Covered stent implantation for calcified nodule to physically hinder its protrusion causing restenosis: a case report

Introduction

Background

Calcified nodule (CN) is a phenotypic feature of calcified plaques which cause acute coronary syndrome (ACS). Despite the use of newer-generation drug-eluting stent (DES), ACS patients attributable to CN have been shown to present an increased risk of target lesion revascularization (TLR) after percutaneous coronary intervention (PCI) (Table 1) (1-6). Sugane et al. reported that the presence of CN was associated with a 7.9-fold greater likelihood of experiencing TLR in ACS patients receiving newer-generation DES (3). Of note, the recurrence of ACS due to in-stent restenosis (ISR) at CN lesion more likely occurred within 12 months after the implantation of newer-generation DES.

Rationale and knowledge gap

Calcified lesions more likely hinder stent expansion, which worsens cardiovascular outcomes after PCI. Debulking devices have been used to modify calcific tissues for achieving optimal acute gain. One observational study investigated the efficacy of rotational atherectomy on TLR rate in patients exhibiting CN. In this study, modification of CN with rotational atherectomy did not reduce TLR rate compared to PCI without rotational atherectomy (2). Mechanistically, pathological and intravascular imaging studies reported the re-protruding nodules of calcification as a potential mechanism causing ISR after DES implantation (7,8). These observations suggest the need for another therapeutic approach to prevent this dynamic protrusion of calcification tissue through struts of an implanted stent. The covered stent has been developed to seal coronary artery perforation due to PCI procedure. Given that the covered stent is surrounded by circumferential membrane (9), it may be effective to prevent the protruding of CN after stent implantation.

Objective

We report a case who received the implantation of one covered stent due to coronary artery perforation after stent implantation at coronary lesion exhibiting CN. Since this case does not experience any clinically-driven TLR after covered stent implantation, this case report will discuss the potential benefit of covered stent to treat CN by analyzing intravascular ultrasound (IVUS) and optical coherence tomography (OCT) imaging. We present this case in accordance with the CARE reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-216/rc).

Case presentation

A 79-year-old man presented to the emergency department with his prolonged chest pain. He had a history of hypertension and adrenal hypertrophy, however he did not take any medications prior to his admission. He did not take hemodialysis. His initial blood pressure was 163/127 mmHg and heart rate was 82 beats per minute at the emergency department. There was no remarkable physical examination including cardiac murmurs and respiratory sounds. The electrocardiogram showed atrial fibrillation and ST-segment elevation in leads I, II, aVL and V4–6. In addition, echocardiography showed a reduced wall motion at posterolateral region. On laboratory data, his creatinine was 1.02 mg/dL, hemoglobin A1c was 5.9%, low density lipoprotein cholesterol was 112 mg/dL, and no evidence of elevation of cardiac enzyme at the presentation. He was diagnosed as ST-segment elevation myocardial infarction, and therefore emergent coronary angiography was conducted. Coronary angiogram revealed one severe stenosis at the middle segment of his right coronary artery (RCA) (Figure 1A), moderate stenosis at middle segment of left anterior descending artery and middle segment of left circumflex artery (Videos S1,S2). Primary PCI was performed under the guidance of IVUS imaging (AltaView^TM, Terumo, Tokyo, Japan). IVUS imaging prior to PCI revealed a convex shape of the luminal surface, convex shape of the luminal side of calcium, an irregular luminal surface, and an irregular leading edge of calcium at his culprit lesion, suggesting the presence of type 1 eccentric CN (Figure 1B, Video 1). The device delivery was difficult due to the coronary artery tortuosity and moderate stenosis at the proximal segment of his RCA, we implanted one 4.0 mm × 15 mm DES (Resolute Onyx^TM, Medtronic, Dublin, Ireland) at the proximal segment of his RCA. And then, we conducted the intervention to the culprit lesion. Following balloon angioplasty with 3.0 mm × 15 mm non-compliant balloon catheter at 14 atm (Sapphire NC24^TM, Orbusneich Medical, Hong Kong, China), one 4.0 mm × 15 mm DES (Resolute Onyx^TM, Medtronic) was implanted at 12 atm (Figure 1C). However, stent underexpansion was observed by coronary angiography after stent implantation. The post-dilatation of the implanted stent was undergone by using the stent balloon catheter at 16 atm. After this procedure, he complained chest pain and then his hemodynamic status was suddenly deteriorated. Coronary angiography revealed the occurrence of coronary artery perforation at the segment receiving DES implantation (Figure 1D). A 4.0 mm × 15 mm non-compliant balloon (Sapphire NC24^TM, Orbusneich Medical) was used to seal coronary artery perforation site (10 atm for 120 seconds). However, coronary perforation was still observed. After the insertion of intra-aortic balloon pumping catheter, we decided to implant one 3.5 mm × 15 mm covered stent (PK Papyrus^TM, Biotronik, Berline, Germany) (Figure 1E,1F). Then, post-dilatation of the implanted covered stent was undergone by using the 4.0 mm × 8 mm non-compliant balloon (Sapphire NCpro^TM, Orbusneich Medical) at 14 atm. These procedures resulted in successfully sealing coronary artery perforation site. The IVUS imaging after post dilatation of covered stent, demonstrated optimal stent apposition and stent expansion (Figure 1G, Video 2). The stent was dilated almost to a regular circle. Because of successful PCI, his symptom was recovered and ST segment elevation at electrocardiogram was resolved. He started taking 100 mg of aspirin and 3.75 mg prasugrel and 30 mg edoxaban once daily. Aspirin was stopped when he discharged, the others had been kept 1 year after the PCI.

