Angioscopic Findings of Stenosis Versus Occlusion in Femoropopliteal Artery Disease

Abstract

Background:

Despite the increase in the number of patients with peripheral artery disease (PAD), the pathophysiology is not fully elucidated. Recently, angioscopy with a 0.48-megapixel equivalent resolution camera became available for patients with PAD. We aimed to compare the plaque component between native stenosis and occlusion in the femoropopliteal artery using this modality.

Materials and Methods:

Thirty-two consecutive patients who underwent endovascular treatment for native femoropopliteal artery disease with angioscopy were studied. The major angioscopic classifications of each lesion were defined as follows: atheromatous plaque (AP) was defined as luminal narrowing without any protrusion, calcified nodule (CN) was defined as a protruding bump with surface irregularity, a mainly reddish thrombus was defined as organizing thrombus (OG), and organized thrombus (OD) was defined by more than half of the thrombus showing a whitish intima-like appearance.

Results:

A total of 34 lesions (stenosis, n=18; occlusion, n=16) from 32 patients were included. All stenotic lesions showed AP or CN (n=8 [44%], n=10 [56%], respectively), whereas all occluded lesions showed OG or OD (n=5 [31%], n=11 [69%], respectively), which amounted to a statistically significant difference (p<0.001). In occluded lesions, stiff wires (>3 g) were required to cross all lesions classified as OD, whereas this was not always necessary for lesions classified as OG (11 [100%] of 11, 1 [25%] of 5, respectively; p=0.04). Yellow color plaques were observed to a similar degree in all angioscopic classifications. Major adverse limb events, defined as amputation and any reintervention at 12 months, were highly variable, depending on the angioscopic findings, and tended to be more frequently observed in CN and OD (13% in AP, 40% in CN, 0% in OT, and 36% in OD, p=0.25).

Conclusion:

Angioscopy revealed varying components in stenosis and occlusion with different degrees of clinical impact. This may provide new information on the pathophysiology of PAD.

Keywords

angioscopy calcified nodule thrombus peripheral artery disease

Introduction

Lower extremity peripheral artery disease (PAD) is the third leading cause of atherosclerotic cardiovascular morbidity, following coronary artery disease (CAD) and stroke, the incidence rates of which are increasing worldwide as society ages concomitant with conventional risk factors such as hypertension (HT), diabetes mellitus (DM), dyslipidemia (DL), smoking, and chronic kidney disease (CKD).^1
–3 Based on the symptoms and disease severity, patients are generally treated with exercise therapy, medical therapy, endovascular therapy (EVT), or bypass surgery.² In the past decade, EVT has become more popular than bypass surgery as various interventional devices, including nitinol stents, drug-eluting stents, drug-coated balloons, and atherectomy devices, have been developed.^4,5

The femoropopliteal artery is the most frequent location within PAD requiring EVT, which sometimes demands complex procedures for lesions, including total occlusion.^6,7 Indeed, approximately 30% to 50% of femoropopliteal artery lesions showed total occlusion in a real-world EVT registry.^8
–10 In contrast, the prevalence of total occlusion in chronic coronary syndrome (CCS) from percutaneous coronary intervention (PCI) registry was reported to be 3% to 5%, and showed a considerable difference between PAD and CAD.^11
–13 A few pathological studies have explained this dissimilarity by demonstrating the presence of thrombi in approximately 75% of peripheral arteries with significant stenosis, two-thirds of which are suggested to be associated with remote embolic events.^14,15 However, there are almost no clinical data describing why or how more occlusion exists in PAD than in CAD.

Angioscopy, which can directly visualize thrombus, plaque, and the vessel wall, has made many advances in its development and usage over the past decades.¹⁶ Recently, the Zemporshe® angioscope (OVALIS, Osaka, Japan), which is equipped with a 0.48-megapixel equivalent resolution camera, has become available for the examination of PAD patients. This device was reported to clearly visualize the thrombus and neointima following stent implantation in several studies.^17
–20

Using high-resolution angioscopy, we compared the features of stenotic and occlusive lesions in patients with native femoropopliteal artery disease.

Materials and Methods

Patients

Between August 2018 and February 2020, 32 consecutive patients who underwent endovascular treatment for femoropopliteal arterial lesions with angioscopy were included. Cases with in-stent restenosis were not included. This study was approved by our institutional ethical committee.

