Plaque Composition & Dynamics

Correlation Between OCT-Derived Intrastent Dimensions and Fractional Flow Reserve Measurements After Coronary Stent Implantation and Impact on Clinical Outcome

Sebastian Reith, MD1;  Simone Battermann1;  Martin Hellmich, PhD2;  Nikolaus Marx, MD1;  Mathias Burgmaier, MD1

Sebastian Reith, MD1;  Simone Battermann1;  Martin Hellmich, PhD2;  Nikolaus Marx, MD1;  Mathias Burgmaier, MD1

Abstract: Background. Insufficient stent expansion, vessel wall injury, and tissue prolapse, all frequently unrecognized by coronary angiography, are predictors of future major adverse cardiac event (MACE) after percutaneous coronary intervention (PCI). Optical coherence tomography (OCT) provides accurate visualization of these features of inadequate stent deployment, whereas reduced fractional flow reserve (FFR) values after PCI indicate functional significance of a residual intrastent stenosis. Objective. To investigate the relationship of OCT-derived intrastent lumen dimensions and FFR-derived hemodynamic relevance immediately after coronary stent implantation and to evaluate the clinical impact of these parameters at follow-up. Methods. In 66 stable patients with a coronary de novo lesion, treated by stent implantation, post-stenting FFR and OCT data were compared and related to MACE at follow-up. Results. There was a significant correlation between remaining OCT-derived intrastent percent area stenosis (%AS) and post-stent FFR (r² = 0.491; P<.001). According to receiver operating characteristic (ROC) analysis, both final FFR and intrastent %AS predicted MACE at 20 months (FFR: area under the curve [AUC] = 0.768; 95% confidence interval [CI], 0.562-0.973; and optimal cut-off = 0.905; %AS: AUC = 0.807; 95%CI, 0.613-1.000; and optimal cut-off = 16.85%) with moderate diagnostic efficiency. Intrastent %AS (16.60 ± 4.75% vs 7.01 ± 3.49%; P<.001) and the 20-month cumulative incidence of MACE (35.9% vs 5.3%; P=.01) were significantly greater in patients with FFR ≤0.905 (n = 26; 39.4%) compared with FFR >0.905 (n = 40; 60.6%). Conclusion. OCT-derived residual intrastent %AS is associated with decreased FFR following stent implantation and both are predictors for clinical outcome at follow-up. 

J INVASIVE CARDIOL 2015:27(5):222-228

Key words: fractional flow reserve, hemodynamics, major adverse cardiac events


Optimal stent deployment with maximal expansion is considered to be a prerequisite for the prevention of stent malapposition and consecutively in-stent restenosis, as well as for the occurrence of acute or subacute stent thrombosis. However, with high-pressure stenting techniques, there is an enhanced risk of vessel damage within the stented segment or at its edges. This includes stent edge dissection, as well as plaque compression and penetration of stent struts into the underlying plaque, as well as thrombus or tissue prolapse into the stented vessel lumen.1 This damage is often undetected by angiography. In contrast, intravascular ultrasound (IVUS) may identify regions of insufficiently expanded stent areas in up to 70% of angiographically apparently well-deployed stents.2,3

Optical coherence tomography (OCT), an intravascular imaging modality with a 10-fold higher resolution compared to IVUS, enables the more accurate identification of intraluminal vessel and stent contours, as well as more sensitive detection of various vessel wall injury types after percutaneous coronary intervention (PCI).4-7 

As fractional flow reserve (FFR) measurement is a well-acknowledged diagnostic tool to evaluate the hemodynamic relevance of intermediate grade coronary lesions,8 several studies and registries have also investigated the impact of FFR after PCI in assessing the quality of stent deployment, regarding residual intrastent stenosis as determined by IVUS and its long-term prognostic value.9-12 However, to date, a correlation between OCT-derived intraluminal dimensions and FFR-derived functional relevance after stenting and its potential clinical impact has not been examined.

Thus, the objective of this study was to evaluate the relationship of OCT-derived final stent dimensions and hemodynamic assessment as determined by FFR after PCI. We also aimed to determine the prognostic value of unfavorable acute morphologic and/or hemodynamic results of stent deployment. 


