Original Title: Mechanisms of Very Late Drug-Eluting Stent Thrombosis Assessed by Optical Coherence Tomography. Reference: Masanori Taniwaki et al. Circulation. 2016 Feb 16;133(7):650-60.
The physiopathological mechanisms behind DES thrombosis have not been fully described yet. The potential causes behind this adverse event were assessed using optical computed tomography (OCT).
Between August 2010 and December 2014, 64 patients with instent very late thrombosis were included as part of an international OCT registry.
Very late thrombosis occurred at median 4.7 years after the original procedure (range 3.1 to 7.5 years).
After restoration of flow, OCT pullbacks were performed to analyze 38 first generation DES and 20 new generation DES; a possible cause was observed 98% of times.
The most frequent findings were strut malapposition (34.5%), neo atherosclerosis (27.6%), uncovered struts (12.1%) and stent underexpansion (6.9%).
Uncovered struts and malapposition were more frequent in thrombosed regions vs. non thrombosed.
Maximum stent length with absence or malapposed intimal covering (3.40 mm vs 1.29 mm; p<0.001) was a very strong predictor of thrombosis, but not malapposition distance (distance separating struts from intimal covering).
The combination of malapposition and absence of covering was consistent in both DES generations.
Conclusion
The most frequent causes of very late thrombosis were malapposition, neoatherosclerosis, uncovered struts and underexpansion, across first and new generation DES.
The maximal length of malapposed or uncovered struts showed the highest correlation with very late thrombosis.
