Optical Coherence Tomography of De Novo Lesions and In-Stent Restenosis in Coronary Saphenous Vein Grafts (OCTOPUS Study)

Abstract

Background: The OCTOPUS registry prospectively evaluates the procedural and long-term outcomes of saphenous vein graft (SVG) PCI. The current study assessed the morphology of de novo lesions and in-stent restenosis (ISR) in patients undergoing PCI of SVG.

Methods and Results: Optical coherence tomography (OCT) of SVG lesions in consecutive patients presenting with stable CAD and ACS was carried out. Thirty-nine patients (32 de novo and 10 ISR lesions) were included in the registry. ISR occurred in 5 BMS and 5 DES. There were no differences in the presence of plaque rupture and thrombus between de novo lesions and ISR. Lipid-rich tissue was identified in both de novo lesions and in ISR (75% vs. 50%, P=0.071) with a higher prevalence in BMS than in DES (23% vs. 7.5%; P=0.048). Calcific de novo lesions were detected in older grafts as compared with non-calcific atheromas (159±57 vs. 90±62 months after CABG, P=0.001). Heterogeneous neointima was found only in ISR (70% vs. 0, P<0.001) and was observed with similar frequency in both BMS and DES (24% vs. 30%, P=0.657). ISR was detected earlier in DES than BMS (median, 50 months; IQR, 18–96 months vs. 27 months; IQR, 13–29 months, P<0.001).

Conclusions: OCT-based characteristics of de novo and ISR lesions in SVG were similar except for heterogeneous tissue, which was observed only in ISR. (Circ J 2016; 80: 1804–1811)

Approximately 50–60% of saphenous vein grafts (SVG) occlude within 10 years after coronary artery bypass grafting (CABG).^1,2 Twelve months after CABG, accelerated atherosclerosis seems to be the primary factor responsible for graft failure in SVG.³ Multiple factors trigger accelerated atherosclerosis including vein graft arterialization, low shear stress, increased pro-thrombotic milieu within the SVG wall, poor run-off and discrepancy between the graft and native vessel diameter leading to slow flow.^4–6 Endothelial damage during the vein harvesting and implantation also contribute to accelerated atherosclerosis.⁷ Significant SVG disease is treated by percutaneous coronary intervention (PCI) because redo CABG is associated with high periprocedural morbidity and mortality.^8,9 Both bare metal stents (BMS) and drug-eluting stents (DES) are used for this purpose, and there is a paucity of data on the superiority of DES over BMS. PCI of SVG is inferior to PCI of native vessels, with a 25% long-term risk of major adverse cardiac events.¹⁰ Given that in-stent restenosis (ISR) develops in the same environment as de novo SVG lesions, the question arises as to whether the morphology of SVG stent failure mimics the de novo SVG lesions. Notably, atheroma that forms within the implanted stent in native coronary arteries resembles the atherosclerosis of the native vessel.¹¹

Intravascular imaging allows for the assessment of atherosclerosis in vivo. Optical coherence tomography (OCT) enables characterization of the morphology and composition of de novo SVG lesions and ISR of SVG with superior resolution.^12,13 Within the OCTOPUS registry, evaluating the periprocedural and long-term outcomes of SVG PCI, OCT characterization of SVG stenosis is needed.¹⁴ The aim of the current OCT analysis was therefore to compare the morphology of de novo SVG lesions with ISR and to characterize the morphology of both types of lesions in BMS and DES.

Methods

OCTOPUS is a prospective registry of intravascular imaging of SVG atherosclerosis, with the aim of evaluating the morphology of de novo and restenotic lesions as well as PCI optimization using OCT. The study conformed to the Declaration of Helsinki and was approved by the local ethics committee. All patients gave written informed consent.

Inclusion/Exclusion Criteria

Patients with a history of CABG with SVG presenting with stable coronary artery disease (CAD) and confirmed ischemia on non-invasive tests, as well as patients presenting with acute coronary syndrome (ACS), were enrolled. Ostial lesions and those located within anastomosis were excluded from the OCT analysis.

The study exclusion criteria were as follows: age <18 years old, glomerular filtration rate <45 ml/min/1.72 m², significant valve disease, left ventricular ejection fraction <35% and contrast allergy. Time to imaging was defined as the time from CABG to presentation for de novo SVG lesions, and the time from index PCI of SVG to repeated angiography for clinically overt ISR.

