Abstract
Background
Saphenous vein graft (SVG) lesions occurring in the chronic phase after coronary artery bypass graft (CABG) surgery are typically characterized by friable atherosclerotic plaques, whereas stenosis due to calcified nodules (CNs) is rare. Intravascular lithotripsy (IVL) is an effective treatment for severely calcified coronary artery lesions, but its application in SVG lesions remains limited.
Case summary
An 84-year-old man with a history of two prior CABG procedures was referred to our hospital with angina pectoris. Coronary angiography revealed severe stenosis in the proximal segment of the SVG to the left anterior descending artery. Intravascular ultrasound demonstrated that a large CN was responsible for severe stenosis at the lesion site. Initial treatment consisted of drug-coated balloon (DCB) therapy following predilatation with a cutting balloon. Because restenosis occurred 9 months later, repeat DCB therapy following more aggressive lesion preparation with high-pressure non-compliant balloon dilatation was performed. Despite repeated DCB treatments, angiographic restenosis recurred 17 months after the initial intervention. Optical coherence tomography (OCT) confirmed a persistent CN, and IVL was performed using a 3.0 × 12 mm ‘Shockwave’ IVL balloon to modify the CN, followed by scoring balloon dilatation and implantation of a 3.5 × 28 mm drug-eluting stent. Final OCT demonstrated improved lumen expansion compared with previous interventions, with a favourable procedural outcome.
Discussion
This case highlights the rarity of CNs in SVG lesions and suggests that IVL may be a reasonable treatment option for CNs in this setting.
Keywords: Calcified nodule, Case report, Saphenous vein graft, Intravascular lithotripsy, Percutaneous coronary intervention
Learning points.
Calcified nodules rarely develop in saphenous vein graft lesions and may cause recurrent restenosis.
Intravascular lithotripsy can be an effective treatment option for calcified nodules, even in SVG lesions.
Introduction
Saphenous vein graft (SVG) disease remains a major cause of late adverse events following coronary artery bypass graft (CABG) surgery. SVG lesions are typically composed of friable atherosclerotic plaques with a high risk of distal embolization, whereas heavily calcified lesions are uncommon.1 Calcified nodules (CNs), a distinct subtype of calcified atherosclerotic plaque, have been reported predominantly in native coronary arteries and are associated with stent underexpansion and restenosis.2
Intravascular lithotripsy (IVL) has recently emerged as a therapeutic modality to modify severely calcified lesions and improve stent expansion.3 However, there are few reports describing the use of IVL for CNs in SVG lesions. Here, we report a case of recurrent restenosis due to a CN in an SVG lesion, which was ultimately treated with IVL-assisted percutaneous coronary intervention (PCI).
Summary figure
Case presentation
An 84-year-old man with a history of CABG surgery at the age of 49 years [SVG to the right coronary artery (RCA), SVG to the left anterior descending artery (LAD), and SVG to the diagonal branch (Dg)] and redo-CABG at the age of 69 years [left internal thoracic artery (LITA) to Dg] was referred to our hospital because of worsening effort angina. There were no abnormal findings on physical examination. Cardiovascular risk factors included hypertension and hyperlipidaemia.
Coronary angiography demonstrated chronic total occlusion in the proximal segment of the RCA and the left main trunk (Figure 1A and B), patency of both LITA–Dg and SVG–RCA (Figure 1C and D), and severe stenosis with calcification in the proximal segment of the SVG to the LAD (Figure 1E, Video 1).
Figure 1.
Initial coronary angiography. Initial coronary angiography showed chronic total occlusion in the proximal segment of the right coronary artery and the left main trunk (arrow and arrowhead in A and B). The left internal thoracic artery to the diagonal branch and the saphenous vein graft (SVG) to the right coronary artery were patent (C and D). Severe stenosis with calcification was observed in the proximal segment of the SVG to the left anterior descending artery (arrow in E).
Intravascular ultrasound (IVUS) revealed severe luminal narrowing caused by protrusion of a CN (Figure 2A–D, Video 2).
Figure 2.
