This was a single center, retrospective observational study conducted at Saitama Medical Center, Jichi Medical University. Legs with symptomatic LEAD that underwent OFDI-guided EVT were reviewed during the period between February 2022 and February 2024. The inclusion criteria were as follows: (1) legs with symptomatic LEAD undergoing EVT in FP arteries with significant stenosis, and (2) the entire FP arteries evaluated by OFDI before the use of stents or drug-coated balloons. The exclusion criteria were: (1) entirely suboptimal OFDI images that could not be analyzed for any reason, and (2) restenotic lesions undergoing previous EVT in the FP arteries. This study received approval from the institutional review board of Saitama Medical Center, Jichi Medical University (S25-098), and written informed consent was waived due to the retrospective study design. All clinical information was obtained through a review of hospital records. The definition of patient characteristics has been previously described.

A 6-Fr guide sheath was introduced through either the ipsilateral or contralateral common femoral artery. The guide sheath tip was positioned at the ostium of the superficial femoral artery (SFA) at a minimum. A 0.014-inch guidewire was advanced into the below-the-knee arteries. OFDI (Fastview [Terumo, Tokyo, Japan]) was subsequently inserted into the most distal segment of the vessel. Pure dextran was flushed to clear the luminal blood. To block the blood flow from upstream, manual compression of the common femoral artery or balloon inflation attached to a guiding catheter (Optimo PPI sheathless kit [Tokai Medical Products Inc., Aichi, Japan]) was employed. The OFDI catheters were automatically pulled back at a rate of 20 mm/s (160 frames/s) from the popliteal artery to proximal SFA. OFDI imaging was repeated until the catheter reached the guide catheter. If the OFDI catheter could not cross a lesion or imaging quality was insufficient due to residual blood, a balloon was used to improve image quality.

OFDI was performed from the SFA to the popliteal artery according to conventional definitions. To assess the prevalence of each finding by location, the information of each tissue characteristic was collected according to the locations of proximal, middle, and distal SFA and popliteal artery. Both findings at the culprit and nonculprit sites were collected. The main causes at the culprit sites were classified into the following: (1) rupture, (2) erosion, (3) eruptive calcified nodule, (4) healed plaque, (5) calcified plaque, and (6) lipidic plaque. ^,, The culprit site was defined as the segment with angiographically significant stenosis of ≥90%. If there was a segment with <visually 25% stenosis over more than a 5-mm interval, the site was identified as the separated culprit site. Identification of culprit lesions based on the above definition was performed retrospectively.

Acute thrombus was defined as protruding mass with an irregular surface lacking superficial high intensity, irrespective of signal attenuation. Acute thrombus was classified into rupture, erosion, and eruptive calcified nodule ( Figure 1 ). ^, Plaque rupture was defined by a discontinuous fibrous cap with a cavity inside the plaque, along with superficial thrombus. ^,, Lipid component, including cholesterol crystals, is present at the ruptured or adjacent site. Plaque erosion was defined by a thrombus attached to the luminal surface with an intact fibrous cap. ^, Unlike plaque rupture, there is no disrupted fibrous cap or a cavity surrounded by a fibrous cap. Superficial lipidic or calcified plaque is not directly connected to the thrombus. Eruptive calcified nodule were defined as convex structures with superficially high intensity and signal attenuation, showing surface irregularity due to calcific nodules and thrombus. ^,, Healed plaque was defined by the following criteria: (1) at least 2 layers with different optical signal density and distinct demarcation between superficial and the underlying plaque, (2) a smooth surface with no signal attenuation in superficial plaque ( Figure 2 ). ^,

Consecutive OFDI images of eruptive calcified nodule, erosion and plaque rupture. ( A ) Thrombus connected to calcific nodules ( white arrow ). (B) Eruptive calcified nodule showing obvious surface irregularity ( yellow arrowheads ) with signal attenuation. ( C ) Protruding mass showing mild surface irregularity (blue arrowheads). ( D ) Thrombus with signal attenuation (orange arrow). ( E ) Thrombus with less signal attenuation and no superficial lipid or calcification connected to the thrombus. ( F ) Smooth surface without a disrupted fibrous cap. ( G ) disrupted fibrous cap with a cavity ( green arrowheads ) and thrombus without signal attenuation (red arrow). ( H ) Thrombus connected to an intact fibrous cap overlying a cavity ( green arrowheads ). ( I ) Thrombus overlying superficial lipid ( gray arrowheads ). OFDI = optical frequency domain imaging.

Consecutive OFDI images of healed plaque. Healed plaque 1: ( A ) Two different layers with clear delamination indicating healed plaque on the luminal side. ( B ) Low-intensity plaque with clear delamination and smooth surface. ( C and D ) The area of healed plaque gradually decreased. Healed plaque 2: ( E ) Healed plaque with intermediate-intensity plaque and underlying plaque with signal attenuation. F. Clear delamination separating intermediate-intensity plaque and underlying plaque. ( G and H ) Area of healed plaque gradually decreased. White arrowheads indicate clear delamination separating healed plaque and underlying plaque. OFDI = optical frequency domain imaging.

