Predictors of Stent Underexpansion for Severely Calcified Lesions After Debulking

Abstract

Background: There are few studies regarding the predictors of stent underexpansion (SUE) in post-debulking calcified lesions. We investigated predictors of SUE in severely calcified lesions after debulking using optical coherence tomography-guided rotational atherectomy (RA) or orbital atherectomy (OA).

Methods and Results: As a post hoc analysis of the DIRO trial, we compared various parameters, including calcium and lipid parameters (lipid-rich plaque, thin cap fibroatheroma [TCFA], maximum lipid arc, mean lipid arc, lipid length, and lipid volume index), between groups with adequate stent expansion (ASE) and SUE. To find predictors of SUE, multivariable analysis was performed using significant factors from the univariable analysis. We also evaluated adverse events 8 months after the procedure. The SUE group consisted of 57 (65.5%) patients. After suitable debulking of severely calcified lesions using RA or OA, there was no correlation between calcium parameters and SUE; however, the lipid parameters of maximum lipid arc ≥224° and TCFA were significantly and independently correlated with SUE Approximately 45% of severely calcified lesions contained lipid-rich plaques. Adverse events occurred more frequently in the SUE than ASE group.

Conclusions: The role of calcium parameters in predicting SUE in severely calcified lesions after suitable debulking using RA or OA is weak; however, maximum lipid arc and TCFA are important predictors of SUE.

It has been reported that patients with stent underexpansion (SUE) are at high risk of adverse outcomes, including stent thromboses and in-stent restenoses, especially in the case of calcified lesions.^1,2 Although there have been several reports on the predictors of SUE in calcified lesions,^2,3 little is known about the predictors of SUE in severely calcified lesions after suitable debulking using rotational atherectomy (RA; Boston Scientific, Marlborough, MA, USA) or orbital atherectomy (OA; Cardiovascular System Inc. [CSI], St. Paul, MS, USA). However, in the real world, even though stents are implanted after suitable debulking, adverse events are occasionally experienced in patients with severely calcified lesions. In addition, we have frequently found calcified lesions to be combined with lipid-rich lesions, but we usually focus on the severity of the calcified lesions when treating calcified lesions.

Conversely, the recently published Does Optical Coherence Tomography Optimize Results of Stenting (DOCTORS)⁴ and ILUMIEN III⁵ trials have revealed that optical coherence tomography (OCT)-guided percutaneous coronary intervention (PCI) results in improved stent expansion compared with angiography- or intravascular ultrasound (IVUS)-guided PCI, and this may be correlated with better clinical outcomes. Particularly in the case of calcified lesions, OCT can provide more important information than angiography or IVUS.^6,7 Therefore, to achieve adequate stent expansion (ASE), OCT is useful, especially for severely calcified lesions.

Thus, the aim of the present study, a post hoc analysis of the Direct Comparison of RA Versus OA for Calcified Lesions Guided by OCT (DIRO) trial (UMIN000037284),⁸ was to investigate predictors of SUE, including lipid lesion parameters, in severely calcified lesions after suitable debulking using RA or OA.⁸

Methods

Study Population

The DIRO trial was a single-center prospective randomized trial that included patients with severely calcified lesions who were scheduled to undergo RA or OA at Osaka Rosai Hospital between August 2019 and October 2021. In this trial, the target lesion had to be a de novo calcified lesion with an arc of more than 180° assessed by OCT, or angiographically severe calcifications if the OCT catheter could not be advanced distal to the lesion before any intervention. The DIRO trial included 50 patients who underwent RA and 50 who underwent OA. Of these patients, 12 patients with poor OCT images and 1 patient with a stent-free strategy were excluded from the present study. Thus, 87 patients were analyzed in this post hoc analysis of the DIRO trial (Figure 1).

Figure 1.

Study population. ASE, adequate stent expansion; DIRO, Direct Comparison of RA Versus OA for Calcified Lesions Guided by OCT; OA, orbital atherectomy; OCT, optical coherence tomography; RA, rotational atherectomy; SUE, stent underexpansion.

