Objective: To observe and characterise vessel injury after stenting using optical coherence tomography (OCT), to propose a systematic OCT classification for periprocedural vessel trauma, to evaluate its frequency in stable versus unstable patients and to assess its clinical impact during the hospitalisation period.
Setting: Stenting causes vessel injury.
Design and interventions: All consecutive patients in whom OCT was performed after stent implantation were included in the study. Qualitative and quantitative assessment of tissue prolapse, intra-stent dissection and edge dissection were performed.
Results: Seventy-three patients (80 vessels) were analysed. Tissue prolapse within the stented segment was visible in 78/80 vessels (97.5%). Median number of tissue prolapse sites was 8 (IQR 4–19), mean (SD) area 1.04 (0.9) mm2. Intra-stent dissection flaps were visible in 69/80 vessels (86.3%) (median number 3 (IQR 1.25–6), maximum flap length 450 (220) μm). Fifty-five out of 80 vessels (68.8%) showed dissection cavities (median number 2 (IQR 0–4.75), maximum depth 340 (170) μm). Edge dissection was visible in 20 vessels (mean (SD) length flap 744 (439) μm). The frequency of tissue prolapse or intra-stent dissection was similar in stable and unstable patients (95.6% vs 100%, p = 0.5 for tissue prolapse; 91.1% vs 82.9%, p = 0.3 for intra-stent dissection). There were no events during the hospitalisation period.
Conclusions: OCT allows a detailed visualisation of vessel injury after stent implantation and enables a systematic classification and quantification in vivo. In this study, frequency of tissue prolapse or intra-stent dissections after stenting was high, irrespective of the clinical presentation of the patients, and was not associated with clinical events during hospitalisation.
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Coronary stent implantation generally creates a certain degree of injury on the vessel wall. Pathological studies have demonstrated plaque compression by the stent and penetration of the struts into the underlying plaque.1 High-pressure stenting techniques have proved to be useful for an optimal stent implantation in order to reduce the risk of restenosis and subacute thrombosis. However, this stent deployment strategy may also increase the risk of vessel damage in the stented segment or at the edges.2
Optical coherence tomography (OCT) is a high-resolution imaging technique which allows a detailed assessment of the anatomical relation between the stent and the vessel wall.3 4 As a consequence, various degrees of vessel injury after stent implantation are frequently detected with this technique even when they are not visible by cine-angiography or intravascular ultrasound. The different types of acute vessel damage caused by stenting that can be seen by OCT and their frequency in different clinical scenarios have not been described yet. Furthermore, the clinical implications of these OCT findings are not well established.
The objectives of this study were to observe and characterise vessel injury after stenting using OCT, to propose a systematic OCT classification for periprocedural vessel trauma, to evaluate its incidence in stable versus unstable (unstable angina IB/IIB/IIIB Braunwald classification and ST elevation myocardial infarction (MI)) patients and to assess its clinical impact during the hospitalisation period.
Patients and methods
All consecutive patients in whom OCT was performed after stent implantation between January 2007 and December 2008 were included in the study. All patients gave informed consent.
The OCT acquisition was performed using a commercially available system for intracoronary imaging (LightLab Imaging, Westford, Massachusetts, USA). The ImageWire (LightLab Imaging) consists of an optical fibre core (125 μm) covered by a protective sheath with a maximum outer diameter of 0.019″. The acquisition technique has been previously described.5 6 In seven cases the occlusive technique was used, in which a proximal, low-pressure (0.4 atm) occlusion balloon (Helios, Goodman, Nagoya, Japan) is inflated with simultaneous distal flush delivery (lactated ringer; flow rate 0.8 ml/s) to remove blood from the vessel lumen. Images were acquired during a pullback rate of 1.0 mm/s. In 73 cases OCT was acquired with the non-occlusive technique. In this case, the ImageWire was positioned distal to the region of interest using a double lumen catheter (Twin Pass catheter; Vascular Solutions, Minneapolis, USA) that had been previously placed in the artery over a conventional guide wire. The automated pullback was performed at 3 mm/s while the blood was removed by the continuous injection of iso-osmolar contrast (Iodixanol 370; VisipaqueGE Health Care, Ireland) at 37° C through the guiding catheter. The data was stored on CD for offline analysis.
