Neointimal vulnerability on optical coherence tomography and slow flow during percutaneous coronary intervention of healed neointima
Authors: Amano H , Kojima Y , Hirano S , Oka Y , Aikawa H , Matsumoto S , Noike R , Yabe T , Okubo R , Ikeda T 
Published: October 2022

Abstract

Backgrounds
Healed plaques in native coronary artery indicate the repair phenomenon of ruptured fibrous caps and erosions [1, 2, 3]. Healed plaques associated with plaque vulnerability [4]. A similar phenomenon is considered to occur in neointima after stent implantation [5]. However, there are few reports in the literature regarding neointimal vulnerability and procedure outcomes of healed tissue in neointima.

Objective
The aims of this study are to investigate clinical characteristics, slow flow during percutaneous coronary intervention (PCI), and neointimal vulnerability of healed neointima by optical coherence tomography (OCT).

Methods
We treated 67 lesions by PCI for in-stent restenosis (ISR) and conducted OCT examinations. Healed neointima was defined as neointima having one or more layers with different optical densities and a clear demarcation from underlying components. ISR with healed neointima was found in 49% (33/67) of the lesions. The angiographic slow flow was defined as a decrease of at least 1 grade in TIMI flow during PCI or final TIMI flow grade 0 and 1 or 2, with no evidence of thrombus, spasm, or dissection. Stents with a strut thickness ≥100 μm were classified as thick [6].

Results
Compared to ISR without healed neointima, ISR with healed neointima showed significantly longer stent age (102±72 months vs. 31±39 months, p&lt;0.001), lower high-density lipoprotein cholesterol (HDL-C) at ISR (42±12 mg/dl vs. 53±16 mg/dl, p=0.005), higher triglycerides at ISR (178±84 mg/dl vs. 138±67 mg/dl, p=0.039), lower frequency of dual antiplatelet therapy (42% [14/33] vs. 74% [25/34], P=0.017), lower use of angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker (ACE-I or ARB) (61% [20/33] vs. 91% [31/34], P=0.028), lower usage of second-generation drug-eluting stents (DESs) (36% [12/33] vs. 63% [22/34], P=0.029), higher usage of thick-strut stents (42% [14/33] vs. 15% [5/34], P=0.012), larger neointimal area (6.8±2.6 mm2 vs. 5.2±1.8 mm2, P=0.005), higher incidence of lipid-laden neointima (70% [23/33] vs. 32% [11/34], P=0.002), thin-cap fibroatheromas (58% [19/33] vs. 21% [7/34], P=0.002), neointimal rupture (45% [15/33] vs. 9% [3/34], P=0.001), thrombus (36% [12/33] vs. 3% [1/34], P=0.001), macrophage accumulation (70% [23/33] vs. 15% [5/34], P&lt;0.001), microvessels (73% [24/33] vs. 32% [11/34], P=0.001), neoatherosclerosis (76% [25/33] vs. 38% [13/34], P=0.002), and lower incidence of stent underexpansion (15% [5/33] vs. 44% [15/34], P=0.010). There were no relations between with healed neointima and slow flow during PCI or procedural myocardial infarction.

Conclusions
ISR with healed neointima was associated with neointimal vulnerability, stent age, stent type, stent strut thickness, stent expansion, antiplatelet therapy, HDL-C and triglycerides levels, and use of ACE-I or ARB. There were no relations between with healed neointima and slow flow during PCI.

Funding Acknowledgement
Type of funding sources: None.