OCT Stent Placement


Coronary Stenting

Intracoronary stent applications where OCT has a potentially major impact include assessing stent placement to predict outcomes, evaluating stents at time points after placement to assess continued drug therapy, as an experimental tool for understanding the biology of coronary interventions, identifying high risk TCFAs for potential catheter based therapeutics (next section), and guiding non-stent coronary interventions. 

Percutaneous coronary stenting is an important procedure in cardiology and has almost completely replaced other forms of catheter based coronary interventions.  However, even when added to optimal medical therapy in stable angina, it may relieve pain but generally does not largely reduce the risk of death, nonfatal myocardial infarction, or major cardiovascular events.36, 58-61  The recent COURAGE trial published in the NEJM emphasize this point, “Conclusion: As an initial management strategy in patients with stable coronary artery disease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy.”36  This is not surprising as most ACS are caused by lesions not detected by angiography.  However, if a culprit TCFA that has a high probability of leading to ACS can be more accurately defined, intracoronary interventions may play a more critical role in reducing mortality and not just morbidity.  In other words, if PCI is applied directly to high risk TCF, improved risk stratification is a prerequisite.  This will be dealt with in a later section.

DES are now becoming the standard over bear metal stents for catheter based coronary interventions because of their lower rate of late luminal loss.  This comes at a small but significant cost, the risk of late acute luminal occlusion from thrombosis with DES. The occurrence of late stent thrombosis after drug-eluting stent implantation currently is estimated at a constant rate, 0.6% per year for up to 3 years.37-41 It is likely due to susceptibility to late thrombosis because of delayed re-endothelialization over the stent struts. Generally, dual anti-platelet therapy is extended to or beyond a year in an attempt to decrease mortality from these late events. The American Heart Association (AHA) and American College of Cardiology (ACC) recommend that dual antiplatelet drug therapy be continued at least 12 months after SES implantation for the prevention of stent thrombotic occlusion, after substantial debate at the FDA.42  The optimal duration of anti-platelet is currently unknown as are the long-term effects of these medications as described below.  Studies are enrolling using OCT to assess optimal antiplatelet therapy, including DAPT trial, (12 versus 30 months of therapy) funded by the FDA along with several other sponsors and the RAPID trial (treatment ranging from 30 days to 2 years).

3.3 OCT Imaging of Coronary Stents

OCT can define stent structure and position in vivo to a degree greater than any current clinical imaging technology, which may be of benefit in identifying stent subgroups (ex; overlap, apposition, etc) more susceptible to late acute occlusion.25, 43, 44 In addition, OCT provides more precise information than IVUS about stent position and neointimal proliferation on drug-eluting struts and makes it possible to quantify the thickness of tissue in the proximity of the stent struts, relevant to looking at different time points.9, 25, 45, 56  In vivo OCT imaging of stents and neointima is shown in figure 7.  OCT has demonstrated its greatest utility with coronary interventions to date, which will be examined here, as a research tool in studying the mechanisms behind these late coronary occlusions. 

While most experimental OCT work focuses on stent positioning abnormalities 3 - 12 months after it has been introduced, some work has looked at initial stent placement abnormalities. Unfortunately, stent characteristics visualized at day zero that predict late thrombosis have yet to be identified.  OCT can aid with real-time stent apposition as demonstrated by Diaz-Sandoval, et al.47, Regar, et al.48, and Suzuki, et al.49, 50. Regar, et al., for example, successfully demonstrated the application of OCT to assess the final stent area and recoil in real-time in their study.48 Suzuki, et al. analyzed the interstrut angles after the deployment of drug-eluting stents.49 Despite angiographic optimization with high pressures and adequately sized balloons, as identified by OCT, malapposed stent struts are frequently found in complex coronary lesions and more often following the implantation of a thicker stent strut and closed cell design.51 So while OCT can define stent structure to a level greater than any currently available imaging technology, markers have yet to be identified at the time of stent placement to be predictive of late thrombotic occlusion. Ultimately, combination with other nonimaging markers may be useful such as biochemical markers, genetic marker, etc.., which has not been examined to date.

In terms of late changes at the stent site, in addition to its ability to visualize strut apposition to the vessel wall, it is also a powerful tool for assessing neointimal coverage on stent struts (figure 7).  This makes it an important modality for assessing both stent malapposition and intimal coverage at later time points. Malapposition may develop long after the stent has been placed.  The clinical importance of late stent malapposition is still controversial.  It is suggested to occur for primarily two reasons.  First, antiproliferative and antimetabolic effects of the drug may prevent the growth of tissue in the space between the struts and vessel wall. Second, local arterial hypersensitivity reactions secondary to the polymer and drug can induce vessel positive remodeling out of proportion to the increase in persistent intimal hyperplasia. Early IVUS studies suggest that the risk of late stent thrombosis is higher in patients with LASM (late acquired stent malapposition) compared with those without LASM.52, 53  Other IVUS and OCT studies failed to identify LASM as a predictor of clinical adverse events.51, 54 An additional issue which should at least be raised id do these uncovered stents represent potential sites for bacteria attachment in the long run.

But the lack of complete neointima coverage at 12 months has been documented by several groups.  In one study, about 90% struts were completely covered by neointimal proliferation at 12 months follow-up, and the thickness of neointima on overlapping and non-overlaping segments were similar.55  Similar results have been found by other groups.56 In one of these studies extended to 12 months, the results revealed that the neointima coverage and thickness at 12 months were greater than at 6 months (P<0.001). This could indicate the steady progression of neointimal proliferation within the SES. However, only a few SES showed full coverage by neointima, with most of the SES containing uncovered struts, even at 12 months. 

Therefore, OCT has been an excellent tool to better understand late thrombosis with DES.  As stated, antiplatelet therapy is needed in patients with DES that has recently been reviewed by Eisenstein et.al.57  However, the long term effects of dual anti-platelet therapy is unknown, as well as how to subcategorize patients in terms of therapy length.  OCT should be a powerful tool in further understanding the complexity of DES placement and subsequent anti-platelet therapy protocols.  As stated, trials are ongoing to identify optimal anti-platelet therapy are ongoing.

So the area where OCT has already proven to be a powerful tool is in the understanding of late thrombosis in DES placement.  Other areas in intracoronary interventions where OCT has a potential major impact on coronary interventions includes assessing stent placement, evaluating stents at time points after placement to assess continued drug therapy, identifying high risk TCFAs for potential catheter based therapeutics (next section), and guiding non-stent coronary interventions.