotting factors with subsequent fibrin formation.

Leukocytic infiltration of the arterial wall, triggered in particular by polymers used for DES coating, are considered important, however, the exact cascade of cellular and molecular events initiating thrombus formation within coronary stents resulting in late ST remains to be delineated.

Therefore, it will be a major objective of PRESTIGE to dissect the basic pathophysiology leading to late ST. To achieve this, PRESTIGE will generate a collaborative platform integrating the expertise of excellent European groups with a major focus on platelet and endothelial biology and coagulation. By combining their different scientific and technological knowledge, PRESTIGE will help to gain fundamental insight into the pathophysiology of the early steps initiating late ST and reveal similarities and dissimilarities of the processes involved in late ST as opposed to normal haemostasis.

WP1 Leader: Prof. Dr M. Jandrot-Perrus
Co-Leader: Prof. Dr S. Massberg


Prof. Dr Adnan Kastrati
Project Coordinator
German Heart Centre Munich
TU Munich

Per Larsen
Project Manager
German Heart Centre Munich
TU Munich

Dr Hans Sawade
neoplas GmbH