Procedure for Angioscopy

Under local anesthesia, either a contralateral or ipsilateral approach through the common femoral artery was selected with 6-French normal guiding catheter (Destination®: Terumo, Tokyo, Japan). An occlusion balloon-tipped guiding catheter (Optimo®: Tokai Medical, Kasugai, Japan) was used when fast blood flow was anticipated. For angioscopic observation, a Zemporshe® angioscope (OVALIS, Osaka, Japan) with 0.48-megapixel equivalent resolution and full color (diameter 1.8 mm) was used in all cases. After the administration of unfractionated heparin (100 IU/kg) through the inserted guiding catheter, angioscopic observation was performed at the stenotic site or just proximal to the stenotic or occluded site in femoropopliteal arterial lesions. To clear blood during angioscopic examinations under angiographic guidance, a total of 20 to 80 mL of dextran was injected. The injection flow rate was manually adjusted depending on the visibility. Pre-ballooning was only performed when necessary. Multiple angioscopic observations (before and after ballooning or stenting) were performed if possible.

Lesion Assessment

Lesions were divided into stenotic and occlusive lesions with or without a microchannel structure based on the angiographic findings. The severity and complexity of the lesion was assessed based on the TransAtlantic Inter-Society Consensus (TASC) II classification.² The clinical presentation (claudication/chronic limb threatening ischemia), Fontaine classification, and Rutherford classification were also applied according to previous studies.^8
–10

Angioscopic Assessment

Based on the angioscopic findings prior to ballooning, femoropopliteal lesions were classified into 4 types (atheromatous plaque, calcified nodule, organizing thrombus, and organized thrombus).²¹ Atheromatous plaque was defined as luminal narrowing without any protrusion or thrombus, the surface color of which is usually a combination of white and yellow. Calcified nodule was defined as a protruding bump with surface irregularity. Organizing thrombus was defined as lesions predominantly composed of reddish thrombus. When more than half of the thrombus showed whitish intima-like appearance, it was classified as an organized thrombus. The maximum yellow color grade in each lesion was graded as follows: grade 0, white; grade 1, light yellow; grade 2, yellow; and grade 3, intensive yellow.²² All the classifications were performed by 2 experienced observers (K.T. and H.M.). The intraobserver and interobserver correlation coefficients were considerably high (0.97 and 0.95, respectively).

Treatment and Clinical Outcome

The treatment strategy for the procedure and medication was left to each operator. Wires to cross femoropopliteal lesions were basically escalated step-by-step from soft wire to stiff wire. The clinical outcome at 12 months, including restenosis and major adverse limb event (MALE), defined as amputation and any revascularization were also assessed. Angioscopic lesion classifications were compared between femoropopliteal arterial stenosis and occlusion. The relationship between angioscopic lesion classifications and the passed wire was also assessed. Based on the tip load, wires were classified as soft (≤1 g), intermediate (>1–3 g), and stiff wire (>3 g). The patients were clinically followed and duplex ultrasonography was evaluated at 12 months. Major adverse limb events were defined as minor and major amputation and any revascularization. Restenosis was defined as loss of patency with a peak systolic velocity ratio of ≥2.4.

Statistical Analyses

The normality of data was tested with the Shapiro-Wilk test. Continuous variables were expressed as the mean±standard deviation or median value [25th percentile–75th percentile], as appropriate, unless otherwise specified. Categorical variables were expressed as the number (percentage). Comparisons of continuous variables with normal distribution were tested by the Student t test. Comparisons of continuous variables with non-normal distribution were tested by the Wilcoxon test. Categorical variables were compared using the χ² or Fisher exact test. All statistical analyses were 2-tailed, and p values of <0.05 were considered to indicate statistical significance. All statistical analyses were performed using the JMP software program (Version 15; SAS Institute, Cary, North Carolina).