The 87 patients in this study were divided into 2 groups, namely an ASE group and a SUE group, according to OCT findings just after stent implantation. SUE was defined as a minimum stent area/mean (proximal and distal) reference area of <80% if both reference areas were available, <90% if only the distal reference area was available, or <70% if only the proximal reference area was available (Figure 2). In this study, we used the conventional method of underexpansion.^9–11 We compared various parameters, including coronary risk factors and OCT parameters, between the 2 groups.

Figure 2.

Representative case with both calcified and lipid lesions and stent underexpansion. A severely calcified lesion is present mainly in a proximal site and both a lipid-rich and calcified lesion are present in a distal site. After stenting, the minimum stent area (MSA; 2.99 mm²) was found at the border of the lipid and calcified lesions. This case showed stent underexpansion (proximal reference area: 5.78 mm²; distal reference area: 3.68 mm²; mean reference area: 5.18 mm²; minimum lumen area/mean reference area: 72.7%). TCFA, thin cap fibroatheroma.

This study adhered to the Declaration of Helsinki.

Interventional Procedures

For severely calcified lesions, suitable debulking using RA or OA was attempted as follows. In the RA group, the burr size was usually selected such that the burr to artery ratio did not exceed 0.7. Burr upsizing was considered based on OCT findings that included the calcium thickness and wire bias obtained after the initial RA. The preset burr speed was mostly set at 180,000 r.p.m. In the OA group, a 1.25-mm classic crown burr was used. All patients were initially treated with a low speed (80,000 r.p.m.). An OCT examination was performed after the low-speed atherectomy. The speed was increased to high (120,000 r.p.m.) when OCT pullback revealed that the reference lumen diameter was >2.5 mm, the guidewire was not attached to normal vessel wall in the lesion, and tissue modification did not exceed the media layer. We defined the suitable atherectomy when we could perform the above-mentioned procedures using RA or OA in the present study. After the atherectomy, the procedure was continued according to the standard of care. OCT pullbacks were performed just after the atherectomy and at the end of the procedure.

OCT Examination and Analysis

Frequency domain OCT examinations were performed with the Dragonfly^TM imaging catheter and OPTIS^TM imaging system (Abbott Vascular, Santa Clare, CA, USA) during the PCI and 8 months after stent implantation. OCT images were analyzed offline using the Medical Offline Review Workstation (Abbott Vascular) at 1-mm intervals according to current guidelines.¹²

In the present study, calcified plaque was defined as a signal-poor or heterogeneous region with a sharply delineated border.¹² The calcium arc was measured at 1-mm intervals and the maximal total calcium arc and mean calcium arc were recorded.¹³ The calcium volume index was calculated as the average calcium arc multiplied by calcium length.¹⁴

A plaque was considered to be lipid-rich if lipids were present for more than 90° of at least 1 cross-section of the plaque.^12,15 The lipid arc was measured first at 1-mm intervals and then in each frame at its largest portion, with the maximum value recorded. A thin-cap fibroatheroma (TCFA) was defined as a lipid-rich plaque with a fibrous cap thickness of <65 µm. Lipid length was measured using the total number of lipid plaque frames, frame rate, and pullback speed. The lipid volume index was calculated as the mean lipid arc multiplied by lipid length.

Clinical Outcomes

Adverse events were evaluated 8 months after the procedure and included all-cause death, cardiovascular death, myocardial infarction, target vessel revascularization, major bleeding, definite stent thrombosis, and stroke.^16,17 In this study, major bleeding was defined as Bleeding Academic Research Consortium bleeding event Types 3 and 5.¹⁶ We also investigated vascular healing, which was evaluated using follow-up OCT examinations.

