Intracoronary Imaging and Histopathological and Spectroscopic Findings
Lorenz Räber, Salvatore Brugaletta, Kyohei Yamaji, Crochan J. O’Sullivan, Shuji Otsuki, Tobias Koppara, Masanori Taniwaki, Yoshinobu Onuma, Xavier Freixa, Franz R. Eberli, Patrick W. Serruys, Michael Joner, Manel Sabaté and Stephan Windecker
Potential Mechanisms in the Pathogenesis of Very Late Scaffold Thrombosis
Uneventful scaffold resorption results in positive remodeling with lumen expansion, intact intima, and normal vessel hemodynamics (upper right). In the presence of relevant areas of malapposed or uncovered scaffold struts, late scaffold discontinuity may cause dislocation of strut remnants into the lumen. This may lead to disturbed hemodynamic flow and activation of the thrombotic cascade potentially that result in very late scaffold thrombosis (lower left). Restenosis in the absence of relevant neointimal hyperplasia represents another potential mechanism in very late scaffold thrombosis (lower right).