Results

A total of 34 femoropopliteal arterial lesions (stenosis, n=18; occlusion n=16) from 32 patients were included. The baseline patient characteristics are summarized in Table 1. Two patients had both stenosis and occlusion; their patient characteristics were included in the occlusion group. In this study population, hemodialysis was only found in 4 patients of the stenosis group. Accordingly, the creatinine level, estimated glomerular filtration rate, low-density lipoprotein (LDL) cholesterol level, and prevalence of CAD showed considerable differences. There were no marked differences in other factors, including the mean age, sex, hypertension, diabetes, dyslipidemia, smoking, atrial fibrillation, hemoglobin A1c (HbA1c) level, high-density lipoprotein (HDL) cholesterol level, triglyceride level, number of antiplatelet drugs, and anticoagulation therapy.

Table 1.

Patient Characteristics.

	Stenosis (n=16)	Occlusion (n=16)	p value
Age, years	78±7	74±9	0.11
Male, n (%)	11 (69)	8 (50)	0.47
Hypertension, n (%)	13 (81)	13 (81)	1.00
Diabetes, n (%)	9 (56)	10 (63)	1.00
Dyslipidemia, n (%)	14 (88)	11 (69)	0.39
Smoking, n (%)	14 (88)	10 (63)	0.22
Hemodialysis, n (%)	4 (25)	0	0.10
Coronary artery disease, n (%)	8 (50)	2 (13)	0.05
Atrial fibrillation, n (%)	2 (13)	1 (6)
Cre, mg/dl	1.0 (0.8–5.3)	0.8 (0.7–1.0)	0.03
eGFR, ml/min	50 (12–66)	65 (52–74)	0.03
HbA1c, %	6.2 (5.6–7.6)	7.4 (6.1–8.0)	0.18
LDL, mg/dL	91 (66–105)	108 (84–145)	0.06
HDL, mg/dL	52 (46–59)	49 (32–57)	0.25
TG, mg/d:	112 (83–155)	128 (87–184)	0.53
No. of antiplatelet drug, n (%)			1.00
1	1 (6)	2 (13)
2	15 (94)	14 (88)
Anticoagulation therapy, n (%)	3 (19)	1 (6)	0.60

Abbreviations: Cre, creatinine; eGFR, estimated glomerular filtration rate; HbA1c, hemoglobin A1c; HDL, high-density lipoprotein cholesterol level; LDL, low-density lipoprotein cholesterol level; TG, triglyceride.

The lesion characteristics are shown in Table 2. There were no significant differences in clinical presentation, lesion length, Fontaine classification, or Rutherford classification. In the occlusion group, the TASC classification was significantly worse, and stenting was selected more frequently. Two-thirds of cases in which plain old ballooning (POBA) was performed included a scoring balloon (stenosis, 4 of 6; occlusion, 1 of 3). Angiography revealed a microchannel structure in 3 (18%) occluded lesions. There were no differences in the rate of restenosis (stenosis vs occlusion: 17% vs 19%; p=1.00) or MALE (stenosis vs occlusion: 28% vs 25%; p=1.00) although both rates were substantially high.

Table 2.

Lesion Characteristics.

	Stenosis (n=18)	Occlusion (n=16)	p value
Clinical presentation, n (%)			1.00
Claudication	14 (78)	13 (81)
Chronic limb threatening ischemia	4 (22)	3 (19)
Lesion length, mm	45 (10–78)	105 (60–135)	0.01
Angiographical channel, n (%)	NA	3 (19)
TASC, n (%)			<0.01
A	12 (67)	1 (6)
B	4 (22)	11 (69)
C	2 (11)	3 (19)
D	0	1 (6)
Fontaine, n (%)			0.55
1	0	0
2	14 (78)	12 (75)
3	0	1 (6)
4	4 (22)	3 (19)
Rutherford, n (%)			0.31
1	0	0
2	8 (44)	10 (63)
3	6 (33)	2 (13)
4	0	1 (6)
5	4 (22)	2 (13)
6	0	1 (6)
Treatment, n (%)
POBA	6 (33)	3 (19)	0.01
DCB	11 (61)	4 (25)
BMS	0	1 (6)
DES	1 (6)	8 (50)
Clinical outcome at 12 months (%)
Restenosis	3 (17)	3 (19)	1.00
MALE	5 (28)	4 (25)	1.00

Abbreviations: BMS, bare metal stent; DCB, drug-coated balloon; DES, drug-eluting stent; MALE, major adverse limb event; POBA, plain old ballooning; TASC, TransAtlantic Inter-Society Consensus.