Statistical Analysis

Statistical analyses were performed using JMP 17 statistical software (SAS Institute Inc., Cary, NC, USA). Categorical variables are presented as numbers and percentages and were compared using either the χ² or Fisher’s exact test, as appropriate. Continuous variables are presented as the median with interquartile range (IQR) and were compared using the Mann-Whitney U test. Subsequently, a univariable logistic regression model was built and variables with P<0.05 were included in the multivariable logistic regression model in addition to clinically important confounders including age, diabetes, hypertension, and dyslipidemia. Two-sided P<0.05 was considered statistically significant.

Results

Patient Characteristics

The ASE group consisted of 30 patients and the SUE group consisted of 57. The patient characteristics are presented in Table 1. There were no significant differences between the 2 groups regarding age, body mass index, sex, coronary risk factors, and past history of medical therapy for coronary artery disease. In addition, there were no significant differences between the 2 groups in laboratory data and ejection fraction assessed by echocardiography.

Table 1.

Patient Characteristics

	ASE group (n=30)	SUE group (n=57)	P value
Age (years)	74 [71–78]	76 [68–80]	0.60
BMI (kg/m2)	23 [21–28]	24 [22–26]	0.50
Male sex	23 (77)	37 (65)	0.33
Diabetes	17 (57)	36 (63)	0.65
Hypertension	27 (90)	44 (77)	0.24
Dyslipidemia	21 (70)	37 (65)	0.81
Current smoker	1 (3)	3 (5)	1.00
Hemodialysis	8 (27)	17 (30)	0.81
Previous MI	9 (30)	13 (23)	0.60
Prior PCI	17 (57)	25 (44)	0.27
Prior CABG	1 (3)	3 (5)	1.00
LDL-C (mg/dL)	69 [58–90]	87 [61–105]	0.16
HbA1c (%)	6.4 [5.8–7.1]	6.3 [5.8–7.2]	0.75
Hemoglobin (mg/dL)	12.2 [10.8–13.1]	11.7 [10.9–13.3]	0.87
Creatinine (mg/dL)	0.74 [0.78–5.61]	0.83 [0.71–4.36]	0.49
CRP (mg/dL)	0.11 [0.05–0.25]	0.12 [0.06–0.28]	0.26
NT-proBNP (pg/mL)	235 [135–1,736]	774 [140–2,680]	0.68
Ejection fraction (%)	65 [59–71]	65 [59–70]	0.85

Unless indicated otherwise, data are given as the median [interquartile range] or n (%). ASE, adequate stent expansion; BMI, body mass index; BNP, B-type natriuretic peptide; CABG, coronary artery bypass grafting; CRP, C-reactive protein; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; PCI, percutaneous coronary intervention; SUE, stent underexpansion.

Regarding the debulking device, the median final burr size was 1.75 mm (IQR 1.5–2.0 mm) and the rotational speed was 181,120±7,225 r.p.m. in RA group (n=50). In the OA group (n=50), the median sanding time was 133 (IQR 80–228 s).

Lesion and Procedural Characteristics

The distribution of target lesions, debulking device, and other procedural factors for stenting and pre- and postdilation were similar between the 2 groups (Table 2). The incidence of the use of predilation was similar (93% and 100% in the ASE and SUE groups, respectively), as was the use of modified balloons, such as cutting or scoring balloons, and conventional balloons. The balloon size and maximum pressure for the pre- and postdilation did not differ significantly. Stent factors, including stent number, diameter, and length, were also similar between the 2 groups.

Table 2.