Intravascular ultrasound (IVUS) findings and initial intervention. (A) Angiographic localization of the lesion with corresponding IVUS cross-sections (B–D). IVUS revealed calcified nodules protruding into the vessel lumen and causing severe luminal narrowing (arrowheads in B–D). The lesion was treated with predilatation using a cutting balloon (E), followed by drug-coated balloon angioplasty (F). Final angiography after the initial intervention confirmed acceptable lesion dilatation without flow limitation (G). Recurrent restenosis was observed 17 months after the initial percutaneous coronary intervention (H).
The lesion was initially treated with 3.5 × 15 mm cutting balloon angioplasty at 12 atm (Figure 2E), followed by 3.0 × 15 mm paclitaxel-coated drug-coated balloon (DCB) therapy (Figure 2F). Angiographic results were acceptable, without flow limitation (Figure 2G, Video 3). However, follow-up coronary angiography at 9 months demonstrated significant restenosis at the treated SVG. At that time, IVL was not yet available at our institution. In addition, rotational or orbital atherectomy was considered less favourable because of the potential risk of distal embolization in an SVG lesion. Given concerns about recurrent failure after drug-eluting stent (DES) implantation in CN lesions, we selected a more aggressive lesion-preparation strategy using a non-compliant (NC) balloon inflated at a higher pressure than during the initial PCI. After 3.25 × 15 mm NC balloon angioplasty at 23 atm, repeat DCB therapy was performed. Final IVUS demonstrated an increased minimal lumen area (MLA) compared with that after the initial PCI (see Supplementary material online, Figure S1A and B).
Despite these interventions, follow-up angiography performed due to recurrent angina 17 months after the initial PCI revealed recurrent restenosis (Figure 2H). Optical coherence tomography (OCT) again demonstrated protrusion of a CN within the lesion (Figure 3A–D, Video 4). Considering that the lesion was refractory to conventional predilatation with NC or cutting balloons and a DCB-based strategy, and given the potential risk of distal embolization associated with debulking devices such as rotational or orbital atherectomy, IVL was selected. In total, 80 pulses were delivered using a 3.0 × 12 mm ‘Shockwave’ IVL balloon (Figure 3E). Post-IVL OCT showed the presence of cracks on the calcium surface (Figure 3F–H). Additional lesion preparation was then performed using a 3.5 × 15 mm scoring balloon at 24 atm. Subsequent OCT imaging demonstrated a larger MLA than that observed on the final IVUS examinations during the initial and second PCI procedures (see Supplementary material online, Figure S1C). Finally, a 3.5 × 28 mm DES was implanted (Figure 4A), with satisfactory angiographic and OCT results (Figure 4B, Video 5). No periprocedural complications occurred. At 6 months after the procedure, the patient remained free from recurrent angina.
Figure 3.
Optical coherence tomography (OCT) and intravascular lithotripsy. (A) Angiographic localization of the lesion with corresponding OCT cross-sections (B–D). OCT demonstrated recurrent protrusion of a calcified nodule into the vessel lumen, resulting in restenosis (arrowheads in B–D). Intravascular lithotripsy (IVL) was performed using a 3.0 mm Shockwave IVL balloon (E). Post-IVL OCT revealed cracks in the calcium surface, indicating effective calcium modification (arrows in F–H; F–H are identical cross-sections to B–D).
Figure 4.
Final angiographic result. A 3.5 × 28 mm drug-eluting stent was implanted in the saphenous vein graft lesion (A). Final angiography showed a satisfactory result (B).
Discussion
CNs are rare in SVG lesions because these lesions typically consist of friable atherosclerotic plaques that are prone to distal embolization. Because the presence of a CN is associated with recurrent restenosis, as observed in this case, SVG lesions with a CN may require a different treatment strategy from more typical SVG lesions.