Figure 1A–D shows representative images of the angioscopic findings, and video images are available in the online Supplemental Video 1A–D. Atheromatous plaque is shown in Figure 1A, which was characterized by luminal narrowing with a continuous intima, without any protrusion or thrombus. The surface color of the intima is usually a combination of white and yellow. A calcified nodule is shown in Figure 1B, which was characterized by irregular bump mimicking coral reef or cauliflower. These findings were often observed in angiographically calcified lesions. Organizing thrombus is shown in Figure 1C, which was characterized by reddish thrombus. Organized thrombus is shown in Figure 1D, which was characterized by thrombus with mixed coloration.

Each lesion was classified, according to the predominant angioscopic findings, as stenotic or occluded (Figure 2). Among the 18 stenotic lesions, calcified nodules were the most frequent angioscopic finding (n=10, 56%), followed by atheromatous plaque (n=8, 44%). Among 4 hemodialysis patients, 1 showed a calcified nodule, whereas 3 showed atheromatous plaque. In the 16 occluded lesions, all lesions showed organizing (n=5, 31%) or organized (n=11, 69%) thrombus. There were marked differences in the angioscopic findings of stenotic lesions and occluded lesions (p<0.001). There was no marked difference in the maximum yellow color grade (Figure 3); however, calcified nodules showed a relatively lower yellow color grade (median value [interquartile range]: atheromatous plaque 2 [1.3–2.8], calcified nodule 1 [1–2], organizing thrombus 2 [1–2], and organized thrombus 2 [1–2], p=0.35). The lesion length was 28 mm in atheromatous plaque, 60 mm in calcified nodule, 120 mm in organizing thrombus, and 100 mm in organized thrombus (p=0.07). Restenosis was observed in 30% of calcified nodules (3 of 10) and 27% of organized thrombi (3 of 11; p=0.21). Major adverse limb events at 12 months were observed in 40% of calcified nodules (4 of 10), 36% of organized thrombi (4 of 11), and 13% of atheromatous plaques (1 of 8) (p=0.25).

The relationship between the passed wire and the angioscopic findings was assessed (Table 3). The 19 stenotic lesions were easily crossed with a soft wire, regardless of the angioscopic findings. Stiff wire was needed to cross all lesions with organized thrombus without a microchannel structure, whereas it was not needed to cross an organizing thrombus without a microchannel structure. In both organizing and organized thrombus, the angiographic channel led to easier passing by a soft wire. The passed wires showed significant variability in stenotic and occluded lesions, which was partially associated with the angioscopic findings (p<0.001).

Table 3.

Angioscopic Finding and Passed Wire.

	Passed wire
	Soft (≦1 g)	Intermediate (1g<, ≦3g)	Stiff (3g<)
Stenosis (total number=18)
Atheromatous plaque (n=8)	8	0	0
Calcified nodule (n=10)	10	0	0
Occlusion (total number=16)
Organizing thrombus (n=4)	2	1	1
Organizing thrombus with channel (n=1)	1	0	0
Organized thrombus (n=9)	0	0	10
Organized thrombus with channel (n=2)	2	0	0
p value	p<0.0001

In this study population, angioscopy-related complications, including vessel dissection and perforation, were not observed. Similarly, dextran did not induce volume overload or unexpected bleeding.

Discussion

The major finding of this study was as follows. In stenotic lesions, the most frequent angioscopic finding was calcified nodule, followed by atheromatous plaque. On the contrary, all occluded lesions exhibited organizing or organized thrombus. Regarding wire crossing, in the absence of a microchannel structure on angiography, an organizing thrombus required a less stiff wire in comparison with organized thrombus. The maximal yellow color grade and the rates of restenosis and MALE varied according to the angioscopic findings.