Lesion and Procedural Characteristics

	ASE group (n=30)	SUE group (n=57)	P value
Lesion location			0.89
Left anterior descending artery	23 (77)	41 (72)
Circumflex artery	3 (10)	7 (12)
Right coronary artery	4 (13)	9 (18)
Predilation	28 (93)	57 (100)	1.00
Predilation with modified balloon	17 (57)	37 (65)	0.15
Predilation modified balloon
Maximum diameter (mm)	3.3 [2.8–3.23]	3 [2.8–3.3]	0.49
Maximum pressure (atm)	12 [12–12]	12 [10–14]	0.76
Predilation with conventional balloon	14 (47)	28 (49)	0.49
Predilation conventional balloon
Maximum diameter (mm)	3 [2.9–3.3]	3 [2.8–3.5]	0.89
Maximum pressure (atm)	16 [12–20]	20 [12–22]	0.51
Debulking device (RA)	19 (63)	24 (42)	0.07
No. stents	1 [1–2]	1 [1–2]	0.85
Maximum stent diameter (mm)	3 [3–3.5]	3.5 [2.8–3.5]	0.30
Mean stent diameter (mm)	3 [2.8–3.3]	3 [2.8–3.4]	0.92
Total stent length (mm)	38 [27–55]	40 [33–51]	1.00
Postdilation	27 (90)	48 (84)	0.53
Postdilation maximum balloon diameter (mm)	3.5 [3–3.5]	3.3 [3–3.5]	0.97
Postdilation maximum pressure (atm)	20 [20–23]	20 [20–22]	0.20

Unless indicated otherwise, data are given as the median [interquartile range] or n (%). ASE, adequate stent expansion; RA, rotational atherectomy; SUE, stent underexpansion.

OCT Findings

Both proximal and reference areas could be detected in 60 (69%) patients, only the proximal reference area could be detected in 17 (20%) patients, and only the distal reference area could be detected in 10 (11%) patients. In pre-OCT analyses, the ASE group had a significantly lower the incidence of a TCFA (1% vs. 11%, P=0.040) and a significantly lower maximum lipid arc area (median 151.6° [IQR 115.1°–176.9°] vs. 194.0° [IQR 119.8°–304.3°]) than the SUE group, whereas there were no significant differences in other parameters between the 2 groups (Table 3). All lesions had calcified plaques and approximately 45% had lipid-rich plaques. A representative case that included both calcified and lipid lesions is shown in Figure 2. This lesion had a severely calcified lesion at a proximal site and a lipid-rich lesion at a distal site. Calcium parameters, including the maximum calcium arc, mean calcium arc, maximum calcium thickness, calcium length, and calcium volume index, were comparable between the 2 groups.

Table 3.

Optical Coherence Tomography Findings

	ASE group (n=30)	SUE group (n=57)	P value
Pre
Distal reference lumen area (mm2)	4.73 [3.36–6.14]	4.55 [3.63–5.66]	0.959
Proximal reference lumen area (mm2)	6.85 [5.82–7.96]	8.17 [6.51–9.41]	0.069
Mean reference lumen area (mm2)	6.01 [4.91–7.96]	6.52 [5.45–7.74]	0.284
Minimum lumen area (mm2)	1.32 [1.3–1.48]	1.37 [1.04–1.69]	0.446
Presence of calcified plaque	30 (100)	57 (100)	–
Maximum calcium arc (°)	281.3 [231.9–356.1]	331.1 [374.1–358.7]	0.119
Mean calcium arc (°)	155.3 [11.2–190.2]	158.2 [130.0–207.6]	0.560
Maximum calcium thickness (mm)	1.21 [1.06–1.32]	1.22 [1.04–1.38]	0.541
Calcium length (mm)	22.5 [17.5–28.3]	25 [20–31]	0.378
Calcium volume index	3,071 [1,866–4,929]	3,658 [2,527–5,450]	0.345
Presence of calcium nodule	14 (47)	23 (40)	0.651
Presence of lipid-rich plaque	13 (43)	25 (44)	0.962
TCFA	1 (3)	11 (19)	0.040
Maximum lipid arc (°)	151.6 [115.1–176.9]	194.0 [119.8–304.3]	0.048
Mean lipid arc (°)	111.4 [1,000.9–126.0]	120.0 [62.5–165.0]	0.325
Lipid length (mm)	5 [3–8]	6 [3–9]	0.620
Lipid volume index	575 [378–764]	650 [365–1,276]	0.538
Post
Minimum lumen area (mm2)	4.76 [3.66–5.43]	4.69 [3.75–6.14]	0.319
Mean lumen area (mm2)	7.14 [5.97–8.26]	7.08 [5.78–8.10]	0.996
Minimum stent area (mm2)	4.77 [3.70–5.40]	4.45 [3.57–5.93]	0.160
Mean stent area (mm2)	6.97 [5.93–7.91]	6.76 [5.50–7.66]	0.947
% Malapposed struts	5.90 [2.50–8.97]	6.74 [2.57–11.40]	0.755
Maximum malapposition distance (mm)	0.43 [0.28–0.60]	0.44 [0.30–0.61]	0.767
Follow-up
Mean NIH thickness (μm)	105 [79–133]	109 [85–141]	0.447
% Uncovered struts	1.99 [0.27–4.01]	1.01 [0.31–4.09]	0.880
% Malapposed struts	0.27 [0–1.10]	0.29 [0–1.28]	0.774