OCT

Optical coherence tomography was performed for SVG stenosis ≥50% on angiography. The St Jude Ilumien Optis Medical system was used for OCT. The OCT Dragonfly catheter was advanced into the SVG via guiding catheter and over a 0.014-in coronary guidewire. All OCT was performed using automated pullback triggered by the hand injection of contrast flush. All patients received unfractionated heparin before OCT to achieve Activated Cloting Time >300 s. Distal protection devices were used in all SVG PCI.

OCT Analysis

The OCT analysis was performed at an independent core laboratory at Krakow Cardiovascular Research Institute (www.KCRI.org) according to the previously validated criteria.¹⁵ The OCT region of interest (ROI) was defined as the lesion length limited by areas without atheroma or neointimal hyperplasia for de novo SVG lesions and as the stent length for ISR of SVG surrounded by 5-mm margins. Serial cross-sectional OCT images of the vessel at 1-mm intervals for both de novo SVG lesions and ISR of SVG were scrutinized. Cross-sectional area (CSA), and vessel lumen diameter were measured every 1 mm. The smallest values for both parameters were defined as minimum lumen diameter (MLD) of the minimum CSA.

The OCT analysis of ISR included the measurement of minimum stent diameter and CSA. Neointimal area was defined as the difference between stent and lumen CSA. The OCT reference lumen area and reference diameter were estimated at the site of the largest CSA within the analyzed SVG for both de novo SVG lesions and ISR SVG. Percentage lumen diameter and area stenosis were defined as the relative decrease in luminal diameter and CSA of the target lesion compared with the reference lumen diameter and CSA.

We also assessed the ratio of uncovered and malapposed stent struts in patients with ISR. Malapposition was defined as distance between the stent strut blooming and vessel contour >0.2 mm.

Tissue was classified as homogenous for signal-rich regions; lipid for signal-poor regions with diffuse borders and high signal attenuation; calcified for signal-poor regions with sharp edges; and heterogeneous for poor-signal regions without signal attenuation. The length of an arc of lipid and calcium that occupied the vessel wall circumference was measured and expressed in degrees.^16,17 The maximum lipid arc and calcium arc were measured. The thickness of the fibrous cap that covered the lipid core was measured in the thinnest part of a signal-rich zone that separated the lipid content from the vessel lumen (µm). The fibrous cap thickness was a mean of 3 measurements. OCT-defined thin-cap fibroatheroma (TCFA) was a lipid-rich plaque with fibrous cap thickness <65 µm. Also, the presence of plaque rupture, luminal thrombus, intimal tear, tissue friability and the presence of venous valves was noted during OCT analysis. Intimal tear was defined as a micro-cavity between SVG lumen and its media; intimal rupture as a micro-cavity of intima connected with the SVG lumen; and tissue friability as a signal-free zone overlaid with signal-rich tissue inside of the SVG wall.¹⁸ Offline OCT analysis was performed using CAAS Intravascular 2.0 (Pie Medical Imaging), and the results of intraobserver variability for standard protocols have been presented previously.¹⁹

Statistical Analysis

Continuous parameters were reported as mean±SD or median (IQR). Discrete data are summarized as frequencies and group percentages. Analysis was performed per lesion. Statistical analysis included different intra-class correlations between groups (>1 lesion per patient). Adjusted Wald test and the chi-squared test with Rao and Scott adjustment were used for comparison of continuous and categorical data, respectively. P<0.05 was considered statistically significant. The analysis was performed in R: language and environment for statistical computing (R Core Team 2014, Vienna, Austria).

Results

Patient Characteristic

Forty patient gave informed consent for the study, but, due to poor OCT in 1 patient, 39 patients were included in the registry. Twenty-nine patients had 32 de novo SVG lesions and 10 patients had 10 ISR lesions imaged. PCI was performed in 22 of the de novo SVG lesions and in all 10 ISR lesions. These 22 de novo SVG were treated with OCT-guided PCI and the region to treat covered ROI. In cases of diffusely degenerated SVG with parietal atheroma, the selection of segment to treat was based on angiography.

The patients consisted of 32 men (mean age, 68.9±7.2). Mean duration from CABG to the index procedure was 139±59 months, and for ISR, the mean time from index PCI of the SVG to repeat angiography was 38±28 months. Twenty patient (51%) had stable CAD and 19 (49%) had ACS (unstable angina, n=16; non-ST-segment elevation myocardial infarction, n=3).

There were no significant differences in baseline patient characteristics and medical therapy between patients with SVG de novo lesions and ISR (Table 1).