Study population. Sixty-six patients with a coronary de novo lesion and concomitant PCI and stent implantation due to stable angina and/or documented ischemia on stress test were enrolled in the present analysis between August 2011 and September 2013.

All lesions were investigated by OCT and FFR before and immediately after stent implantation. Clinical history, laboratory tests, and QCA analysis were performed in all patients. Inclusion criteria were the presence of a coronary stenosis, eligible for OCT and FFR examination, written informed consent to the study protocol, and conformation to institutional guidelines. Exclusion criteria were left main, bifurcation, serial and bypass graft lesions, acute coronary syndromes, left ventricular ejection fraction (LVEF) <30%, contraindications to adenosine administration, hemodynamic, or rhythmic instability, renal insufficiency (serum creatinine level >1.5 mg/dL), and pregnancy. 

The study was approved by the local Ethics Committee and was in accordance with the Declaration of Helsinki on ethical principles for medical research involving human subjects.

Quantitative coronary angiography. We performed standardized QCA after intracoronary administration of nitrates (200 µg) and recorded two orthogonal views of every major coronary vessel. QCA data analysis included reference lumen diameter, minimal lumen diameter (MLD), percent diameter stenosis, and lesion length. These data were determined by an experienced reader. Offline imaging analysis was performed with a validated QCA software (Philips Inturis Cardio View, QCA V3.3; Pie Medical Imaging).

Follow-up. Clinical follow-up was obtained by telephone contact or during outpatient visits. A major adverse cardiac event (MACE) was classified as any death, myocardial infarction (MI)/non-ST elevation myocardial infarction (NSTEMI), or target lesion revascularization (TLR) within the follow-up period. In case of more than one clinical event in a single patient, the first event was taken for analysis. The decision for recatheterization and TLR was based on the interventionalist’s discretion.

FFR measurements. FFR measurements were performed using a 0.014˝ coronary pressure sensor-tipped Certus wire (St. Jude Medical Systems, AB) and were in accordance with the recently published recommendations for standardization, recording, and reporting of FFR measurements.13 Maximal hyperemia was induced by intracoronary administration of 200 µg adenosine. FFR was calculated as the ratio between intracoronary and aortic pressure. Preinterventional stenoses were considered to be hemodynamically relevant if FFR was ≤0.8.8 The FFR guidewire was hereafter used for stent implantation. Accuracy of postinterventional FFR measurements was assured by assessing the pressure curves as previously described.13 In case of a suspected drift between aortic and pressure-wire pressures,13 the FFR sensor was pulled back to the guiding catheter and equalization of pressures was performed again. Postinterventional FFR was determined distal to the stent as described above if coronary angiography documented an optimal interventional result, defined as ≤10% residual diameter stenosis by visual estimation. If FFR did not normalize after PCI, FFR was measured proximally to the stent to exclude a relevant lesion of the native proximal vessel segment. In the case of a persistent trans-stent gradient ≤0.8, an FFR delta <0.1 compared to the baseline FFR value, or stent malapposition documented by OCT, additional balloon inflation with a non-compliant balloon was performed. Final FFR measurement for analysis was taken when FFR was >0.8, FFR delta was ≥0.1, and adequate stent apposition and/or maximum balloon burst pressure was achieved. 

OCT image acquisition and analysis. OCT image acquisition was performed using the frequency-domain OCT C7XR system and the DragonFly catheter (St. Jude Medical Systems; Lightlab Imaging, Inc). The removal of blood was achieved with the non-occlusion OCT technique by injection of iodixanol iso-osmolar contrast (GE Healthcare) through the guiding catheter, followed by an automated pull-back at a rate of 20 mm/s. The required amount of contrast was 10-15 mL/pullback at a flow rate of 4 mL/s, and the cumulative examination time was approximately 3 minutes for each single OCT image acquisition.

Subsequent offline and pull-back analyses were performed by two independent observers as previously described14 and in accordance with the recently published consensus for quantitative and qualitative assessment.4,15,16 The analysts were blinded to the clinical and interventional results; in cases of divergent results, they reached a consensus measurement. 