One of the most surprising findings of our study was that calcified nodules were the most frequent type of stenotic lesion. The vascular lumen was highly constricted by calcified nodules, but not occluded. Calcified nodules are traditionally considered a rare cause of thrombosis in acute coronary syndrome (ACS).²¹ Pathologically, plaque rupture (60%–70%) is the most common cause of acute local thrombosis, followed by plaque erosion (20%–30%) and calcified nodule (5%) in ACS, whereas the main lesions of CCS were fibrous, fibroatheroma, or fibrocalcific plaque with or without nodular calcification.²¹ This has been confirmed by coronary imaging studies using optical coherence tomography (OCT).^23,24 Lee et al also showed that 54% of calcified nodules presented as stable angina.²⁵ Thus, calcified nodules can cause both ACS and CCS in CAD. In PAD, a few reports mentioned calcified nodules.^26,27 However, the recognition of calcified nodules in PAD is probably low because intravascular imaging is less frequently used in PAD and intravascular ultrasound, which is the most major intravascular imaging device in PAD, but not the best tool for identifying calcified nodules.^28,29 Optical coherence tomography is likely to be superior to intravascular ultrasound (IVUS); however, angioscopy may provide a clearer, more detailed view of the morphology and surface properties as calcified nodules mimicked red thrombus on OCT.^28
–30 Torii et al reported that the plaque type was classified as calcified nodule in a substantial number of cases of femoropopliteal disease.²⁷ Horimatsu et al also reported that 29% of patients with PAD had a calcified nodule that was evenly distributed throughout the length of the artery.³¹ Calcified nodules are believed to be associated with tortuous location represented by the middle of the right coronary artery.^21,25 The femoropopliteal artery is also a representative tortious artery with frequent bending motions. Therefore, the high frequency of calcified nodules, which were identified in stenotic lesions in our data, seems to be a reasonable finding.

In our study, pathologically, atheromatous plaque could be either fibroatheroma or fibrocalcific plaque.²¹ Fibrocalcific plaque is basically a more advanced plaque than fibroatheroma; however, fibroatheroma and fibrocalcific plaque sometimes overlap.^21,32 In contrast to other intravascular imaging modalities, underlying calcification is not clear on angioscopy. Thus, it may be difficult to separate fibroatheroma and fibrocalcific plaque by angioscopy. The yellow color grade has been used to assess lipids by angioscopy.³³ In our study, yellow plaque was frequently observed, not only in atheromatous plaque but also near organized or organizing thrombus lesions, whereas the frequency was not as high in calcified nodules. However, after ballooning, yellow material, which was suggested to be the lipid core, was often expressed in atheromatous plaque although it was not always easy to visualize after the procedure.

In occluded lesions, the underlying etiology of thrombosis, such as plaque rupture, erosion, or calcified nodule, was not distinguishable due to the presence of thrombus, which narrows the visual field of angioscopy.²¹ If remote thrombotic events from the upper stream cause occlusion, it is also difficult to determine the etiology using any intravascular imaging device.^15,27 Our study showed how occlusion and stenosis differ in femoropopliteal lesions, but it was not able to show why the rate of occlusion in PAD was higher than that in CAD. To address the latter question would be beyond the ability of our study. This may be due to differences in the anatomical scale and the clinical feature of a considerable proportion of patients being asymptomatic.³⁴ Peripheral artery disease often remains unrecognized and underdiagnosed as general physicians and patients are unaware of its clinical manifestations, including impaired walking, classic intermittent claudication, and critical limb ischemia; furthermore, the associated adverse cardiovascular events and limb outcomes are also not widely recognized.³⁴ According to the Edinburgh Artery Study, among patients with an ankle brachial index of ≤0.90, only 15% reported classic intermittent claudication, whereas 35% reported no exertional leg symptoms.³⁵ Thus, for occlusive lesions, the time from the thrombotic event to the diagnosis may contribute to the different features between CAD and PAD.

Angioscopy provides forward observation of the vessel, whereas other intravascular imaging modalities provide a side view. This feature of angioscopy was beneficial for differentiating organizing thrombus and organized thrombus before wire crossing. Total occlusion can be divided into short duration or long duration, based on the presence or absence of fibrin.³⁶ Conceptually, the thrombus shifts from organizing to organized over time, making the lesion harder.³⁶ Accordingly, in cases involving organizing thrombus with abundant relatively fresh red thrombus, it was easy to pass a soft wire through the lesion, whereas organized thrombus required a stiff wire. Angioscopy finding was helpful to make decisions in occluded lesions for wire step-up, which resulted in the difference in passed wire for organized thrombus without angiographical channel. Other intravascular imaging may be helpful for understanding whether the wire is within the true lumen or not during the procedure for total occlusion.³⁷ However, predicting the hardness of total occlusion would be difficult, using other intravascular imaging modalities. Forward observation by high-resolution angioscopy was likely to be beneficial to recognized calcified nodules, as recognizing calcified nodule in other intravascular imaging is not straightforward.²⁸ As calcified nodule can lead to stent underexpansion, DCB tended to be selected for cases with calcified nodule lesions in our population.²⁹ Unfortunately, angioscopy cannot be used to measure the vessel size, which is easily accomplished with other intravascular imaging modalities; this is a major shortcoming of this approach. Thus, when assessing atheromatous plaques, other intravascular imaging modalities can provide more information, including the nature and size of the plaque, whereas angioscopy can only demonstrate the surface color.