Table 1. Patient Characteristics

	De novo lesion patients (n=29)	ISR patients (n=10)	P-value
Age (years)	69.07±7.56	68.50±6.25	0.832
Male	24 (83)	8 (80)	0.778
BMI (kg/m2)	28.5 (26–32)	30 (28–32)	0.344
NSTEMI	1 (3)	2 (20)
Unstable angina	10 (35)	2 (20)
Stable angina	18 (62)	6 (60)	0.456
Risk factors
Hypertension	26 (90)	8 (80)	0.811
Hyperlipidemia	25 (86)	8 (80)	0.960
Diabetes mellitus	13 (45)	6 (60)	0.644
Current smoking	2 (7)	2 (20)	0.566
Time from CABG (months)	143 (100–212)	180 (126–210)	0.499
No. vein grafts:
1	4 (14)	3 (30)
2	18 (62)	4 (40)
3	7 (24)	3 (30)	0.400
Arterial graft (LIMA-LAD)	26 (90)	8 (80)	0.811
Pharmacological therapy
Aspirin	28 (97)	9 (100)	0.530
Thienopyridine	2 (7)	1 (10)	0.765
β-adrenergic antagonist	25 (86)	10 (100)	0.404
Calcium channel antagonist	4 (14)	4 (40)	0.188
ARB/ACEI	20 (69)	9 (90)	0.371
Statin	29 (100)	10 (100)	0.999
Other lipid-lowering therapy	6 (21)	1 (10)	0.876
Oral anti-diabetics	5 (17)	4 (405)	0.219
Insulin	2 (7)	2 (25)	0.414
Laboratory results
Hemoglobin	14.08 (12.90–15.22)	13.60 (11.97–14.64)	0.449
WBC	6.32 (5.69–7.24)	6.57 (6.22–7.45)	0.390
Platelets	184 (161–228)	200 (181–221)	0.547
Total cholesterol (mg/dl)	162.29±58.52	151.12±39.70	0.609
LDL-C (mg/dl)	78 (68–98)	71 (60–98)	0.501
HDL-C (mg/dl)	41 (32–48)	41 (35–56)	0.503
Triglyceride (mg/dl)	132 (103–157)	100 (82–188)	0.376
GFR (ml/min/1.73 m2)	71 (53–88)	74 (71–89)	0.545

Data given as mean±SD, median (IQR) or n (%). ACEI, angiotensin-converting-enzyme inhibitor; ARB, angiotensin II receptor blocker; BMI, body mass index; CABG, coronary artery bypass grafting; GFR, glomerular filtration rate; HDL, high-density lipoprotein cholesterol; ISR, in-stent restenosis; LDL-C, low-density lipoprotein cholesterol; LIMA-LAD, left internal mammary artery to left anterior descending artery; NSTEMI, non-ST-segment elevation myocardial infarction; SVG, saphenous vein grafts; WBC, white blood cells.

Angiographic Characteristics

In patients with ISR, there were 5 BMS (Multilink) and 5 DES (2 Promus Elements, 2 Cypher, 1 Resolute Integrity). There was no difference in the location of lesions between SVG de novo lesions and ISR (Table 2). The time to imaging, however, was shorter for ISR of SVG compared with de novo SVG lesions (Table 3).

Table 2. Angiography Data

	De novo SVG lesions (n=32)	ISR of SVG (n=10)	P-value
SVG to left anterior descending artery	3 (9)	2 (20)
SVG to circumflex artery	18 (56)	6 (60)
SVG to right coronary artery	11 (35)	2 (20)	0.590

Data given as n (%). Abbreviations as in Table 1.

Table 3. OCT Data

	De novo SVG lesions (n=32)	ISR of SVG (n=10)	P-value
Time to imaging (months)	139±59	38±28	<0.001
ROI length (mm)	13.15±6.16	17.70±7.55	0.061
Reference lumen CSA (mm2)	6.80 (4.58–9.18)	7.7 (6.6–8.7)	0.128
Reference minimum diameter (mm)	3.01±0.68	3.07±0.53	0.829
Minimum lesion lumen CSA (mm2)	2.71 (1.34–4.19)	1.5 (1.00–2.81)	0.104
Minimum lumen diameter (mm)	1.88±0.65	1.23±0.43
Area stenosis (%)	61.00 (42.72–77.63)	79.01 (58.20–87.59)	0.036
Diameter stenosis (%)	37.33±17.25	59.02±15.36	0.001
Lipids	24 (75)	5 (50)	0.077
Minimum cap thickness (μm)	80 (60–101)	81 (65–87.5)	0.623
Plaque rupture	4 (12.5)	0	0.751
TCFA	7 (33)	1 (20)	0.966
Maximum lipid arc (°)	269 (163–317)	247 (218–277)	0.930
Plaque calcification (°)	14 (44)	1 (10)	0.117
Maximum calcification arc (°)	86.89±54.19	166	–
Mixed plaque	12 (38)	1 (10)	0.104
Macrophages	20 (62)	2 (20)	0.020
Cholesterol clefts	5 (16)	0	0.188
Neovascularization	4 (13)	1 (10)	0.833
Heterogeneous tissue	0	7 (70)	<0.001
Thrombus	9 (28)	0	0.146
Dissection	1 (3)	0	0.533
Intimal tear	2 (6)	0	0.967
Intimal rupture	2 (6)	0	0.967
Tissue friability	6 (19)	0	0.336
Plaque within the SVG valve	6 (19)	0	0.336

