When used to guide percutaneous coronary interventions (PCI), intracoronary imaging is associated with improved clinical outcomes . Intracoronary imaging guidance during PCI reduces in-stent restenosis and repeat revascularization after bare-metal stent placement and has been shown to reduce major adverse cardiac events (MACE), stent thrombosis, target vessel myocardial infarction, and target lesion revascularization after drug-eluting stent (DES) placement . These benefits have been attributed to the use of larger diameter stents and more aggressive post-dilation when intracoronary imaging is used to guide PCI, thus achieving larger lumen areas within the stent than are achieved with angiographic guidance alone .
The evidence supporting improved clinical outcomes when intracoronary imaging is used to guide PCI has largely been derived from studies of intravascular ultrasound (IVUS). Compared to IVUS, which uses sound to generate an image having an axial resolution of approximately 100 μm, optical coherence tomography (OCT) uses light to generate an image having an axial resolution of approximately 15 μm. Owing to this superb spatial resolution, OCT has been shown to be superior to IVUS in identifying various morphologic findings post-PCI, including tissue protrusion, thrombus, stent edge dissections, and strut malapposition, and also more accurately identifies true lumen size compared to IVUS, which tends to overestimate vessel areas . Furthermore, OCT detects neo-intimal coverage of stent struts more accurately than IVUS . Despite these factors favoring OCT, the superiority of OCT over IVUS with respect to improving clinical outcomes has not been demonstrated. In fact, both imaging techniques appear to result in similar degrees of stent expansion . Recent evidence does support, however, the superiority of OCT-guided PCI over angiographic-guided PCI, in that OCT guidance improves post-PCI stent area and post-PCI fractional flow reserve , and has been associated with improved clinical outcomes in at least one observational study .
The evidence supporting intracoronary imaging guidance for PCI has been mostly limited to lesions that are not chronic total occlusions (CTO). Hence, studies evaluating intracoronary imaging in CTO interventions are clearly needed and the publication of the study by Sherbet et al. in this issue of the journal is thus timely. In their analysis from the ACE-CTO study, Sherbet et al. performed OCT imaging in the target vessel of 62 patients eight months after undergoing DES placement within a CTO. The most important observations made by the investigators were that at eight months 9.3% of all struts were malapposed and that 88.7% of all patients had at least one malapposed strut. In addition, approximately 80% of patients had at least one strut that was uncovered by neointimal tissue.
The study by Sherbet et al. is notable for several reasons. First, the authors should be congratulated on completing this study, as their analysis of >44,000 stent struts surely took considerable effort. Second, this study is noteworthy as the largest yet to evaluate OCT findings during follow up after CTO stenting. Third and most importantly, the authors, who represent a well-respected group of CTO interventionalists, demonstrate that even among the most experienced CTO operators, strut malapposition is exceedingly common months after stent placement in a CTO. The high frequency of late strut malapposition observed in this study is of potential concern, as prior studies in non-CTO lesions have linked late malapposition with both delayed stent healing and late stent thrombosis . As pointed out by the authors, this high frequency of late strut malapposition during follow-up is in contrast to much lower rates of late malapposition previously demonstrated in DES implanted in non-CTO lesions . Whether the high frequency of late strut malapposition after CTO stenting contributes to the higher rate of stent failure characteristic of CTO lesions compared to non-CTO lesions remains unknown.
One of the major limitations of the study by Sherbet et al. is that OCT findings at the time of PCI were not reported. Accordingly, the frequency of acute strut malapposition by OCT at baseline among the patients in this study is unknown. Therefore, it cannot be determined whether the late malapposition observed at follow up represents late-persistent or late-acquired malapposition. Whereas late-persistent malapposition has been previously demonstrated to occur more frequently at stent edges and is predicted by the degree of acute strut malapposition, late-acquired malapposition is frequently located in the body of the stent rather than at the edges and is associated with the presence of tissue prolapse at the time of the acute intervention . In a prior study of non-CTO lesions, late-persistent malapposition was more common than late-acquired malapposition . In contrast, Sherbet et al. speculate that late-acquired malapposition may be favored over late-persistent malapposition as the mechanism underlying the high rate of observed late malapposition after CTO stenting. If correct, this might represent an important difference in the response of CTO and non-CTO lesions to DES implantation. As the authors explain, a high rate of late-acquired malapposition after CTO stenting might be attributable to gradual luminal enlargement after CTO recanalization and the development of aneurysmal segments during follow up. Their additional argument is that late-acquired malapposition is more likely because IVUS, which was performed at baseline in 74% of patients, did not detect high rates of acute malapposition. However, it is important to note that IVUS does not identify malapposition nearly as frequently as OCT , and therefore acute malapposition at baseline may have been missed. Furthermore, late-persistent malapposition is associated with the performance of PCI on calcified lesions and implantation of longer stent lengths, both of which are common characteristics of CTOs . Additional studies, in which OCT is performed both at baseline and during follow up, will be required to determine the relative frequency of late-acquired and late-persistent malapposition at follow-up after CTO stenting.
As with all important scientific observations, those made by Sherbet et al. generate several questions to be investigated in future studies. Perhaps the most important question that remains is whether intracoronary imaging guidance during CTO interventions results in improved clinical outcomes in a manner analogous to PCI of non-CTO lesions. There are two points worthy of consideration in this regard. First, in non-CTO PCI the reduction in MACE with intracoronary imaging guidance appears to be greatest among complex interventions . Second, the use of intracoronary imaging during implantation of long coronary stents (≥28 mm in length) in non-CTO lesions has now been demonstrated in the context of a randomized controlled trial to improve clinical outcomes . Considering that CTO interventions are both complex and often characterized by implantation of long coronary stents, routine use of intracoronary imaging to guide CTO stenting may be beneficial and certainly deserves to be investigated in future clinical studies.
Disclosures: Ryan D. Madder, MD has received speaker honoraria from St Jude Medical and research support from Infraredx.

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