In this small study, the clinical outcome at 12 months was highly variable, with calcified nodules and organized thrombus tending to be associated with worse outcomes. Previously, Kobayashi et al reported that calcified nodules showed the worst clinical outcome in ACS of CAD, which was consistent with the findings of our study.³⁸ Total occlusion in femoropopliteal lesions has been reported to be associated with worse outcomes.³⁹ In our study, we separated organizing thrombus and organized thrombus. An interventional approach at the stage of organized thrombus may require a more complex procedure in comparison with the stage of organizing thrombus, as the stage is likely to be more advanced.

Limitations

This study was associated with several limitations. Our study was performed in a single center with a relatively small number of patients. Although angioscopic observation was performed by multiple experienced observers, these observations could still be subjective. Our study focused on symptomatic patients; cases of early stage disease may have different characteristics. For these reasons, our results may not be applicable to all patients. However, this type of assessment has never been performed by angioscopy. We therefore believe that our study is significant.

Conclusion

Using angioscopy, stenotic lesions showed calcified nodules and atheromatous plaque, whereas occluded lesions showed organizing and organized thrombus, suggesting an association with the duration or hardness of occlusion. These results may provide new information on the pathophysiology of PAD. Further studies with a larger study population are needed.

Supplemental Material

sj-docx-1-jet-10.1177_15266028221079759 – Supplemental material for Angioscopic Findings of Stenosis Versus Occlusion in Femoropopliteal Artery Disease

Supplemental material, sj-docx-1-jet-10.1177_15266028221079759 for Angioscopic Findings of Stenosis Versus Occlusion in Femoropopliteal Artery Disease by Kazuma Tashiro, Hiroyoshi Mori, Takahiro Tezuka, Ayumu Omura, Daisuke Wada, Hiromoto Sone, Yosuke Takei, Masahiro Sasai, Tokutada Sato and Hiroshi Suzuki in Journal of Endovascular Therapy

Footnotes

Author’s Note

Hiroshi Suzuki is now affiliated to Showa University Fujigaoka Hospital, Yokohama, Japan.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Hiroyoshi Mori

Supplemental Material

Supplemental material for this article is available online.

References

Fowkes

FGR

Rudan

, et al. Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis. Lancet. 2013;382(9901):1329–1340. doi:10.1016/S0140-6736(13)61249-0.

Norgren

Hiatt

Dormandy

, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg. 2007;45(suppl 1):S5–S67. doi:10.1016/j.jvs.2006.12.037.

Usui

Ninomiya

Nagata

, et al. Albuminuria as a risk factor for peripheral arterial disease in a general population: the Hisayama study. J Atheroscler Thromb. 2011;18(8):705–712. doi:10.5551/jat.7682.

Wright

Steffens

Huilgol

RL.

Vascular surgery trends in Australia: 2001–2015: less open surgery, less limb loss and more endovascular intervention. ANZ J Surg. 2019;89(4):309–313. doi:10.1111/ans.14878.

Wendt

Kristiansen

Krohg-Sørensen

, et al. Norwegian trends in numbers of lower extremity revascularisations and amputations including regional trends in endovascular treatments for peripheral arterial disease: a retrospective cross-sectional registry study from 2001 to 2014. BMJ Open. 2017;7(11):e016210. doi:10.1136/bmjopen-2017-016210.

Higashitani

Uemura

, et al. Clinical outcome and diverse risk factors for different therapeutic target locations of peripheral artery disease. J Atheroscler Thromb. 2020;27(8):769–779. doi:10.5551/jat.52647.