Figure 1 Coronary angiography and IVUS images before and after PCI. (A) Severe stenosis at the middle segment of his RCA [a-d correspond to IVUS images in (B)]. (B) IVUS images of CN (asterisks). (C) Implantation of drug-eluting stent. (D) Coronary artery perforation (red arrow) at segment receiving drug-eluting stent (white dotted line). (E) Covered stent implantation. (F) Final coronary angiography (white line = implanted covered stent; white dotted line = implanted drug eluting stent) [a’-d’ correspond to IVUS images in (G)]. (G) IVUS images at segment receiving covered stent. CNs (asterisks) did not erupt into the stent. IVUS, intravascular ultrasound; PCI, percutaneous coronary intervention; RCA, right coronary artery; CN, calcified nodule.

Seven months after the PCI, follow-up coronary angiography and OCT (Dragonfly Opstar^TM, Abott Vascular, Chicago, IL, USA) imaging were conducted to evaluate his RCA. Any ISR was not observed in his RCA (Figure 2A). Furthermore, OCT imaging elucidated a small amount of neointimal proliferation without any protruding feature of CN through the segment receiving a covered stent (Figure 2B, Video 3). One year after the PCI, he discontinued taking 3.75 mg of prasugrel. Of note, he did not experience any clinically-driven TLR or no adverse events for 2 years after PCI. The timeline of the imaging and treatment was summarized in Figure 3.

Figure 2 Follow-up coronary angiography and OCT imaging at 7 months after PCI. (A) In-stent restenosis did not occur at segment receiving covered stent (white line) [a-h correspond to OCT images in (B)]. Dotted white line indicates the implanted drug-eluting stent. (B) Protruding of CN was not observed at segment receiving covered stent by OCT imaging (g’ is an enlargement of the frame of g). OCT, optical coherence tomography; PCI, percutaneous coronary intervention; CN, calcified nodule.