Unless indicated otherwise, data are given as the median [interquartile range] or n (%). ASE, adequate stent expansion; NIH, neointimal hyperplasia; TCFA, thin-cap fibroatheroma; SUE, stent underexpansion.

Post-OCT analyses revealed that the minimum and mean lumen areas and minimum and mean stent areas were comparable between the 2 groups. The percentage of malapposed struts and the maximum malapposition distance were also similar between the 2 groups. At the 8-month follow-up, the mean neointimal hyperplasia thickness and the frequency of uncovered and malapposed struts were comparable between the 2 groups.

Factors Correlated With SUE

A receiver operating characteristic curve revealed that the suitable cut-off value for the maximal lipid arc to predict SUE was 224°. Univariable logistic regression analysis showed that the incidence of a TCFA and the maximum lipid arc (≥224°) were significantly correlated with SUE (Table 4). Multivariable logistic regression analysis including age, diabetes, hypertension, and dyslipidemia also revealed that both the incidence of a TCFA and the maximum lipid arc (≥224°) were independently and significantly correlated with SUE.

Table 4.

Factors Correlated With Stent Underexpansion

	Univariate			Multivariate
	OR	95% CI	P value	OR	95% CI	P value
Age	1.85	0.67–5.68	0.243	1.64	0.18–18.04	0.662
TCFA	7.73	1.41–144.61	0.014	9.38	1.67–129.08	0.025
Maximal lipid arc (≥224°)	8.57	1.57–159.80	0.009	13.15	1.60–209.25	0.014
Diabetes	1.31	0.53–3.23	0.556	4.95	0.79–36.69	0.091
Hypertension	0.38	0.08–1.30	0.127	0.14	0.01–1.27	0.082
Dyslipidemia	0.79	0.30–2.02	0.631	0.70	0.11–4.43	0.695

CI, confidence interval; OR, odds ratio; TCFA, thin-cap fibroatheroma.

Eight-Month Clinical Outcomes

During the 8-month-follow-up, target vessel revascularization was observed in 7% of lesions in the SUE group but in 0% of lesions in the ASE group (P=0.29; Table 5). No patients in the ASE group experienced death from any cause, cardiovascular death, or myocardial infarction, whereas these three outcomes were observed in 2 (4%) patients each in the SUE group (P=0.54). All major bleeding in this study was Type 3a (transfusion with overt bleeding). There were no significant differences in major bleeding between the ASE and SUE groups (10% vs. 9%, respectively; P=1.00). The incidence of other clinical outcomes, including definite stent thrombosis and stroke, did not differ between the 2 groups (Table 5).

Table 5.