Katsuki

Yamaji

Hiramori

, et al. Ten-year clinical outcomes for patients undergoing lower extremity endovascular interventions. J Vasc Surg. 2020;72(5):1626–1635.e3. doi:10.1016/j.jvs.2020.02.026.

Iida

Takahara

Soga

, et al. Shared and differential factors influencing restenosis following endovascular therapy between TASC (Trans-Atlantic Inter-Society Consensus) II Class A to C and D lesions in the femoropopliteal artery. JACC Cardiovasc Interv. 2014;7(7):792–798. doi:10.1016/j.jcin.2014.01.168.

Okuno

Iida

Shiraki

, et al. Impact of calcification on clinical outcomes after endovascular therapy for superficial femoral artery disease. J Endovasc Ther. 2016;23(5):731–737. doi:10.1177/1526602816656612.

10.

Ishihara

Iida

Okamoto

, et al. Potential mechanisms of in-stent occlusion in the femoropopliteal artery: an angioscopic assessment. Cardiovasc Interv Ther. 2017;32(4):313–317. doi:10.1007/s12928-016-0411-3.

11.

Nairooz

Parzynski

Curtis

, et al. Contemporary trends, predictors and outcomes of perforation during percutaneous coronary intervention (from the NCDR Cath PCI Registry). Am J Cardiol. 2020;130:37–45. doi:10.1016/j.amjcard.2020.06.014.

12.

Tadano

Kotani

J-I

Kashima

, et al. Predictors of clinical outcomes after coronary implantation of bioresorbable polymer sirolimus-eluting Ultimaster stents in all-comers: a report of 1,727 cases. Catheter Cardiovasc Interv. 2019;94(1):91–97. doi:10.1002/ccd.28076.

13.

Othman

Seth

Zein

, et al. Percutaneous coronary intervention for chronic total occlusion—The Michigan experience: insights from the BMC2 Registry. JACC Cardiovasc Interv. 2020;13(11):1357–1368. doi:10.1016/j.jcin.2020.02.025.

14.

Narula

Dannenberg

Olin

, et al. Pathology of peripheral artery disease in patients with critical limb ischemia. J Am Coll Cardiol. 2018;72(18):2152–2163. doi:10.1016/j.jacc.2018.08.002.

15.

Narula

Olin

Narula

Pathologic disparities between peripheral artery disease and coronary artery disease. Arterioscler Thromb Vasc Biol. 2020;40(9):1982–1989. doi:10.1161/ATVBAHA.119.312864.

16.

Litvack

Grundfest

Lee

, et al. Angioscopic visualization of blood vessel interior in animals and humans. Clin Cardiol. 1985;8(2):65–70. doi:10.1002/clc.4960080202.

17.

Hoyano

Ozaki

Nishida

, et al. High-resolution angioscopy of endoluminal stent graft at 6 months after implantation. Circ J. 2019;83(9):1970. doi:10.1253/circj.CJ-18-1229.

18.

Ihara

Nojima

Adachi

, et al. Paclitaxel particle distribution 3 months after drug-coated balloon treatment-zemporshe ® angioscopy assessment. Circ Rep. 2020;2:135–136. doi:10.1253/circrep.CR-19-0133.

19.

Nishimoto

Fukuhara

Miyamoto

, et al. Edge restenosis of a polytetrafluoroethylene-covered stent in the superficial femoral artery: insights from an imaging assessment with an electronic high-resolution angioscope. Cardiovasc Interv Ther. 2020;35(1):98–100. doi:10.1007/s12928-019-00583-z.

20.

Tsujimura

Ishihara

Iida

, et al. Angioscopic assessments at 3 months after fluoropolymer-based paclitaxel-eluting stent implantation for femoropopliteal endovascular intervention. Circ J. 2020;84(11):1999–2005. doi:10.1253/circj.CJ-20-0551.

21.

Virmani

Kolodgie

Burke

, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20(5):1262–1275. doi:10.1161/01.ATV.20.5.1262.

22.

Ueda

Asakura

Yamaguchi

, et al. The healing process of infarct-related plaques: insights from 18 months of serial angioscopic follow-up. J Am Coll Cardiol. 2001;38(7):1916–1922. doi:10.1016/S0735-1097(01)01673-4.

23.