Definitions of acute effects of stent implantation in OCT
Analysis encompassed the intra-stent segment, defined by the first and the last cross section with a visible strut, and the adjacent vessel segments 5 mm proximal and distal to the stent (edge segments).
Tissue prolapse: convex-shaped, protrusion of tissue between adjacent stent struts towards the lumen, without disruption of the continuity of the luminal vessel surface7 (fig 1). Protrusion of tissue between struts was considered tissue prolapse only if the distance from the arc connecting adjacent stent struts to the greatest extent of protrusion was >50 μm.
Intra-stent dissection: disruption of the luminal vessel surface in the stent segment. It can appear in two forms: (a) dissection: the vessel surface is disrupted and a dissection flap is visible; (b) cavity: the vessel surface is disrupted and an empty cavity can be seen (fig 2).
Edge dissection: disruption of the luminal vessel surface in the edge segments (within 5 mm proximal and distal to the stent, no struts are visible) (fig 3).
Thrombus: irregular mass with dorsal shadowing protruding in the lumen (mural thrombus) or a luminal mass with dorsal shadowing that is not connected to the vessel wall (fig 4).
Quantitative OCT analysis of the acute effects of stent implantation
The analysed region comprised the intra-stent and edge segments. The lumen and stent area were measured in 1 mm intervals along the pullbacks. In the proximal and distal edge segments, the lumen area was measured. In cases of tissue prolapse the number of sites with tissue prolapse was counted. Tissue prolapse length was defined as the distance from the arc connecting adjacent stent struts to the greatest extent of protrusion (the maximum and average tissue prolapse length were calculated). The area of tissue protruding between the stent struts was also measured (tissue prolapse area) (fig 1). When there were signs of intra-stent dissection the number of dissection flaps or cavities was counted and the length of the flap (from its tip to the joint point with the vessel wall) or the maximum depth of the cavity (from the lumen to the deepest cavity point inside the vessel wall) was measured (fig 2). When edge dissection was present the length of the dissection flap (in a similar way as described for intra-stent dissection flap) was measured. The presence of thrombus was qualitatively assessed and the number of frames with visible thrombus was recorded. When incomplete stent apposition (defined as separation of at least one stent strut from the vessel wall not related with a side branch) was visible, the maximum distance from the endo-luminal surface of the strut to the vessel wall was measured (maximum incomplete stent apposition length) To take into account differences in the stent length, the number of tissue prolapse sites, number of dissection flaps and number of cavities were normalised by the stent length and expressed per mm.
The analysts were blinded to the clinical and procedural characteristics.
The presence of events (death, MI, target lesion revascularisation, target vessel revascularisation and stent thrombosis) during the hospitalisation period following stent implantation was registered. MI included reinfarction (defined as recurrence of symptoms together with ST elevation or new left bundle branch block and an increase in cardiac enzymes following stable or decreasing values) or spontaneous MI (diagnosed by a rise in creatine kinase-MB fraction of three times the upper limit of normal together with symptoms and either new ST elevation or left bundle branch block).
Continuous variables are expressed as mean (SD) or median and interquartile range. Categorical variables are expressed as percentages. Comparisons between groups were performed with χ2 for categorical variables. Continuous variables were compared with the Student t test when they had a normal distribution and with a non-parametric test (Mann–Whitney) when their distribution was not normal.
Clinical and procedural characteristics
Seventy-three patients, 80 vessels were included in the study. Table 1 shows the clinical and procedural characteristics.
Acute effects of stent implantation assessed by OCT
The mean (SD) lumen area measured by OCT was 7.16 (1.7) mm2. The minimum lumen area in-stent was 5.65 (1.7) mm2. The mean and minimum stent areas were 7.40 (1.9) and 5.70 (1.76) mm2, respectively.