The following quantitative and qualitative assessments were taken before intervention:

  • Minimal lumen area (MLA) and MLD at the frame with the smallest intraluminal area. 
  • Reference lumen area at the reference cross-section with the largest lumen within 10 mm proximal or distal to the MLA and before any side branch.4 Percent area stenosis (%AS) was calculated as ([reference lumen area – MLA]/reference lumen area) x 100.
  • Stenosis length, measured as the segment around the MLA with a cross-sectional area of at least 50% compared to the predefined reference segment lumen area.

The OCT examination was performed after the initial stent deployment and was repeated in the case of a documented stent malapposition after every consecutive additional balloon dilatation. Definite postinterventional OCT acquisition for data analysis was performed after final balloon inflation and after final FFR measurement, and encompassed the frame with the smallest intraluminal area within the stented segment (defined as the minimal stent area [MSA]). The intraluminal contour area and stent contour area were documented in this cross-sectional image (Figure 1). The maximal stent area (SA) was defined as the frame with the largest stent contour area within the entire stent. Intrastent %AS was calculated as ([maximal SA – minimal intraluminal contour area]/maximal SA) x 100. Tissue prolapse was defined as a convex-shaped protrusion of tissue between adjacent stent struts toward the lumen without disruption of the continuity of the luminal vessel surface.6,17 Thrombus was defined as an irregular mass with dorsal shadowing, protruding into the lumen without connection to the vessel wall. Moreover, stent edge dissections were recorded within 5 mm adjacent to the stent at the proximal and distal segment of the native vessel. 

Statistical analysis. Statistical analyses were performed with SPSS (IBM Corporation). Categorical variables were summarized as count (percentage), continuous variables as mean ± standard deviation. Continuous variables were compared with Wilcoxon-Mann-Whitney, Student’s or Welch’s t-test, contingent on distributional characteristics. Pearson’s χ2 test was used to test for the association of nominal variables. 

Linear regression analysis was performed to determine the association between post-stenting OCT-derived parameters and FFR. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and optimal cut-off values were calculated from the receiver operating characteristic (ROC) curve to predict MACE rate at 20 months. This follow-up time of 20 months was predetermined in this study as a suitable clinical intermediate follow-up time for MACE. Given that the mean follow-up of our patient cohort was 15.11 ± 7.70 months (Table 1), cases with a shorter follow-up time and without events were included in the analysis as censored cases. 

Assuming a MACE rate of 10% over 20 months of follow-up and a true area under ROC curve of 0.8, a total of 58 patients (ie, 6 events) are required to test the null hypothesis H0 (area under curve [AUC] = 0.5) vs the alternative hypothesis HA (AUC >0.5) with a power of 80%.18 A similar sample size was used in other studies investigating the effect of FFR and clinical outcome.12

Values with the highest Youden index (sensitivity + specificity – 1) were identified as optimal cut-off values. A classification of the diagnostic efficiency of FFR and intrastent %AS according to the values of the AUC was used, as described elsewhere.19 MACE rates were estimated using the Kaplan-Meier method and differences in time-to-event distributions between groups were compared using the log-rank test. A P-value <.05 was considered statistically significant.


Baseline characteristics and procedural data. Sixty-six patients (mean age, 68.97 ± 9.67 years) with a coronary lesion of at least intermediate degree (≥40% by QCA) were enrolled in the analysis. Clinical baseline characteristics are outlined in Table 1. Single-vessel disease was present in 20 patients (30.3%) and multivessel disease was present in the remaining 46 patients (69.7%). The average QCA values were 64.96 ± 15.93% for percent diameter stenosis, 9.30 ± 4.76 mm for lesion length, 0.90 ± 0.41 mm for MLD, and 2.55 ± 0.63 mm for reference diameter.

There were no periprocedural or postprocedural complications associated with the intracoronary use of FFR and OCT. Predilatation was performed in 32 lesions (48.5%) and postdilatation was performed in 27 lesions (40.9%). The overall procedural-related data are provided in Table 2. In 2 cases, there were persistent hyperemic postinterventional trans-stent pressure gradients of 0.65 and 0.77 (both 0.50 before PCI), even after additional non-compliant balloon inflation at burst pressure and exclusion of stent malapposition. 

