Incomplete Stent Apposition… Do We Still Need to be Convinced?

Some things have to be believed to be seen!
    – Ralph Hodgson, Poet (1871-1962)

One of the cornerstones of contemporary stent implantation during percutaneous coronary revascularization is the need for adequate stent expansion with apposition of stent struts to the vessel wall. In most cases, this is achieved with high-pressure dilatation using a non-compliant balloon, so called post-dilatation. The value of adequate stent expansion and stent strut apposition is related to both reductions in repeat revascularization from restenosis and in-stent thrombosis.^1-5

The critical importance of adequate stent apposition was identified by several investigators in the bare-metal stent (BMS) era using intravascular ultrasound (IVUS) and many of these lessons have either been reproduced or extended in the current drug-eluting stent (DES) era. The study by Kume et al in this issue of the Journal, in particular, sheds some new light on this phenomenon.⁶ However, when interpreting studies examining incomplete stent apposition, it is important to be familiar with the definitions and descriptions of incomplete stent apposition (ISA), as the timing of the observation has important implications in terms of the pathology. On IVUS assessment, ISA is defined as presence of one or more stent struts clearly separated from the vessel wall, with evidence of blood speckle behind the struts in a segment not associated with any side branches.^1-3 In general, ISA can be categorized into either baseline ISA when it is identified at the time of initial stent implantation or late acquired ISA, identified at follow-up. Interestingly, some patients with baseline ISA have been shown to achieve resolution on follow-up and were thus classified as resolved ISA as opposed to persistent ISA, when incomplete stent apposition is observed both at baseline and at follow-up. However, when complete stent apposition is achieved during initial stent deployment and ISA is observed during follow-up, it is considered to be a late acquired ISA.

During initial stent implantation, the most common cause of ISA is undersizing of stent diameter compared to the reference segments. However, several mechanisms have been proposed for both persistent and late acquired ISA, including positive arterial remodeling, dissolution of jailed thrombus or plaque debris, inhomogeneous stent expansion due to severe calcified lesion, chronic stent recoil, and more recently, the use of DES.² However, in the absence of baseline IVUS assessment, it is often difficult to differentiate persistent versus late acquired ISA, particularly when DES are used. The risk of late ISA has been a persistent concern since the first reports with sirolimus-eluting stents. In a recent meta-analysis, DES use was associated with higher incidence of late acquired ISA compared with BMS (6.5% vs 2.6%, respectively), although the clinical effects of late ISA in the long term have not yet been fully elucidated.⁴

Among existing technologies, IVUS and OCT probably provide the most accurate assessment of the presence of ISA. However, reverberation and side-lobe artifacts with the strong reflective nature of metallic struts can sometimes make it difficult to detect distance between struts and vessel wall. In addition, the perceived complexity of the procedure and the additional need for contrast and radiation during the delivery of the IVUS catheter are often used as barriers for greater adoption in clinical practice. However, the study by Kume et al⁶ should serve as a wake-up call for interventional cardiologists who perform few to no IVUS assessments of their stent implantation practices. To begin with, the experience that the authors describe occurred within the context of a multicenter randomized clinical trial, a scenario where sites were presumably chosen for their high-quality interventional work and their experience in performing stent implantation. Even in this context, nearly one in four patients had at least one segment of ISA, the majority of it either in the proximal or distal edge of the stent, which leads one to wonder how much more prevalent it might be in the real world. Secondly, the authors identified that the most powerful predictor of ISA was larger reference vessel to stent ratio, especially in the proximal stent edge. The most logical explanation for this finding is that the larger reference vessel diameter represents the natural taper of the vessel from a proximal to distal end and the likely tendency of the operators to conservatively size the stent to the distal reference segment, which may result in substantial mismatch, especially when long stent lengths are implanted. An alternative explanation for the higher rate of proximal and distal edge ISA is that operators are often careful not to extend the footprint of the post-dilatation balloon beyond the stent edge, often related to concerns of edge dissection. In doing so, there remains the risk of not adequately expanding the proximal or distal edge and thus contributing to ISA. 

So, what lessons does this article have to offer to interventional cardiologists? To begin with, it should serve to sensitize us about the high frequency of ISA in clinical practice. Even though there is no hard evidence that identifying and addressing ISA results in tangible clinical benefits, there is enough corroborating evidence relating to adequate stent expansion and late stent thrombosis that supports an aggressive approach toward identifying and treating ISA. Therefore, whereas it is not necessary to perform an IVUS assessment on all lesions, it should be considered in selected subgroups, ie, those at higher risk for ISA, such as long lesions requiring a longer length stent, lesions requiring atherectomy prior to stent implantation, lesions with heavy calcification, bifurcation lesions, and lesions located in moderate to severely tortuous vessels. Performing IVUS assessments in these selected subgroups would over a period of time provide an objective measure of the performance of DES in these conditions and thus allow the operator to choose to post-dilate these stents to reduce the frequency of ISA. Although the risk of late stent thrombosis may be quantitatively small with ISA, it is a potentially treatable cause and could have a significant effect on an individual patient prognosis. Changing this mindset does require us to believe that ISA can occur even with the best of techniques and that it is better to see it and address it than not. Our patients deserve nothing less!

References

1. Ako J, Morino Y, Honda Y, et al. Late incomplete stent apposition after sirolimus-eluting stent implantation: a serial intravascular ultrasound analysis. J Am Coll Cardiol. 2005;46(6):1002-1005.
2. Cook S, Wenaweser P, Togni M, et al. Incomplete stent apposition and very late stent thrombosis after drug-eluting stent implantation. Circulation. 2007;115(18):2426-2434. 
3. Honda Y, Grube E, de La Fuente LM, Yock PG, Stertzer SH, Fitzgerald, PJ. Novel drug-delivery stent: intravascular ultrasound observations from the first human experience with the QP2-eluting polymer stent system. Circulation. 2001;104(4):380-383. 
4. Sanchez-Recalde A, Moreno R, Barreales L, et al. Risk of late-acquired incomplete stent apposition after drug-eluting stent versus bare-metal stent. A meta-analysis from 12 randomized trials. J Invasive Cardiol. 2008;20(8):417-422. 
5. Serruys PW, Degertekin M, Tanabe K, et al. Intravascular ultrasound findings in the multicenter, randomized, double-blind RAVEL (RAndomized study with the sirolimus-eluting VElocity balloon-expandable stent in the treatment of patients with de novo native coronary artery lesions) trial. Circulation. 2002;106(7):798-803.
6. Kume T, Waseda K, Ako J, et al. Intravascular ultrasound assessment of post procedural incomplete stent apposition. J Invasive Cardiol. 2012;24(1):13-16.

____________________________________

From the Division of Cardiology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Address for correspondence: Vankeepuram S. Srinivas, MBBS, MS, The Division of Cardiology, Montefiore Medical Center, Albert Einstein College of Medicine, 1825 Eastchester Road, Suite W1-120, Bronx, NY 10468. Email: vsriniva@montefiore.org