Data given as mean±SD, median (IQR) or n (%). CSA, cross-sectional area; mixed plaque, both lipids and calcifications present within the lesion; OCT, optical coherence tomography; ROI, region of interest; TCFA, thin-cap fibrous atheroma. Other abbreviations as in Table 1.

De Novo SVG Lesions vs. ISR of SVG

Six de novo SVG lesions (19%) and 1 ISR lesion (10%) consisted of homogenous tissue only (P=0.522); 12 de novo SVG lesions (37.5%) and 3 ISR lesions were lipid-rich only (P=0.669); 2 de novo SVG lesions (6%) and no ISR lesions were exclusively calcific plaque (P=0.423). Both lipids and calcification were observed simultaneously in 12 de novo SVG lesions (37.5%) and 1 ISR lesion (10%; P=0.104). There were more mixed (lipid and calcified) de novo SVG lesions observed in 132-month follow-up after CABG (Table 4).

Table 4. De Novo SVG Lesion Characteristics vs. Time From CABG

Characteristics	Time from CABG (months)
	<60	60–132	>132
Homogenous tissue only	2 (67)	1 (7.0)	3 (20)
Lipid-rich only	0	10 (72.0)	2 (13)
Calcified tissue only	0	0	2 (13)
Both lipid and calcified tissue	1 (33)	3 (21)	8 (54)

Data given as n (%). P=0.001. Abbreviations as in Table 1.

The lumen area stenosis and lumen diameter stenosis were higher for ISR than in de novo lesions (Table 3). There were no differences in the length of ROI, reference lumen CSA, reference minimum diameter, minimum lesion CSA, or minimum lesion diameter between de novo SVG lesions and ISR lesions (10%).

There were no differences in the presence of cholesterol clefts, neovascularization, lipids, degree of lipid arc, minimum cap thickness, presence of TCFA or plaque rupture between de novo SVG lesions and ISR lesions. Macrophage accumulation, however, was noted more frequently in de novo SVG lesions. Also, the presence of calcification and maximum lipid arc between de novo SVG lesions and ISR lesions were similar, but calcification occurred in older grafts (159±92 vs. 90±62 months, P=0.001) (Figure 1). Only 1 de novo SVG lesion was detected within a venous valve (Figure 2).

Figure 1.

Representative optical coherence tomography of de novo saphenous vein graft lesions. (A) Lipid-rich plaque; (B) ruptured lipid-rich plaque; (C) calcified de novo lesion; (D) thrombus within the lesion; (E) intimal tear; (F) tissue friability.

Figure 2.

De novo saphenous vein graft (SVG) lesion involving venous valve. (A) Angiogram of SVG with de novo lesion (white dashed lines); (B) longitudinal optical coherence tomography (OCT) reconstruction of the lesion. (b) Double lumen created by the presence of venous valve (arrow).

Thrombi, dissections, intimal tear, intimal rupture, and tissue friability were detected only in de novo SVG lesions. Heterogeneous tissue was detected only in ISR of SVG, and time to imaging was shorter for the stent with identified heterogeneous neointima (45±31 vs. 128±65 months; P=0.002). OCT analysis is summarized in Table 3.

SVG ISR for BMS and DES

Time to imaging was shorter for DES compared with BMS (Table 3). There were no differences in lumen CSA, lumen diameter, stent CSA, or vessel CSA, although BMS were less frequently underexpanded as compared with DES [1 (20%) vs. 4 (80%), P=0.21]. No discrepancies were observed in the ratio of malapposed and uncovered stent struts between BMS and DES. There was a higher prevalence of lipid in BMS compared with DES but no difference in the degree of lipid arc (Table 5). There was no difference in the volume of heterogeneous neointima between BMS and DES. Layered neointima was not observed in ISR lesions. OCT data are summarized in Table 5 (Figure 3).