In this patient, a strategy of predilatation with NC or cutting balloons followed by DCB therapy failed to achieve durable results. Previous studies have reported that treatment of CNs with a DES is associated with a high risk of major adverse cardiac events due to repeat reintervention caused by re-protrusion of calcified masses through stent struts, as well as stent thrombosis resulting from stent underexpansion or malapposition.4,5 Therefore, DCB therapy has been explored as an alternative strategy for CNs. However, clinical outcomes of DCB therapy for CNs have remained suboptimal.6 This may be attributable to insufficient plaque preparation. IVL-assisted PCI for CNs has been reported to achieve stent expansion comparable to that observed in non-CN lesions, suggesting that IVL may serve as an effective lesion preparation modality for CNs in SVGs.7
Although evidence supporting DCB use in SVG lesions remains limited, a small retrospective study reported comparable short-term outcomes between DCB and DES in de novo SVG lesions.8 SVG atherosclerosis develops through progressive arterialization of the vein graft under systemic arterial pressure, with vascular smooth muscle cell proliferation contributing to neointimal hyperplasia.1 Therefore, antiproliferative drug delivery by DCB may have a mechanistic rationale in SVG lesions.
It is important to confirm optimal lumen expansion by intravascular imaging both after adequate lesion preparation and after final device treatment. In this case, OCT imaging after IVL treatment and subsequent high-pressure dilatation with a scoring balloon revealed a larger MLA than on the final IVUS examinations during the first and second PCI procedures, suggesting that adequate lesion preparation may contribute to improved procedural outcomes.
Although debulking devices such as rotational or orbital atherectomy are established treatment options for calcified lesions, their use in SVG lesions should be approached with caution due to the risk of distal embolization.
CNs in SVG lesions have rarely been reported, and evidence regarding the optimal treatment strategy remains limited. Given that IVL is an established calcium-modification technique for CNs in native coronary arteries, it may also represent a reasonable therapeutic option for SVG lesions when intravascular imaging identifies a CN.
Conclusion
This case illustrates that CNs, although rare, can occur in SVG lesions and cause recurrent restenosis. IVL may be an effective treatment strategy for CNs in SVG lesions.
Supplementary Material
Acknowledgements
None.
Contributor Information
Daisuke Irie, Department of Cardiovascular Division, Ijinkai Takeda General Hospital, 28-1 Ishidamoriminamicho, Kyotoshi Fushimi-ku, Kyoto 601-1495, Japan.
Hibiki Iwakoshi, Department of Cardiovascular Division, Ijinkai Takeda General Hospital, 28-1 Ishidamoriminamicho, Kyotoshi Fushimi-ku, Kyoto 601-1495, Japan.
Atsushi Hosokawa, Department of Cardiovascular Division, Ijinkai Takeda General Hospital, 28-1 Ishidamoriminamicho, Kyotoshi Fushimi-ku, Kyoto 601-1495, Japan.
Yoshio Sasaki, Department of Cardiovascular Division, Ijinkai Takeda General Hospital, 28-1 Ishidamoriminamicho, Kyotoshi Fushimi-ku, Kyoto 601-1495, Japan.
Ryoji Kitamura, Department of Cardiovascular Division, Ijinkai Takeda General Hospital, 28-1 Ishidamoriminamicho, Kyotoshi Fushimi-ku, Kyoto 601-1495, Japan.
Lead author biography
Daisuke Irie is an interventional cardiologist at Ijinkai Takeda General Hospital. His clinical interests include PCI, heart failure, and echocardiography. He graduated from Kyoto Prefectural University of Medicine, where he obtained his PhD for research on perivascular adipose tissue and atherosclerosis. His research interests focus on coronary intervention and heart failure.
Supplementary material
Supplementary material is available at European Heart Journal – Case Reports online.
Author contributions
Daisuke Irie (Writing—original draft, Writing—review & editing [lead]), Hibiki Iwakoshi (Validation [supporting]), Atsushi Hosokawa (Validation [supporting]), Yoshio Sasaki (Validation [supporting]), and Ryoji Kitamura (Validation [supporting])
Consent: The authors confirm that written consent for submission and publication of this case report has been obtained from the patient in line with COPE guidance.
Funding
No funding was received for this manuscript.
Data availability
The data underlying this article are available in the article and in its online Supplementary material.
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Associated Data
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Supplementary Materials
Data Availability Statement
The data underlying this article are available in the article and in its online Supplementary material.





