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Bioresorbable Vascular Scaffold Collapse Causes Subacute Thrombosis

Rafael J. Ruiz-Salmer√≥n, PhD;  Sof√≠a Pereira, MD;  Daniela de Araujo, MD

July 2014

ABSTRACT: We report a subacute bioresorbable scaffold thrombosis caused by stent collapse into a heavily calcified lesion.

J INVASIVE CARDIOL 2014;26(7):E98-E99

Key words: device failure, complications

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Bioresorbable stents have emerged as a revolutionary tool in coronary interventions. Known by the slogan “do the job and disappear,” their transient scaffolding offers important potential benefits. They minimize the risk of late thrombosis, do not hamper subsequent bypass surgery, and allow coronary lumen follow-up with computed tomography (CT) scan. Furthermore, their ability to restore vascular physiology and to promote positive remodeling makes these devices unique.

The Absorb bioresorbable vascular scaffold (BVS) system (Abbott Vascular) is made from a polymer backbone of semicrystalline poly-L lactide coated with an amorphous poly-D, L-lactide polymer and the antiproliferative drug everolimus. The current Absorb BVS (revision 1.1) has showed optimal efficacy and safety results in the Absorb cohort B trial.1

Scaffold limitations of the Absorb BVS have been described in comparison with contemporary metallic stents: higher, although not significant, acute elastic recoil;2 and greater geometrical distortion with elliptical shape after implantation, especially in calcified lesions.3 Those limitations could be a concern when facing demanding settings, such as severe calcified, intramyocardial, ostial, and/or diffuse lesions.

Case Report. A 62-year-old patient with hypertension and tobacco use as coronary risk factors was admitted to our institution due to an inferolateral ST-elevation myocardial infarction, and successfully thrombolyzed with tenecteplase. Early triage angiography  (Figure 1A) showed severe double-vessel disease: the culprit lesion was located in the mid-codominant circumflex (LCX), and the left anterior descending (LAD) coronary artery presented a calcified diffuse proximal lesion including the ostium, which was confirmed with coronary computed tomography angiography (Figure 1B). Heart-team discussion considered percutaneous complete revascularization using the Absorb BVS based on the appealing concept of complete resorption of the scaffold that would protrude in the left main lumen after treating the ostial LAD lesion. Consequently, after uneventful revascularization of the mid-LCX, the proximal LAD was approached by initial debulking with the use of a 1.5 mm Rotablator burr, followed by 3.0 x 20 mm balloon predilatation, and finally 3.0 x 28 mm Absorb BVS implantation. Excellent angiographic result was achieved, without residual stenosis and with preserved flow in all the main vessels and side branches involved (Figure 1C).

Four days after the procedure, the patient suddenly developed chest pain with left bundle branch block and cardiogenic shock. He was emergently taken to the cath lab, suffering cardiac arrest at arrival. Coronary catheterization revealed LAD scaffold thrombosis extending proximally and occluding the left main. Scaffold rewiring was not possible, even with repeated attempts with different guidewire types. Finally, the patient died and necropsy was requested.

Histopathological study of the LAD and LCX consisted of cross-section at 10 mm intervals along their lengths, from distal to proximal. Macroscopic view of proximal-mid LAD showed heavy calcification throughout the vessel segment; at the area covered by BVS, a huge eccentric plaque of calcium was taking up the majority of the vessel area, surrounding an elliptically shaped lumen. Inside the lumen, scaffold appeared collapsed along its mid and distal parts, and was totally occluded with thrombus (Figure 1D). 

Discussion. To our knowledge, this is the first reported case of definitive subacute bioresorbable scaffold thrombosis. Although the Absorb BVS was implanted successfully, following standard recommendations, some issues should be taken into consideration. First, its geometric expansion could be hampered by a heavily calcified lesion, even though previous rotablation and aggressive predilatation were performed. Second, the lesion was diffuse and the 28 mm scaffold length could not be homogeneously expanded. We hypothesize that the impressive calcium bulge surrounding the vessel lumen could damage the polymeric platform and weaken its scaffolding properties; stent collapse made impossible its rewiring, and therefore, LAD recanalization.

Acknowledgment. The authors express appreciation to Javier Rivera, MD, Sergio Rodriguez-Leiras, MD, and Javier Goicolea, MD, for their support and critical review of this manuscript.

References

  1. Dudek D. Evaluation of the Absorb everolimus-eluting bioresorbable vascular scaffold (Absorb BVS) in the treatment of patients with de novo native coronary artery lesions: 2 year clinical results of absorb cohort B trial. J Am Coll Cardiol. 2012;59(15):E319.
  2. Onuma Y, Serruys PW, Gomez J, et al. Comparison of in vivo acute stent recoil between the bioresorbable everolimus-eluting coronary scaffolds (revision 1.0 and 1.1) and the metallic everolimus-eluting stent. Catheter Cardiovasc Interv. 2011;78(1):3-12.
  3. Brugaletta S, Gomez-Lara J, Diletti R, et al. Comparison of in vivo eccentricity and symmetry indices between metallic stents and bioresorbable vascular scaffolds: insights from the ABSORB and SPIRIT trials. Catheter Cardiovasc Interv. 2012;79(2):219-228.

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From the 1Endovascular Unit; 2Department of Anatomical Pathology; and 3Department of Radiology Hospital Virgen Macarena, Seville, Spain.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted November 5, 2013 and accepted November 11, 2013.

Address for correspondence: Rafael Ruiz-Salmerón, PhD, Endovascular Unit. Hospital Virgen Macarena, Avda Dr Fedriani no. 3, 41009 Seville, Spain. Email: rjruizsalmeron@yahoo.es