Unfavorable bioresorbable vascular scaffold resorption, a cause of restenosis?




Abstract


We report a case of bioresorbable vascular scaffold restenosis which could be caused by abnormal resorption 17 months after implantation.


Highlights





  • Bioresorbable vascular scaffold restenosis was observed by optical coherence tomography.



  • The presence of strut discontinuity was demonstrated in area with restenosis.



  • The strut discontinuity was absent in area without restenosis.



  • Scaffold area was smaller in discontinuity segments than in non-discontinuity ones.



  • Neointima area was larger in discontinuity segments than in non-discontinuity ones.




Introduction


Bioresorbable vascular scaffold (BVS) is a novel approach in percutaneous coronary intervention. It provides transient vessel support with drug delivery capability, without the long-term limitation associated with vessel caging . BVS has obvious potential advantages compared with metallic stent. Late and very late stent thrombosis risks are potentially reduced. Neointimal tissue growth, neoatherosclerosis, and the risk of chronic inflammation as reactions to permanent metal implant may also be reduced . The second generation of bioresorbable vascular scaffold (Absorb BVS 1.1, Abbott Vascular, Santa Clara, CA) was evaluated in the ABSORB cohort B study . In this study, BVS showed a low event rate, and imaging analyses by intravascular ultrasound (IVUS) and optical coherence tomography (OCT) at 6 and 12 months demonstrated low angiographic late loss without any reduction of the scaffold area . At 2-year follow-up, the angiographic late loss remained stable with a late enlargement of the scaffold by OCT .


However, pathophysiology of very late hazards of BVS has not been completely understood. We herein report a case of very late restenosis of BVS assessed by OCT.





Case description


A 61-year-old patient with history of ischemic heart disease, hypertension, diabetes mellitus, and dyslipidemia was admitted for chest pain. 17 months before, he had non-ST segment elevation myocardial infarction and treated with percutaneous coronary intervention (PCI) with BVS implantation in left anterior descending (LAD) and right coronary artery (RCA). At index procedure, AHA types of lesions were B1 in LAD and B2 in RCA. There was no calcification at the lesion sites. In LAD, pre-dilatation was performed with 2.5 mm non-compliant balloon at 20 atm. BVS 3.5 × 28 mm was implanted at 16 atm leading to max diameter of 4.0 mm, and no further post-dilatation was performed. In RCA, pre-dilatation was performed with 3.0 mm non-compliant balloon at 12 atm. BVS 3.5 × 28 mm was implanted at 16 atm leading to max diameter of 4.0 mm, and post-dilatation was not performed, either. Both BVSs were expanded within their theoretical maximum expansion limits.


On admission, there were no ECG changes and no cardiac enzymes elevation. Coronary angiography revealed significant restenosis of the BVS placed in the proximal segment of LAD and of the BVS previously placed in the mid segment of the RCA ( Fig. 1 A and B ). OCT examination in LAD showed significant restenosis at proximal and mid segments of the scaffold, with signs of strut discontinuity ( Fig. 1 C and D). Conversely, no signs of discontinuity were present in non-restenotic segments ( Video 1 ). PCI was performed with final biolimus eluting stent (BES) (Biosensors Inc., Newport Beach, CA) implantation. OCT examination in RCA also showed significant restenosis at mid and distal segment of the scaffold with signs of discontinuity ( Fig. 1 E and F), while no abnormalities were shown at the proximal segment ( Video 2 ). PCI with BES implantation was also successfully performed.




Fig. 1


Angiography and OCT. Angiography showed significant restenosis in LAD scaffold (A) and RCA scaffold (B) (bars indicate location of BVS; arrows indicate the OCT imaging sites). OCT images demonstrated discontinuity (arrowheads) and restenosis in LAD scaffold (C and D) and RCA scaffold (E and F). *Wire artifact.





Case description


A 61-year-old patient with history of ischemic heart disease, hypertension, diabetes mellitus, and dyslipidemia was admitted for chest pain. 17 months before, he had non-ST segment elevation myocardial infarction and treated with percutaneous coronary intervention (PCI) with BVS implantation in left anterior descending (LAD) and right coronary artery (RCA). At index procedure, AHA types of lesions were B1 in LAD and B2 in RCA. There was no calcification at the lesion sites. In LAD, pre-dilatation was performed with 2.5 mm non-compliant balloon at 20 atm. BVS 3.5 × 28 mm was implanted at 16 atm leading to max diameter of 4.0 mm, and no further post-dilatation was performed. In RCA, pre-dilatation was performed with 3.0 mm non-compliant balloon at 12 atm. BVS 3.5 × 28 mm was implanted at 16 atm leading to max diameter of 4.0 mm, and post-dilatation was not performed, either. Both BVSs were expanded within their theoretical maximum expansion limits.


On admission, there were no ECG changes and no cardiac enzymes elevation. Coronary angiography revealed significant restenosis of the BVS placed in the proximal segment of LAD and of the BVS previously placed in the mid segment of the RCA ( Fig. 1 A and B ). OCT examination in LAD showed significant restenosis at proximal and mid segments of the scaffold, with signs of strut discontinuity ( Fig. 1 C and D). Conversely, no signs of discontinuity were present in non-restenotic segments ( Video 1 ). PCI was performed with final biolimus eluting stent (BES) (Biosensors Inc., Newport Beach, CA) implantation. OCT examination in RCA also showed significant restenosis at mid and distal segment of the scaffold with signs of discontinuity ( Fig. 1 E and F), while no abnormalities were shown at the proximal segment ( Video 2 ). PCI with BES implantation was also successfully performed.




Fig. 1

Nov 13, 2017 | Posted by in CARDIOLOGY | Comments Off on Unfavorable bioresorbable vascular scaffold resorption, a cause of restenosis?

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