Table 5. OCT Data vs. Stent Type

	BMS (n=5) 100 cross-sections	DES (n=5) 82 cross-sections	P-value
Time to imaging (months)	50 (18–96)	27 (13–29)	<0.001
Lumen CSA (mm2)	4.5 (2.95–6.35)	5.55 (4.00–6.60)	0.185
Lumen diameter (mm)	2.10 (1.70–2.65)	2.50 (2.10–2.70)	0.083
Stent CSA (mm2)	8.55 (7.50–9.90)	8.30 (7.10–9.30)	0.297
Stent diameter (mm)	3.10 (2.90–3.35)	3.10 (2.80–3.30)	0.313
Total stent struts	1,146	879
Malapposed stents struts	32 (3)	5 (0.5)	0.108
Covered stent struts	1,028 (90)	830 (94)	0.410
Neointimal area (mm2)	2.8 (0.95–5.20)	3.4 (2.2–4.1)	0.649
Heterogeneous tissue	24 (24)	25 (30.5)
Homogenous tissue	52 (52)	50 (61)
Lipids	23 (23)	7 (8.5)
Calcification	1 (1)	0	0.048
Minimum lipid plaque cap thickness (μm)	81 (60–130)	118 (91–136)	0.153
Lipid arc (°)	168 (136–247)	170 (145–217)	0.959
Calcification arc (°)	166	0	–

Data given as median (IQR) or n (%). DES, drug-eluting stent. Other abbreviations as in Tables 1,3.

Figure 3.

Representative patterns of in-stent restenosis of saphenous vein graft for (A–D) bare metal stents and (E–H) drug-eluting stents: (A,E) homogenous tissue; (B,F) heterogeneous tissue; (C,G) lipid-rich tissue; (D) calcification; (H) thin-cap fibroatheroma.

On comparison of the “youngest” 16-mm-long and 35-month-old BMS with the “oldest” 18-mm-long and 20-month-old DES, heterogeneous neointima appeared only in the youngest BMS (3 mm, 19%), and this BMS contained more lipids than the oldest DES (12 mm, 75% vs. 5 mm, 28%; P<0.001) in the group.

Technical Aspects of SVG OCT

OCT imaging was performed only by the hand contrast injection using 10 ml syringe, which was sufficient to present ROI in every patient. The right Amplatz guiding catheter and the right Judkins catheter was used to intubate ostium of SVG in 18 (44%) and in 23 (56%) pullbacks, respectively. Ten pullbacks were repeated due to shallow intubation of the guiding catheter. The median amount of contrast used in 32 OCT-guided PCI was the same as for the other 32 consecutive angiography-guided interventions (200 ml; IQR, 160–250 vs. 200 ml, IQR, 150–250, P=0.720). The patients (n=32) did not have chest pain during imaging, and no ventricular arrhythmia was noted. There was no vessel injury caused by SVG OCT.

Discussion

Previous studies have shown that accelerated atherosclerosis is responsible for de novo SVG graft lesions and ISR in SVG.^4,20,21 The current report focuses on intravascular OCT of SVG lesions and shows that ISR of SVG develops faster compared with de novo SVG lesions and has traits of accelerated atherosclerosis. On OCT tissue characterization, the pattern of ISR is similar for both BMS and DES implanted in SVG. Although the number of patients is limited, it seems that ISR in DES occurs earlier than in BMS.

De novo SVG lesions were lipid rich, calcified, and covered with TCFA, potentially prone to rupture on OCT. These findings are in line with previous histological observations and suggest that the morphology of de novo SVG lesion is similar to that observed in native coronary arteries.²⁰ The present study also confirms previous results from intravascular ultrasound (IVUS), OCT and near-infrared spectroscopy that lipids are commonly distributed along the SVG.^{12,18,22–24} Interestingly, one-fifth of the de novo SVG lesions were observed close to venous valves, a finding not documented previously on OCT,^12,18 but biologically plausible given the turbulence associated with reverse SVG.²⁵

Analogous to lesions of native coronary arteries, atheroma of SVG may rupture and lead to ACS.^18,20 The present report supports these previous observations, and the present incidence of ruptured de novo SVG plaque is similar to that in previous IVUS studies.²² On OCT, however, the de novo SVG lesions not only had a high prevalence of lipid, but also of calcification. Calcification was more common in older SVG, consistent with the previous in vivo IVUS observations.²⁶ The observed tissue friability and the intimal tear within SVG were also seen in previous OCT studies on de novo SVG lesions responsible for ACS.¹⁸