Araki

Soeda

Kim

, et al. Spatial distribution of vulnerable plaques: comprehensive in vivo coronary plaque mapping. JACC Cardiovasc Imaging. 2020;13(9):1989–1999. doi:10.1016/j.jcmg.2020.01.013.

24.

Sugiyama

Yamamoto

Fracassi

, et al. Calcified plaques in patients with acute coronary syndromes. JACC Cardiovasc Interv. 2019;12(6):531–540. doi:10.1016/j.jcin.2018.12.013.

25.

Lee

Mintz

Matsumura

, et al. Prevalence, predictors, and clinical presentation of a calcified nodule as assessed by optical coherence tomography. JACC Cardiovasc Imaging. 2017;10(8):883–891. doi:10.1016/j.jcmg.2017.05.013.

26.

Shimada

Goto

Kubo

, et al. Calcified nodules projecting into the popliteal artery successfully treated through the use of myocardial biopsy forceps. Int Heart J. 2018;59(3):660–663. doi:10.1536/ihj.17-216.

27.

Torii

Mustapha

Narula

, et al. Histopathologic characterization of peripheral arteries in subjects with abundant risk factors: correlating imaging with pathology. JACC Cardiovasc Imaging. 2019;12(8 pt 1):1501–1513. doi:10.1016/j.jcmg.2018.08.039.

28.

Hao

Fujii

Shibuya

, et al. Different findings in a calcified nodule between histology and intravascular imaging such as intravascular ultrasound, optical coherence tomography, and coronary angioscopy. JACC Cardiovasc Interv. 2014;7(8):937–938. doi:10.1016/j.jcin.2013.12.212.

29.

Kawakami

Hao

Takagi

, et al. Drug-eluting stent implantation on calcified nodule: ex vivo intravascular images and histopathology. JACC Cardiovasc Interv. 2015;8(8):e127–e128. doi:10.1016/j.jcin.2015.02.024.

30.

Umemoto

Nakagama

Lee

, et al. Calcified nodule observed on coronary angioscopy. Circ J. 2019;83(10):2083. doi:10.1253/circj.CJ-19-0203.

31.

Horimatsu

Fujii

Fukunaga

, et al. The distribution of calcified nodule and plaque rupture in patients with peripheral artery disease: an intravascular ultrasound analysis. Heart Vessels. 2017;32(10):1161–1168. doi:10.1007/s00380-017-0984-5.

32.

Mori

Torii

Kutyna

, et al. Coronary artery calcification and its progression: what does it really mean? JACC Cardiovasc Imaging. 2018;11(1):127–142. doi:10.1016/j.jcmg.2017.10.012.

33.

Omatsu

Sotomi

Kobayashi

, et al. Quantitative validation of the coronary angioscopic yellow plaque with lipid core burden index assessed by intracoronary near-infrared spectroscopy [published online ahead of print January 22, 2021]. J Atheroscler Thromb. doi:10.5551/jat.60566.

34.

Campia

Gerhard-Herman

Piazza

, et al. Peripheral artery disease: past, present, and future. Am J Med. 2019;132(10):1133–1141. doi:10.1016/j.amjmed.2019.04.043.

35.

Fowkes

FGR

Housley

Cawood

, et al. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol. 1991;20(2):384–392. doi:10.1093/ije/20.2.384.

36.

Sakakura

Nakano

Otsuka

, et al. Comparison of pathology of chronic total occlusion with and without coronary artery bypass graft. Eur Heart J. 2014;35(25):1683–1693. doi:10.1093/eurheartj/eht422.

37.

Tsubakimoto

Isodono

Fujimoto

, et al. IVUS-guided wiring improves the clinical outcomes of angioplasty for long femoropopliteal CTO compared with the conventional intraluminal approach. J Atheroscler Thromb. 2021;28:365–374. doi:10.5551/jat.57166.

38.

Kobayashi

Takano

Tsurumi

, et al. Features and outcomes of patients with calcified nodules at culprit lesions of acute coronary syndrome: an optical coherence tomography study. Cardiology. 2018;139(2):90–100. doi:10.1159/000481931.

39.

Chae

Yoon

, et al. Differential efficacy between stenting and plain balloon angioplasty for femoropopliteal disease with or without total occlusion. Korean J Intern Med. 2020;35(5):1114–1124. doi:10.3904/kjim.2019.039.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.01 MB

0.08 MB