Figure 3 The timeline of the imaging and treatment. The x-axis displays the clinical course, with coronary angiogram, intravascular imaging, and medications. One covered stent was implanted to the coronary perforation in lesion with calcified nodule of his RCA. He started taking 100 mg of aspirin and 3.75 mg prasugrel and 30 mg edoxaban once daily. Aspirin was stopped when he discharged, the others had been kept one year after the PCI. In-stent restenosis did not occur 7 months after the PCI. One year after the PCI, he discontinued taking 3.75 mg of prasugrel. He did not experience any clinically-driven target lesion revascularization or no adverse events for 2 years after PCI. PCI, percutaneous coronary intervention; RCA, right coronary artery.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

In our case presenting ACS attributable to CN, one covered stent successfully sealed coronary artery perforation caused by DES implantation. OCT imaging 7 months after PCI did not demonstrate any protrusion of CN within the implanted covered stent. Furthermore, this case did not experience any clinically-driven TLR for 2 years after PCI even in the presence of the eccentric CN which associated with worse clinical outcome (10). The current case may suggest the potential of covered stent to prevent the continuing protrusion of CN through stent struts.

Strengths and limitations

The strength of this case report is to serially evaluate lesions with CN by using intravascular imaging modality. OCT imaging visualized that the protrusion of CN did not occur 7 months after PCI. These observations suggest the use of covered stent as another therapeutic approach to treat CN. Since this is a case report, future dedicated study is required to investigate whether the use of covered stent reduces TLR rate at CN lesions. We did not conduct OCT imaging at PCI. Therefore, we did not detect whether the fibrous cap was disrupted or not. However, balloon and DES was well dilatated. By the favourable balloon and DES response, this CN might be the eruptive CN. In most case of CN, a greater amount of calcification is often recognized at the adjacent lesion. However, this case had less calcification in the adjacent lesion. It might affect the favourable clinical course. We do not conduct additional follow-up evaluation of CN lesion receiving covered stent by intravascular imaging. Therefore, it remains unknown whether the protrusion of CN occurred later or not. This is only one case report. Further clinical follow-up is required to monitor whether the use of covered stent continues to prevent CN-related ISR.

Comparison with similar researches

As shown in Table 1, published studies investigated the efficacy of newer-generation DES and rotational atherectomy on TLR rate at CN lesions, respectively (1-6). To date, these devices do not necessarily reduce TLR rate at coronary lesions exhibiting CN. Moreover, there are no studies and case reports to evaluate the efficacy of covered stent for this high-risk calcified lesion.

Explanations of findings

Pathophysiologically, protruding of CN through implanted stent struts has been considered as a potential mechanism causing ISR (7). PK Papyrus^TM is covered by polyurethane membrane, which seals coronary perforation site (9). Given that follow-up angiography and OCT did not show any protrusion of CN within the implanted covered stent, polyurethane membrane of this covered stent may be effective to physically hinder the protrusion of calcification tissues into the implanted stent.

Implications and action needed

Covered stent may be effective to physically hinder the re-protrusion of calcification tissues into the lumen. Further clinical follow-up is required to monitor whether the use of covered stent continues to prevent CN-related ISR.

Conclusions

In the current case, coronary perforation occurred after the implantation of DES at culprit lesion exhibiting CN. One covered stent was successfully implanted, which enabled to seal coronary artery perforation. Seven months later, coronary angiography and OCT imaging did not show any ISR, accompanied by the absence of protruding calcification tissues within the implanted covered stent. Furthermore, he did not experience any clinically-driven TLR for 2 years after PCI. Polyurethane membrane of the covered stent may be effective to physically hinder the re-protrusion of calcification tissues into the lumen. Further clinical follow-up is required to monitor whether the use of covered stent continues to prevent CN-related ISR.

Acknowledgments

Funding: None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-216/rc

Peer Review File: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-216/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-24-216/coif). Y.K. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from September 2023 to August 2025. Y.K. has received research support from Kowa, Nipro and Abbott, and honoraria from Nipro, Abbott, Kowa, Amgen, Sanofi, Astellas, Takeda and Daiichi-Sankyo. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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