Clinical outcome. As presented in Table 1, complete follow-up was available in all 66 patients during a mean period of 15.11 months (range, 6-28 months). No patient developed acute or subacute stent thrombosis or required revascularization by coronary artery bypass graft surgery. Two patients with NSTEMI concurrently required TLR, whereas 1 TLR and 1 NSTEMI occurred independently. There were 3 reported deaths of any cause within the study cohort; 1 patient with a final FFR of 0.93 died 15 months after the procedure due to a sudden cardiac death, 1 patient with reduced LVEF of 37% died of decompensated heart failure (final FFR, 0.90), and another patient with a final FFR of 0.86 died due to a traumatic intracerebral hemorrhage. 

OCT-derived intrastent percent area stenosis and fractional flow reserve predict clinical outcome. In linear regression analysis, OCT-derived intrastent %AS was significantly related to post stent FFR (r² = 0.491; P<.001)(Figure 2), whereas no significant correlation was found between FFR and MSA or between FFR and intrastent MLD (both P>.05). 

We then determined the diagnostic efficiency of both post stent FFR and intrastent %AS to predict clinical events. ROC analysis demonstrated a moderate diagnostic efficiency (AUC = 0.768; 95% CI, 0.562-0.973) for final FFR to predict MACE at 20 months at a best cut-off value of 0.905 (sensitivity, 71.4%; specificity, 85.0%; PPV, 62.5%; NPV, 89.5%) (Figure 3). According to this optimal cut-off value, patients were categorized into a group with an FFR ≤0.905 (n = 26; 39.4%) and a group with an FFR >0.905 (n = 40; 60.6%).

The differences in clinical baseline and follow-up characteristics between the two groups are displayed in Table 1, exhibiting a significantly higher clinical event rate in patients with an FFR ≤0.905 compared to those with an FFR >0.905. 

OCT-derived intraluminal stent dimensions in lesions with an FFR ≤0.905 had a higher degree of intrastent %AS (16.60 ± 4.75% vs 7.01 ± 3.49%, respectively; P<.001). Baseline FFR (0.661 ± 0.122 vs 0.739 ± 0.094, respectively; P<.01) as well as postinterventional FFR values (0.862 ± 0.053 vs 0.947 ± 0.027, respectively; P<.001) were significantly lower in lesions with a final FFR ≤0.905 compared to those with an FFR >0.905. There was a weak correlation between these pre- and postinterventional FFR values (r² = 0.186; P<.001), whereas no association could be demonstrated between patients with and without stent edge dissections regarding the incidence of MACE (P>.05; data not shown). Further differences of procedural and OCT data between the groups are displayed in Table 2.  

Moreover, ROC analysis for intrastent %AS to predict clinical events was analyzed and also demonstrated a moderate diagnostic efficiency (AUC = 0.807; 95% CI, 0.613-1.000) at an optimal cut-off value of 16.85% (sensitivity, 85.7%; specificity, 65.0%; PPV, 46.2%; NPV, 92.9%) (Figure 3). 

According to the Kaplan-Meier method, the 20-month cumulative incidence of MACE was significantly greater in patients with an FFR ≤0.905 compared with patients who had an FFR >0.905 (35.9% vs 5.3%, respectively; P=.01) (Figure 4A). Furthermore, patients with an intrastent %AS >16.85% had a significantly higher 20-month cumulative incidence of MACE (51.3%) compared to individuals with an intrastent %AS ≤16.85% (8.0%; P<.001) (Figure 4B).


The present investigation demonstrated the following: (1) Postinterventional intrastent %AS analyzed by OCT shows a significant correlation with post stent FFR values. (2) Final measurements of hemodynamic relevance using FFR and OCT-derived intrastent %AS predict MACE with moderate diagnostic efficiency. (3) Only 60.6% of patients had a post stent FFR value >0.905, which was associated with a better clinical outcome during follow-up and a significantly lower remaining intrastent %AS after PCI according to OCT analysis.