In comparison with de novo SVG lesions, ISR of SVG developed faster and the time from stent implantation to ISR was similar to that observed in native coronary arteries.²⁷ This suggests that similar pathological processes are responsible for the extensive in-stent neointimal hyperplasia in native coronary arteries and SVG.^11,27 Similar to ISR of native coronary arteries, lipid-rich heterogeneous and calcified tissue was observed on OCT in implanted stents in SVG.^17,28,29 Interestingly, the ISR lesions caused higher grade stenosis as compared to de novo SVG. Unfortunately, due to the limited OCT penetration, it was not possible to compare plaque burden in de novo SVG lesions and ISR of SVG and further clarify this phenomenon. We postulate that this may be a result of positive vessel remodeling in de novo SVG lesions, which allows for inward and outward plaque expansion,²³ as opposed to the stent platform, which prevents positive vessel remodeling leading to restrictive ISR.

The time from stent implantation to imaging was shorter in DES than in BMS, in contrast to the exaggerated neointimal hyperplasia observed in BMS implanted into native coronary arteries.³⁰ Surprisingly, we observed more lipid within BMS as compared with DES ISR, possibly indicating that factors other than accelerated atherosclerosis are responsible for this phenomenon, such as neovascularization. Given that lipid was less common in DES, thrombogenicity as a result of poor vessel healing may be responsible for new ISR. The presence of heterogenous neointima reflects a high fibrin content or proteoglycan-rich myxomatous content within the stented segment, and such tissue prevailed over lipids in restenotic DES of SVG.^17,31 Clinical observation confirmed that OCT detected heterogeneous neointima within DES, and that this is correlated with poor outcome.³² Interestingly, heterogeneous neointima was not found in de novo SVG lesions, but only in ISR. This probably reflects a high thrombogenic state of stented SVG, which, together with low shear stress, may speed up the formation of ISR as compared with the formation of de novo SVG lesions.³³ To the best of our knowledge, this is the first report on heterogenous neointima within BMS implanted in SVG, further suggesting that impaired healing within the stent may play a significant role in SVG ISR.

Autopsy and OCT studies suggest that stents implanted in SVG are characterized by delayed vessel healing, and that this is especially pronounced in DES.²¹ In contrast, on OCT of ISR of SVG, stent strut coverage in BMS was similar to that in DES. OCT provides the highest resolution to assess stent strut coverage by neointima in vivo. Nevertheless, it cannot visualize strut endothelialization, which is far beyond OCT resolution, and strut coverage by neointima on OCT is used as a surrogate for endothetialization.³⁴ Thus, some of the struts covered by endothelium without relatively thick neointima might have been misclassified.³⁴ In contrast, the uncovered stent struts were observed more than 12 months after stent implantation into SVG, which, together with heterogenous neointima, suggest the need for prolonged dual antiplatelet therapy. The data from case reports suggest that heterogenous neointima may be responsible for the recurrent ISR of SVG.¹³

Large clinical observational studies suggest that there is no superiority for DES compared with BMS in SVG lesions on long-term follow-up.¹⁰ Moreover, there is no difference between first- and second-generation DES in de novo SVG lesion stenting.³⁵ Perhaps the degree of healing might be related to the particular anatomy and tissue properties of SVG, because the heterogeneous neointima was observed in both BMS and DES. This warrants larger OCT prospective assessment of stent healing after SVG intervention in comparison with native coronary artery intervention.

Study Limitations

The primary limitation of this study was the small sample size. Second, OCT is characterized by relatively shallow beam penetration into the vessel wall, hampering comparison of plaque burden within de novo SVG lesions with ISR of SVG. Third, the different stent follow-up between BMS and DES and smaller DES expansion could bias the results of stent healing Finally, OCT was performed in lesions on an intention-to-treat basis, and therefore it is possible that some of the results may be due to the passage of distal protection devices before OCT.

Conclusions

OCT-based characteristics of de novo and ISR lesions in SVG are similar, except for heterogeneous tissue, which was observed only in ISR. Similar to native coronary arteries, ISR of SVG develops faster as compared with de novo SVG lesions.

Funding

This work was supported by the European Union structural funds (Innovative Economy Operational Program POIG.01.01.02-00-109/09-00) and statutory funds of Medical University of Silesia.

Conflict of Interest

None.

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