Fifty-one out of the 80 vessels (63.8%) showed at least one malapposed strut and the average maximum incomplete stent apposition length was 281 (145) μm. Findings suggestive of thrombus were visible in 36/80 vessels (45%). The median number of frames with visible thrombus was 0 (IQR 0–1) and the median number of frames with thrombus normalised by the stent length was 0 (IQR 0–0.06).
Table 2 shows the frequency and quantitative assessment of tissue prolapse as assessed by OCT.
Table 2 presents the frequency and quantitative measurements of intra-stent dissection as assessed by OCT.
In four cases edge regions were not visible. Twenty vessels out of 76 showed edge dissection. Four vessels showed both proximal and distal edge dissection. The mean (SD) length of the dissection flap was 744 (439) μm.
Acute effects of stent implantation as assessed by OCT in relation to the clinical presentation
The effects of stent implantation in the vessel as assessed by OCT were compared in stable versus unstable (unstable angina IB/IIB/IIIB Braunwald classification and ST elevation MI) patients. Table 3 shows the baseline clinical and procedural characteristics of the two groups.
The frequency of incomplete stent apposition was not different between groups (27/45 (60%) for stable vs 24/34 (70.6%) for unstable p = 0.3). The maximum incomplete stent apposition length was 280 (74) μm for stable and 283 (198) μm for unstable patients (p = 0.9). Structures suggestive of thrombus were visible in 20/45 (44.4%) stable patients vs 16/35 (45.7%) unstable patients (p = 0.9). There were also no significant differences in the median number of frames with visible thrombus between stable 0 (IQR 0–1) and unstable 0 (IQR 0–2) patients (p = 0.9). The median number of frames with visible thrombus normalised by the stent length was 0 (IQR 0–0.05) for stable and 0 (IQR 0–0.08) for unstable (p = 0.7). Table 4 shows the frequency and quantitative assessment of tissue prolapse, intra-stent dissections and edge dissections in patients with stable versus unstable clinical presentation.
There were no events (death, MI, target lesion revascularisation, target vessel revascularisation or stent thrombosis) during the hospitalisation period.
This study proposes a systematic classification and quantification of a variety of acute effects of stent implantation on the vessel wall, as visible by OCT. The main findings are: (a) OCT allows for a detailed visualisation of periprocedural vessel wall trauma in coronary stenting and enables a systematic classification and quantification in vivo; (b) a very high proportion of patients, irrespective of their clinical presentation, showed tissue prolapse or intra-stent dissections visible by OCT after stent implantation, but this finding was not associated with clinical events during hospitalisation.
OCT for the detection of vessel injury after stenting
OCT is a light-based technique which can provide in vivo imaging of the coronary artery with near-histological resolution. This technique has opened new possibilities for the evaluation of stents at follow-up, allowing a very detailed assessment of strut apposition and tissue coverage.8 9 10 11 12 This study demonstrates its ability to detect and distinguish different types of vessel injury during stent implantation. Furthermore, OCT allows not only qualitative but also quantitative evaluation of the acute effects of stenting in vivo. Previous reports have shown that OCT can also visualise vascular effects of other coronary devices such as balloon-induced dissections and cuts made by the blades of a cutting balloon.13 Furthermore, OCT has proved to be useful for the evaluation of strut symmetry or the presence of intracoronary thrombus after stenting.14 15 16
Tissue prolapse after stenting
In a postmortem study, compression of the coronary plaque after stent implantation with protrusion of tissue between the struts was seen in 94% of the patients.1 This is in agreement with our study in which tissue prolapse between the struts was visible in the vast majority of patients. It is in contrast to intravascular ultrasound (IVUS) studies, which have reported a relatively low plaque prolapse incidence ranging from 18% to 35%.17 The higher sensitivity of OCT in comparison with IVUS for the detection of this phenomenon has been previously published.7 18 The clinical impact of the presence of tissue prolapse after stenting, however, is not well established. An IVUS study demonstrated a correlation between creatine kinase-MB elevation post-procedure and the extent of plaque prolapse.17 However, IVUS has failed to show differences in the rate of stent thrombosis or stent restenosis between patients with and without plaque prolapse.19 20 In our study, even when almost all patients had visible tissue prolapse by OCT, no clinical events during hospitalisation occurred. Therefore, non-flow-limiting tissue prolapse as visualised by OCT in our study appears to be a benign phenomenon in the short term that might not require further treatment.
