Post-Stent Evaluation, Stent Thrombosis, and In-Stent Restenosis

, Jagat Narula2, Yuliya Vengrenyuk3 and Samin Sharma4



(1)
Director, Cardiac Catheterization Laboratory, Director, Structural Heart Intervention Program, Director, Interventional Cardiology Fellowship Program, Zena and Michael A. Wiener Professor of Medicine, Icahn School of Medicine at Mount Sinai, Mount Sinai Hospital, New York, New York, USA

(2)
Director, Intravascular Imaging Core Laboratory, Instructor, Department of Medicine, Icahn School of Medicine at Mount Sinai, Mount Sinai Hospital, New York, New York, USA

(3)
Philip J. and Harriet L. Goodhart Chair in Cardiology, Chief of Cardiology, Mount Sinai St. Luke’s Hospital, Professor of Medicine and Radiology, Associate Dean, Arnhold Institute for Global Health, Icahn School of Medicine at Mount Sinai, Mount Sinai Hospital, New York, New York, USA

(4)
Director, Clinical and Interventional Cardiology, President, Mount Sinai Heart Network, Dean, International Clinical Affiliations, Anandi Lal Sharma Professor of Medicine, Icahn School of Medicine at Mount Sinai, Mount Sinai Hospital, New York, New York, USA

 



Electronic Supplementary Material

The online version of this chapter (doi:10.​1007/​978-3-319-62666-6_​4) contains supplementary material, which is available to authorized users.


Keywords
Stent expansionStrut malappositionTissue protrusionIn-stent dissectionRotational atherectomyOrbital atherectomyCutting balloon angioplastyBifurcation lesionIn-stent restenosisAcute and subacute stent thrombosis



4.1 Introduction


Optimization of stent deployment during percutaneous coronary interventions (PCI) is one of the most important factors in achieving favorable immediate and long-term outcomes. Intravascular ultrasound (IVUS) imaging studies demonstrated that the strongest predictor of early stent thrombosis and restenosis is the absolute degree of stent expansion characterized by the minimal stent area (MSA) after PCI [1, 2]. Stent underexpansion is poorly recognized by angiography. By achieving greater stent expansion, IVUS-guided PCI has been associated with significant reduction in the risk of major adverse coronary events (MACE) compared to angiography-guided PCI [3].

Although optical coherence tomography (OCT) has higher resolution compared to IVUS, the limited penetration depth by OCT does not allow visualization of the external elastic membrane (EEM) and assessment of the vessel size, an important measurement used in IVUS-guided trials. Whether OCT-guidance can result in a similar degree of stent expansion compared to IVUS-guided PCI has been under investigation by a series of ILUMIEN trials. In a post hoc analysis of two prospective imaging trials (ILUMIEN II), IVUS and OCT guidance demonstrated a comparable degree of stent expansion [4]. Post-PCI MSA with OCT guidance was non-inferior to that of IVUS-guidance in the first prospective randomized trial, ILUMIEN III. Procedural and 30 day MACE were also similar between the groups [5]. The goal of the next randomized study, ILUMIEN IV , is to determine whether similar clinical outcomes can be obtained after stenting guided by these imaging modalities.

In addition to stent underexpansion, OCT can detect several features of suboptimal stent deployment including edge dissection, malapposition, intrastent plaque protrusion, and reference lumen area narrowing. In-stent minimum lumen area less than 4.5 mm2, distal stent edge dissection more than 200 μm, and the reference lumen area less than 4.5 mm2 at either distal or proximal stent edge were independent predictors of MACE in a retrospective analysis with 1 year follow-up [6]. In contrast, percent stent expansion less than 70%, stent malapposition more than 200 μm, large plaque protrusion and proximal edge dissection more than 200 μm, were not associated with worse clinical outcomes. Multiple reports emphasize the importance of adequate high pressure postdilatation to obtain optimal stent expansion in order to reduce the risks of complications [7]. It is important to select a technique that allows for avoidance of unwanted and potentially dangerous complications caused by vessel overstretching. Postdilatation with noncompliant balloons has been shown to improve MSA without causing deeper injury of the vessel wall with intima-media rupture [7].

Stent thrombosis (ST) is an infrequent but highly morbid complication of PCI with mortality rates of 10–20% during the first year [8, 9]. PCI for ST is associated with a low rate of reperfusion and high rates of recurrent ST, myocardial infarction (MI), and death [1012]. Unfavorable long-term outcomes with a high mortality and ST recurrence rate of 26% were observed after a first definite ST [9]. Premature discontinuation of antiplatelet therapy, renal failure, bifurcation lesion PCI, diabetes, and low ejection fraction were identified as predictors of future thrombotic events [13]. Procedure-related factors including stent underexpansion and residual reference segment stenosis have been shown to play a major role in early ST, which occurs within 1 month of stent implantation [14, 15]. Impaired re-endothelialization, incomplete stent apposition or fracture, hypersensitivity to the drug-eluting stent (DES) polymer, chronic inflammation with outward remodeling, and neoatherosclerotic plaque rupture play important roles in late (1–12 month after stent implantation) and very late ST (more than 12 month after stenting) [16, 17]. Increased risk of ST is also associated with inadequate antiplatelet therapy and/or resistance to antiplatelet treatment [18, 19]. OCT imaging represents a unique tool for ST diagnosis and evaluation. It can help understand whether a procedure-related mechanism is involved in ST and select the most appropriate treatment strategy. Stent underexpansion and strut malapposition are the most common procedural factors leading to ST. In addition, the length of the segment with uncovered struts by OCT was an independent predictor of late stent thrombosis after DES implantation [17]. Therefore, efforts should be made to ensure optimal stent expansion and apposition after stenting. OCT can help identify and correct suboptimal stent implantation, which can prevent ST recurrence in future.

Although introduction of DES dramatically reduced the occurrence of aggressive neointimal proliferation, treatment of in-stent restenosis (ISR) after stent implantation remains a major clinical problem [20]. Treatment of patients with ISR lesions includes conventional coronary balloon angioplasty (BA), cutting and scoring balloon therapy, stenting, atherectomy, and vascular brachytherapy. Intrastent plaque morphology assessment with OCT imaging can positively impact outcomes by optimizing PCI in complex lesions. OCT imaging can provide unique insights into the underlying substrates of ISR by detailed visualization of neointimal tissue and select the best treatment strategy for the patient and to make the decision whether another stent implantation is necessary. While normal neointimal tissue in DES mainly consists of smooth muscle cells and extracellular matrix, recent pathological and imaging studies provided convincing evidence for the presence of atherosclerosis within stent neointima, or neoatherosclerosis [2124]. Neoatherosclerosis is characterized by neointimal formation of lipid-rich plaque and calcification and may represent an important mechanism of DES failure. OCT imaging can provide unique insights into the etiology of in-stent restenosis and help select the most appropriate treatment strategy. Rotational atherectomy has been successfully used in calcified neoatherosclerosis causing undilatable in-stent restenosis [25, 26]. In addition, OCT imaging before stenting can assess the risks for periprocedural myocardial infarction. The unstable features of neoatherosclerosis including thin-cap fibroatheroma and plaque rupture were the most common findings in patients with periprocedural myocardial infarction [27].


4.2 Case 1. Stent Malapposition (Figs. 4.1, 4.2 and 4.3, Videos 4.1, 4.2 and 4.3)




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Fig. 4.1
Coronary angiography and OCT imaging before percutaneous coronary intervention (PCI). A 73-year-old female, ex-smoker, with controlled non-insulin dependent diabetes mellitus (NIDDM), hyperlipidemia and hypertension presented for staged PCI of the RCA. Angiography demonstrated 80–90% eccentric lesion in the proximal RCA (a, arrow). OCT automatic lumen profile feature (c1) was used to assess the degree of stenosis (82.3%), references, and plaque morphology. OCT imaging detected fibrocalcific plaque with spotty (less than one quadrant) calcification proximal to MLA (b2, asterisk), and minimal disease at the proximal (b1) and distal (b4) reference sites with 3 and 3.8 mm lumen diameters respectively. Another spotty calcification was visualized at the proximal reference site (b1, asterisk). Severe (three-quadrant) calcification was detected distal to the lesion (b5, asterisks). Based on the lesion assessment by OCT, a 3.5/23 mm drug eluting stent (DES) was selected for the lesion and implanted after predilatation with a noncompliant balloon


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Fig. 4.2
OCT and intravascular ultrasound (IVUS) /near infrared spectroscopy (NIRS) images after stenting. Large circumferential stent malapposition was detected by OCT at the proximal edge of the stent with maximal malapposition distance of 400 μm (b1, arrows). The lumen and stent areas in the frame were measured 11.4 and 8.7 mm2 respectively. MSA of 8.2 mm2 suggested good stent expansion (b2); there was no malapposition or dissection detected at the distal edge of the stent (b3). In addition to OCT, IVUS/NIRS imaging of the same lesion was performed (d1d3, e1, e2). The MSA location was detected by IVUS manually (d2). IVUS crosssections (d1) and (d3) correspond to the OCT frames (b1) and (b3). OCT image of the proximal stent edge (b1) provides more clear visualization of stent malapposition compared with IVUS (d1). Stent postdilatation was performed with a 4/12 mm noncompliant balloon at 18 atm


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Fig. 4.3
Final post-PCI coronary angiography and OCT images. Proximal stent malapposition was resolved after postdilatation (b1, b2). Maximal stent area increased from 8.7 to 12.9 mm2 and was detected at the proximal edge of the stent (b1). A small intimal in-stent dissection was visualized after postdilatation at the site of MSA (b1, arrow). In this case, detection of large circumferential stent malapposition by OCT imaging led to postdilatation with a noncompliant balloon, which resulted in resolved strut malapposition and minimal tissue injury


4.3 Case 2. Stent Malapposition and Underexpansion (Figs. 4.4, 4.5 and 4.6, Videos 4.4, 4.5 and 4.6)




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Fig. 4.4
Coronary angiography and OCT imaging before PCI. A 62-year-old female, ex-smoker with controlled hypertension and hyperlipidemia presented with CCS Class III angina, shortness of breath with minimal exertion, and ischemic ECG change on stress echocardiography. Coronary angiography showed a 70–80% stenosis and a nonocclusive lesion in the proximal part of the vessel (a, arrows). OCT detected two focal stenoses with lumen area of 3.14 (b1) and 1.6 mm2 (b2). There was no calcification detected by OCT in the segment; a lipid-rich (b1, asterisks) and mostly fibrous (b2) plaques were visualized at the site of stenoses. The distal portion of the OCT pullback was not analyzable due to insufficient blood clearance (c, asterisks). A 3/32 mm everolimus eluting stent was selected for the lesion in order to cover both stenoses


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Fig. 4.5
Coronary angiogram and OCT imaging after stenting. OCT after stent implantation detected stent underexpansion with MSA of 3.9 mm2 (b3). In addition, OCT visualized a proximal plaque protrusion (b1), stent malapposition with the largest distance of 240 μm (b2, arrow), and small intimal in-stent dissections at the distal portion of the stent (b4, b5, arrow). Based on the imaging findings, postdilatation was performed with a 3/20 mm noncompliant balloon at 18 atm


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Fig. 4.6
Angiography and OCT after postdilatation . There was no evidence of stent malapposition after dilatation (b1, b2). In addition to improved stent apposition, OCT showed improved stent expansion after postdilatation with MSA (b2). Slightly deeper intima-media in-stent dissections were detected distal to the site of MSA after postdilatation; the dissections were not visible on angiogram (a). In conclusion, detection of suboptimal stent expansion by OCT resulted in postdilatation, which led to an increase in MSA and a slightly deeper tissue injury


4.4 Case 3. Stent Underexpansion in a Calcified Bifurcation Lesion (Figs. 4.7, 4.8 and 4.9, Videos 4.7, 4.8 and 4.9)




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Fig. 4.7
Coronary angiography and OCT imaging before PCI . A 64-year-old male with controlled hypertension, hyperlipidemia, NIDDM, a history of prior MI, and multiple PCI presented for a staged intervention of the LAD. A 70–80% calcified lesion was detected in the mid-LAD by angiography (a1, a2). OCT pullback confirmed the severity of the disease with MLA of 1.47 mm2 and 66% stenosis measured using automatic lumen profile tool (c). In addition, OCT detected severe circumferential calcification proximal to the MLA site (b1, b2, asterisks) and moderate (1–2 quadrant) calcified plaques at the site of the MLA (b3, b4). Based on OCT analysis of calcium distribution, rotational atherectomy (RA) was performed in the mid LAD using 1.75 mm burr at 150,000 rpm followed by placement of a 3/38 mm DES


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Fig. 4.8
Coronary angiogram (a) and OCT after RA and stenting . Post-stent OCT detected few malapposed struts (b1) and suboptimal stent expansion at the level of circumferential calcification (b2, c). While there was OCT evidence of plaque modifications with RA (b2, asterisk), automatic lumen profile showed a 29% residual stenosis and minimal stent area of 3.5 mm2 after stenting. Postdilatation was performed with a 3.5/15 mm noncompliant balloon at 20 atm for 10 s

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Dec 30, 2017 | Posted by in CARDIOLOGY | Comments Off on Post-Stent Evaluation, Stent Thrombosis, and In-Stent Restenosis

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