Calcification was defined as a structure with a signal-poor or heterogeneous region and sharply delineated borders. Medial or intimal calcifications are in the media or intima, respectively ( Supplementary Figure 1 ). Noneruptive calcified nodule was defined as follows: (1) a convex shape with a smooth surface, (2) superficially high-intensity signal with attenuation, (3) longitudinal connection to calcification. ^,, When medial calcification is assigned into noneruptive calcified nodule, it is required that noneruptive calcified nodule in media is not connected to intimal calcification. Bone formation was defined as a honeycomb sign within calcification. ^, Lipid was defined as a plaque with a signal-poor region and diffuse borders ( Supplementary Figure 1 ). ^, The severity of lipid, intimal and medial calcification was assessed using a quadrant distribution score ranging from 0 to 4 (score 0: 0°; score 1: >0° and ≤90°; score 2: >90° and ≤180°; score 3: >180° and ≤270°; score 4: >270°). Cholesterol crystal was defined as a linear and high-intensity signal with a clear border within the plaque showing low- or intermediate-intensity ( Supplementary Figure 1 ). ^, Macrophages were defined as a confluent punctate, high-intensity signal with a shadow in the underlying tissue ( Supplementary Figure 1 ). ^, Macrophages lack continuity with calcification and longitudinally disappear in the plaque. ^, Thin-capped fibroatheroma was defined as a delineated necrotic core with an overlying fibrous cap, where the minimum thickness of the fibrous cap is less than a predetermined threshold (<65 µm). Offline software QAgio XA7.3 (MEDIS Imaging System, Leiden, The Netherlands) was used to analyze digitally stored OFDI images.

Data are presented as values and % or median (interquartile range) in patient and leg characteristics and OFDI findings. For the location-level analysis (proximal, middle, distal SFA and popliteal artery), the generalized estimating equation (GEE) method was applied. Categorical data were tested by the GEE method using an ordinal logistic model with Fisher’s exact test. The factors associated with acute thrombus and healed plaque were evaluated by the multivariate logistic regression analysis using the GEE method. Variables with p <0.05 in the univariate logistic regression analysis using the GEE were entered into the multivariate logistic regression model. If clinically similar variables remained, we selected 1 variable that we considered to be more clinically relevant to avoid multicollinearity. Statistical analyses were conducted using JMP Pro version 16 and SPSS version 28. A 2-sided p <0.05 was considered statistically significant.

In this study, 54 legs from 44 patients were included ( Figure 3 ). The patient and leg characteristics are listed in Table 1 . Most patients had high-risk features such as diabetes mellitus (73%), coronary artery disease (59%), and hemodialysis (34%). Among 54 legs, 25 (46%) suffered from chronic limb-threatening ischemia.

Study flow chart. EVT = endovascular therapy; OFDI = optical frequency domain imaging.

OFDI data per leg is summarized in Table 2 . Acute thrombus was found in 41 of 54 legs (76%). Eruptive calcified nodules were the majority type (43%), followed by erosion (28%) and plaque rupture (13%). Forty-six legs (85%) showed healed plaque. Legs with both acute thrombus and healed plaque were 33 (61%), whereas there were no legs without acute thrombus or healed plaque ( Supplementary Figure 2 ). Multiple acute thrombus and healed plaque were found in 23 (43%) and 39 (72%), respectively ( Supplementary Figure 3 and Table 2 ). Medial and intimal calcification were detected in 34 (63%) and 52 (96%), respectively. Bone formation was found in the intima (22%) and media (4%). Lipid was detected in 33 (61%), and thin-capped fibroatheroma was not found. OFDI findings by locations are listed in Supplementary Table 1 . Bone formation and medial calcification were less frequently observed in popliteal arteries than in other locations.

Table 2

Optical frequency domain imaging findings

Legs	n = 54
Observed length, cm	33.0 (30.1-35.0)
Ballooning prior to imaging	13 (24.1)
Acute thrombus in all segement	41 (75.9)
Eruptive calcified nodule in all segement	23 (42.6)
Erosion in all segement	15 (27.8)
Plaque rupture in all segement	7 (13.0)
Healed plaque in all segement	46 (85.2)
Multiple acute thrombus in all segement	23 (42.6)
Multiple healed plaque in all segement	39 (72.2)
Medial calcification
Medial calcification	34 (63.0)
Medial calcification quadrant
0	20 (37.0)
1	6 (11.1)
2	9 (16.7)
3	6 (11.1)
4	13 (24.1)
Noneruptive calcified nodule	15 (27.8)
Bone in media	2 (3.7)
Intimal calcification
Intimal calcification	52 (96.3)
Intimal calcification quadrant
0	2 (3.7)
1	12 (22.2
2	15 (27.8)
3	13 (24.1)
4	12 (22.2)
Eruptive calcified nodule	27 (50.0)
Noneruptive calcified nodule	31 (57.4)
Bone in intima	12 (22.2)
Bone in media and intima	12 (22.2)
Lipid	33 (61.1)
Lipid quadrant
0	21 (38.9)
1	9 (16.7)
2	14 (25.9)
3	8 (14.8)
4	2 (3.7)
Thin-capped fibroathereoma	0 (0.0)
Cholesterol crystal	18 (33.3)
Machrophages	36 (66.7)
Microvessel	30 (55.6)
Culprit sites	n = 120
Causes of significant stenosis
Acute thrombus	58 (48.3)
Eruptive calcified nodule	38 (31.6)
Erosion	14 (11.7)
Plaque rupture	6 (5.0)
Healed plaque	55 (45.8)
Lipidic plaque	6 (5.0)
Calcified plaque	1 (0.8)

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