Abstract
Introduction: Third-generation drug-eluting stent (3rd DES) is widely used in percutaneous coronary intervention. Clinical superiority of 3rd DES has been demonstrated, however, pathological response after 3rd DES remains unclear. We aimed to examine the histology after 3rd DESs in low-density lipoprotein receptor knockout (LDLR -/-) minipigs’ coronary arteries. Methods: Using LDLR -/- minipigs, second-generation drug-eluting stents (2nd DESs) and 3rd DESs were deployed in coronary arteries. Two weeks (n = 2) or four weeks (n = 4) after stent implantation, coronary angiography for the follow up was performed. For evaluation of the features of neointima, optical coherence tomography (OCT) examination was performed in all stented vessels. The stent-implanted arteries were dissected immediately after OCT and investigated histologically. Results: OCT analysis for four-week models showed that the thickness of neointima over 3rd DESs was significantly thinner than that over 2nd DESs (3rd DESs; 43.29 ± 3.29 μm vs. 2nd DESs; 61.67 ± 5.51 μm, P = 0.009). In two-week models, numerous inflammatory cells were observed on the luminal side of 2nd DESs’ struts, while this response was absent in 3rd DESs. Fibrin deposition around 3rd DES’s strut was 2347.9 ± 875.6 μm 2 , while that around 2nd DES’s strut was 4738.9 ± 691.0 μm 2 (P = 0.041) in four-week models. Moreover, when defining the density of smooth muscle cells as ratio of hematoxylin-eosin stained area, it was significantly higher in the neointima above 3rd DESs than that above 2nd DESs in four-week models (3rd DESs; 0.373 ± 0.011 vs. 2nd DESs; 0.265 ± 0.030, P = 0.026). Although neointima over 3rd DES was thin, the density of smooth muscle cells that compose the neointima was higher and seemed to be well-matured. Conclusion: Our pathological analysis showed advanced healing process in 3rd DES compared to 2nd DES lesions. This result may attributed to the absence or the presence of polymer applied on the luminal side of struts, which triggers severe inflammation in the early term after stent implantation, leading to formation of fibrin deposition, unnecessary neointimal thickening, and inhibition of neointimal maturation.
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