Clinical Outcomes at 8 Months

	ASE group (n=30)	SUE group (n=57)	P value
All cause death	0 (0)	2 (4)	0.54
Cardiovascular death	0 (0)	2 (4)	0.54
Myocardial infarction	0 (0)	2 (4)	0.54
Target lesion revascularization	0 (0)	4 (7)	0.29
Target vessel revascularization	2 (7)	4 (7)	0.61
Major bleeding	3 (10)	5 (9)	1.00
Definite stent thrombosis	0 (0)	1 (2)	1.00
Stroke	1 (3)	1 (2)	1.00

Unless indicated otherwise, data are given as n (%). ASE, adequate stent expansion; OA, orbital atherectomy; RA, rotational atherectomy; SUE, stent underexpansion.

Discussion

The main findings of this study are that: (1) when suitable lesion preparation was performed using RA or OA for severely calcified lesions, the calcium parameters, including maximum calcium arc and maximum calcium thickness, were not strongly correlated with SUE; (2) approximately 45% of severely calcified lesions included lipid-rich lesions; and (3) after optimized lesion preparation for severely calcified lesions, the maximum lipid arc and TCFA were significantly and independently correlated with SUE.

Calcified Lesions After Suitable Debulking

Several studies have reported a correlation between severely calcified lesions and SUE, which is known to be a common risk factor for stent thrombosis and in-stent restenosis.^2,3,18 Therefore, a more aggressive strategy of lesion modification including RA or OA is needed prior to stent deployment to achieve an efficient interventional treatment.¹⁹ We previously reported that a maximum calcium thickness <880 μm was a useful predictor of acceptable stent expansion,²⁰ but in that study we excluded lesions treated with RA or OA. Another study reported that the maximum calcium arc was associated with SUE.³ However, in the present study, calcium parameters, including maximum calcium thickness and maximum calcium arc, were not correlated with SUE. One reason why the present study did not show any correlation between calcium parameters and SUE may be that all the patients in the DIRO study underwent aggressive debulking of calcium lesions before stenting.⁸ However, we also found that even though suitable debulking was performed for severely calcified lesions, v was evident in over 60% of lesions (66% in the present study). Therefore, we need to focus on parameters other than the calcium grade.

Lipid-Rich Plaque

It has been reported that the presence of a proximal lipid-rich plaque is the most potent independent predictor of a proximal coronary edge dissection after PCI.²¹ Therefore, if the lesion has a lipid-rich plaque, especially at an edge site, it is occasionally necessary to reduce the post-dilatation pressure to avoid an edge dissection after stent implantation. These trends may partially induce SUE. In addition, because lipid-rich plaques and TCFAs have been reported to be correlated with a slow-flow phenomenon, we occasionally decrease the pressure of the stent implantation if the lesion includes lipid-rich plaque and/or a TCFA.²² In the present study, a lipid-rich plaque was found in approximately 45% of severely calcified lesions. Therefore, when treating severely calcified lesions, attention should be paid to any lipid-rich plaque.

Possible Mechanism of SUE in Lesions Including Both Lipids and Calcified Plaque

In this study, after suitable lesion preparation for severely calcified lesions, the contribution of calcium parameters to SUE was weak. Instead, lipid parameters may contribute to SUE. Although the underlying reason for this is not clear, we speculate that the explanation could be as follows. According to our results, severely calcified lesions frequently include a lipid-rich plaque. If the lesion modification for severely calcified plaque was suitable, the impact of the lipid-rich plaque on stent expansion may have been stronger than that of the calcified lesion. As shown in Figure 3, if the lesion had the same hardness throughout, the action of the balloon pressure would be the same for the whole lesion; however, if the lesion has both hard and soft parts (e.g., a calcified part and a lipid-rich part), greater balloon expansion would occur in the soft than hard part, resulting in different expansion within the stent. The border of the soft and hard parts in particular may be most affected and could become deformed, which could induce SUE. In addition, because the operators wanted to avoid dissection and slow flow after stent implantation, they tended to reduce the inflation pressure for stent implantation in the lipid parts compared with the calcified parts, especially when they were using a short non-complaint balloon. However, our data showed the post-dilatation maximum pressure was same between the ASE and SUE groups. In the real world, if physicians dilate balloons at a site near the stent edge or in relatively soft lesions, they usually use relatively low pressure. In the present study, postdilation was performed several times and only the maximum pressure was recorded. These combined mechanisms may have induced SUE in both calcified and lipid-rich lesions after suitable debulking of the calcified lesions. To confirm our hypothesis, we reanalyzed the correlation between the site of lipid-rich plaque and the site of the minimum stent area. There were 38 (43.7%) patients with lipid-rich plaques. We reanalyzed whether SUE sites corresponded to the border regions between calcified and lipid lesions in these 38 patients, using a side branch in the OCT imaging. In 74% (28/38) of cases, SUE was observed around these border regions. Therefore, the results may partially support our speculation.

Figure 3.

Possible mechanism for stent underexpansion in lesions with both lipid and calcified plaque. (Left) If the lesion has the same hardness throughout, the effect of the balloon pressure with be the same on the whole lesion. (Right) However, if the lesion has both hard and soft parts (e.g., calcified parts and lipid-rich parts), greater balloon expansion will occur in the soft parts than in the hard parts, potentially leading to different degrees of stent expansion. The border between the soft and hard parts may be the most affected and can become deformed (Right), which could induce a stent underexpansion. In the present study, because the lipid-rich plaque was predominantly located in the distal region, the minimum stent area (the site of greatest underexpansion) frequently occurred at the border of the lipid-rich and calcified lesions.

Clinical Implications

It has been reported that in severely calcified lesions, the calcium burden, area, and volume assessed by OCT are correlated with underexpansion, but there have been few studies regarding the correlation between these calcium parameters and SUE after suitable debulking of calcified lesions. In fact, in our study, SUE occurred in over 60% of lesions (66% in the present study) even after a suitable debulking of severely calcified lesions, and clinical adverse events at the 8-month follow-up, especially target vessel revascularization, occurred more frequently in the SUE than ASE group. In addition, we showed that the effect of calcium parameters on stent expansion may be weak after suitable modification of calcified lesions using the RA or OA. Thus, the focus should be on parameters other than the calcium grade. According to our results, to achieve ASE, the focus should be on the grade of the lipid-rich plaque in the calcified lesions. If severely calcified lesions include a lipid-rich plaque, that part of the lipid-rich lesion should be carefully evaluated. If the degree of stent expansion is not satisfactory in the part of the lesion with a lipid-rich plaque, it may be better to use a more aggressive post-dilatation pressure, using a short non-complaint balloon to avoid SUE.

Study Limitations

First, this study was a post hoc analysis of the DIRO study, and the sample size was relatively small, but a detailed OCT analysis of the patients with severe calcified lesions after suitable debulking is rare and valuable. Second, we did not evaluate nodular calcification in this study. In the present OCT system, it is occsionally difficult to completely distinguish nodular calcification from lipid-rich plaques because both nodular calcification and lipid-rich plaques show signal attenuation. Therefore, in this study, some lipid-rich plaques may include nodular calcification, and in some lipid-rich lesions the presence of lipids could obscure underlying calcification on OCT. Finally, we only recorded the maximum pressure of the post-dilation balloon in this study, Therefore, it is not clear whether the physicians used the maximum post-dilation pressure at the site near the stent edge or in the region where both calcified and lipid lesions are present.

Conclusions

This study demonstrated that after suitable debulking of calcified lesions using RA or OA, the contribution of calcium parameters to SUE may be weak. Instead, attention should be paid to the maximum lipid arc and TCFA to avoid SUE, because approximately 45% of severely calcified lesions included lipid-rich lesions.

Acknowledgments

The authors thank John Martin for his linguistic assistance with this manuscript.

Sources of Funding

This study did not receive any specific funding.

Disclosures

The authors declare no conflicts of interest.

IRB Information

This study was approved by the Medical Ethics Committees of Osaka Rosai Hospital (Reference no. 2021-20).

Data Availability

The deidentified participant data will not be shared.

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