Several studies have demonstrated that angiography may not precisely evaluate the quality of stent deployment and even additional use of IVUS may not sufficiently identify all features of unsatisfactory acute interventional results.2 The latter is mainly attributed to the low sensitivity of IVUS to assess vessel injury associated with stent implantation, potentially resulting in future clinical events. A number of series have demonstrated that postinterventional FFR measurements may predict morphologic intrastent dimensions20,21 as well as long-term prognostic outcome after balloon angioplasty alone11 or after stenting.11 Whereas Fearon et al20 demonstrated that a post-stent FFR <0.96 predicts a suboptimal stent result based on validated IVUS criteria, the data by Klauss et al 10 and Pijls et al11 focused on clinical outcome and demonstrated that a final FFR value <0.95 is a strong and independent predictor of adverse cardiac events at 6-month follow-up. Similarly, Leesar et al observed a significantly lower cardiac event rate at follow-up if post-stent FFR was ≥0.96.12 

However, compared to these investigations, the design of the present study provides some substantial differences. First, we used a lower FFR cut-off value of 0.905, which was obtained by calculation of the ROC analysis for FFR to predict MACE. Second, we performed intravascular analysis by OCT. In the past, no correlation between angiographic residual stenoses and postinterventional FFR had been observed in a large registry of 750 patients,11 whereas IVUS studies had demonstrated concordance between post-stent FFR measurements and IVUS-determined stent dimensions.20 However, due to its superior resolution when compared with IVUS, the OCT technique offers a more accurate delineation of vessel and stent contours, as well as a better identification of intraluminal obstruction. Thus, using OCT, we were able to precisely quantify the residual degree of intrastent stenosis, potentially resulting in coronary flow limitation. This in turn is reflected by the post-PCI FFR measurement. As we were able to demonstrate a significant correlation between OCT-derived remaining intrastent %AS and FFR, our findings indicate that an FFR value ≤0.905 may predict a suboptimal stent result based on OCT criteria. Third, we used fixed high doses of intracoronary adenosine (200 µg), and the differences of the FFR threshold in our study compared with the values in previous investigations may be related to this. Fearon et al20 and Leesar et al12 used intracoronary adenosine dosages ranging from 15-54 µg, whereas Klauss et al10 used higher doses of up to 150 µg, but with a wide range starting at 30 µg. In this regard, several investigations have indicated a dose-response relationship for the intracoronary application of adenosine for doses >60 µg.22 Recently, the intracoronary use of ≥180 µg adenosine compared with a bolus application of 60 µg resulted in an increased sensitivity of FFR to detect hemodynamically relevant coronary lesions.23 Thus, in the previous investigations, maximal hyperemia may not have been achieved; this may therefore serve as an explanation for the higher FFR cut-off values in their examinations in comparison with ours.

The protrusion of tissue through the stent struts may essentially contribute to the occurrence of residual intrastent lumen narrowing. In a post mortem analysis, compression of the coronary plaque after stent implantation with intraluminal tissue prolapse was notable in 94% of patients.1 Recently, these data were confirmed in vivo by OCT, with a reported tissue prolapse incidence within the stented segment of 97.5%;23 similarly, our findings demonstrated a high tissue prolapse incidence of 93.9%. On the other hand, previous IVUS investigations described distinctly lower incidences of tissue prolapse, ranging between 18%-41%.7 

To date, the true clinical impact of tissue prolapse and its hemodynamic relevance as determined by FFR immediately after stent implantation are not completely elucidated. Whereas Jin et al5 reported no association between tissue prolapse determined by OCT and the clinical event rate during 1-year follow-up, IVUS investigations related significant tissue protrusion with early stent thrombosis24 and early in-stent restenosis25 and proposed that this might be due to the limitation of coronary flow caused by tissue prolapse. However, these differences in clinical outcomes with various imaging technologies may be explained by the ability of OCT to even visualize minor tissue prolapse, whereas IVUS can only detect severe tissue prolapse (which has a higher probability of subsequent stent thrombosis). However, it currently remains unclear if OCT-assessed minor tissue prolapse may similarly result in an increased incidence of stent thrombosis and concomitant clinical events,26 as there is a paucity of data comparing IVUS and OCT with regard to tissue prolapse and MACE rates. In the future, large clinical outcome trials are needed to determine whether the superior resolution of OCT adds further clinically relevant information concerning tissue prolapse, justifying a more frequent use of this imaging technique in routine clinical practice, and moreover to comprehensively understand the definite benefit of OCT toward IVUS after coronary stenting.