Intra-stent and edge dissections
OCT allows the visualisation of the disruption of the endoluminal vessel wall continuity in the intra-stent segment and it can distinguish between the presence of a flap or a region with loss of material (cavity). IVUS (with an axial resolution of around 150 μm) is hampered in distinguishing intra-stent dissections from plaque prolapse. However, by OCT those two entities can be clearly differentiated and might have different clinical implications. In our series, despite a high frequency of visible intra-stent dissections by OCT, no in-hospital events were registered. However, the long-term impact of the presence of vessel wall disruption in the stent segment in the incidence of restenosis or stent thrombosis is not known. The endothelial integrity is important to prevent thrombus deposition, and pathological examinations have associated stent thrombosis with the disruption of the vessel continuity and prolapse of the necrotic core between stent struts.21 Several animal and pathological studies have associated vessel injury with stent restenosis.1 22 On the other hand, non-flow-limiting edge dissections detected by IVUS have not been associated with an increase in acute or long-term events such as restenosis but the impact of intra-stent dissections is not established.23 24 25 Furthermore, the location of a stent strut floating over an empty cavity without direct wall contact might also influence its coverage by tissue at follow-up.26
Acute effects of stent implantation in stable versus unstable patients
In our series, the frequency of tissue prolapse did not differ between stable and unstable patients but the tissue prolapse area was higher in the stable group. This result seems to be in contradiction with the concept of the underlying plaque type in stable and unstable patients. In theory, the plaque type in stable patients might be mainly fibrous while in unstable patients more lipid-rich and/or thrombosed plaques would be expected and those might be more prone to prolapse. However, to the best of our knowledge there are no reported data about differences in tissue prolapse between stable and unstable patients. Furthermore, pre-stent OCT examination was not performed in our sample and therefore no information is available about the underlying plaque type. No differences in the frequency of intra-stent or edge dissections were found between stable and unstable patients.
This study demonstrates the feasibility of a systematic classification and quantification of periprocedural vessel injury in vivo. This might allow the development of an injury score, analogous to the vascular injury score in histopathology, and may help to study vascular healing and to optimise stent design and implantation technique in the future. To date the reasons for stent failure (thrombosis and restenosis) are poorly understood and vessel trauma after stenting might be a missing link to help us improve our understanding of this important clinical problem.27 28
However, correlation with clinical events, both early and late, is required to determine whether these OCT observations have clinical significance, and this should be the aim of future studies.
The lack of clinical events during the study period does not allow a proper correlation of OCT-assessed vessel trauma with clinical outcome and it is the main limitation of the study. Intra-stent dissection and tissue prolapse were almost universal. Therefore identification of their presence alone has no significance. In order to find a more discriminatory OCT measure of vessel trauma we described different quantitative parameters for each type of post-stenting vessel injury. However, the lack of clinical events did not allow us to evaluate which parameter may be clinically significant. We assessed the acute effects of stent implantation visible by OCT and their clinical impact at short-term follow-up. Long-term follow-up studies including OCT imaging are needed in order to better define the clinical implications of these findings. The clinical presentation classification used has limitations as it included syndromes with different physiopathology (unstable angina/NSSTMI and STEMI) in the same group. However, owing to the limited sample size, it was not possible to divide the population into multiple subgroups. We acknowledge that the stent type might influence the vessel trauma observed by OCT. However, owing to the heterogeneity of the population, with different drug-eluting stents and a limited number of bare metal stents, no comparison between stent types was performed.
OCT allows for a detailed visualisation of periprocedural vessel wall trauma in coronary stenting and enables a systematic classification and quantification in vivo. In our study, the incidence of tissue prolapse or intra-stent dissections after stent implantation was high, irrespective of the clinical presentation of the patients, and was not associated with clinical events during the hospitalisation period.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
See Editorial, p 1895
Patient consent Obtained.
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