Taken together, these discrepancies highlight the superiority and enhanced sensitivity of OCT toward both angiography and IVUS to detect various features of suboptimal stent deployment, including tissue prolapse, residual thrombus, stent malapposition, and stent edge dissections.27 

To the best of our knowledge, the present study is hitherto the only investigation regarding the association of postinterventional severity of residual stenosis as assessed by OCT on the one hand and functional severity of the remaining intrastent stenosis as assessed by FFR on the other hand. We were able to demonstrate that a cut-off value of 0.905 for FFR best determines the clinical prognosis after stent implantation. The specific clinical implication of this finding is that measuring FFR following stent implantation is a widely available and convenient method to identify most cases in which the stent is insufficiently deployed despite a reasonable angiographic appearance. Therefore, interventionalists should be encouraged to make use of FFR after PCI more frequently, particularly when this method has initially been used for preinterventional assessment of the coronary lesion and has hereby demonstrated a low baseline FFR value. As we observed a weak but significant correlation between baseline and postinterventional FFR values, this may be related to a greater extent of intraluminal plaque protrusion through the stent struts in more advanced coronary lesions, reflecting lower baseline FFR values. However, regarding the prognostic value in terms of MACE rate, the final FFR value after stent implantation remains more applicable when compared with baseline FFR. Moreover, in case of a reduced post-stenting FFR value, OCT may be a helpful diagnostic adjunct in differentiating possible reasons for unfavorable hemodynamic acute results that require further intervention. Thus, the additive use of OCT may provide a rationale for a distinct concomitant therapeutic strategy.  This may either be further postdilatation with high-pressure inflation (malapposition, tissue prolapse), differentiated antithrombotic therapy, or thrombus aspiration (residual intraluminal thrombus), a conservative approach in case of small stent edge dissections, or even additional stent implantation to cover relevant stent edge dissections. Recently, the CLI-OPCI trial28 demonstrated that the early detection of stent-related adverse features with OCT guidance may have contributed to improved clinical outcome after coronary intervention.     

The low PPV and concurrently high NPV values for both FFR and intrastent %AS to predict MACE are in line with previous IVUS findings20 and suggest that a final FFR >0.905 and a residual intrastent %AS ≤16.85% are highly predictive for future freedom from MACE. 

Thus, these findings may emphasize and strengthen the power of FFR and OCT to guide and optimize coronary interventions, as well as validate the final interventional result. However, further studies are warranted to evaluate the definite impact of FFR and OCT on future interventional strategies.

Study limitations. First, although this study is currently the only OCT investigation exploring the context of intraluminal dimensions, hemodynamic relevance, and clinical prognosis after PCI, the sample size is small and further large-scale prospective studies are required to confirm these data and moreover to validate the cut-off value observed in our study. Second, we cannot exclude that diffuse and complex coronary disease, particularly regarding the high proportion of patients with diabetes (54.5%) and multivessel disease (65.2%), may have accounted for some of the low postinterventional FFR values. In this regard, in contrast to the intracoronary administration of adenosine in this study, an intravenous application of adenosine with a pressure pull-back curve might have identified occult atherosclerotic disease of native coronary vessels adjacent to the stent as the possible underlying cause for persistently low FFR values. Finally, the relatively high MACE rate of the study cohort may reflect the above-mentioned high percentage of patients with diabetes and multivessel disease and may furthermore be potentially overestimated, since (1) the indication for TLR was not standardized and confirmed by FFR and OCT in all cases, but left to the interventionalist’s discretion; and (2) this investigation did not address whether additional postdilatation of suboptimal FFR values might have resulted in less cardiac events. However, similar MACE rates have been observed in a large multicenter registry.11


We demonstrate that final intrastent %AS analyzed by OCT is significantly associated with post-stent FFR measurements. Both FFR and OCT-derived intrastent %AS following stent implantation are predictors of clinical outcome at follow-up.


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From the 1Department of Cardiology, University Hospital of the RWTH Aachen, Germany; and 2Institute of Medical Statistics, Informatics and Epidemiology, University of Cologne, Germany.

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.

Manuscript submitted March 24, 2014, provisional acceptance given June 17, 2014, final version accepted July 21, 2014.

Address for correspondence: Sebastian Reith, MD, Department of Cardiology/Medical Clinic I, University Hospital of the RWTH Aachen, Pauwelsstr. 30, D-52074 Aachen, Germany. Email: