Abstract

Although complete bioresorbable vascular scaffold (BVS) resorption has been demonstrated at 5-year follow-up, whether corresponding vasomotor function restoration occurs remains unknown. The objective was to simultaneously assess the structural healing response along with vasomotor responses at 5-year follow-up of BVS implantation. We studied consecutive patients treated with ABSORB-BVS at 5-year follow-up (n=31), who were recruited from a multicenter registry and were contacted to undergo a research protocol-driven repeat coronary angiogram involving intracoronary optical coherence tomography (OCT) and invasive coronary endothelial function testing. Epicardial endothelium-dependent vasomotion was defined as any vasodilatation after intracoronary acetylcholine (ACh), whereas endothelium-independent vasomotion was defined as any vasodilatation after intracoronary nitroglycerine (NTG), using quantitative coronary angiography. The mean implantation time point was 60.5 ± 4.6 months. OCT imaging demonstrated complete scaffold resorption in all patients. New coronary lesions (stenosis &gt;50%) were found in 5 patients (16.1%), 3 of them underwent ad hoc percutaneous revascularization (9.7%). Intracoronary ACh (27 patients) and NTG testing (30 patients) was performed. Quantitative coronary angiography analysis demonstrated vasoconstriction after ACh administration and lack of response to NTG in BVS segments (mean lumen diameter=2.00 ± 0.61 mm at baseline vs 1.74 ± 0.70 mm post-ACh, p &lt;0.001; 2.05 ± 0.54 mm at baseline vs 2.03 ± 0.50 mm post-NTG, p=0.69). OCT lumen analysis demonstrated similar vasoconstrictive responses to ACh (mean lumen area=5.31 ± 2.26 mm<sup>2</sup> at baseline vs 5.12 ± 2.55 mm<sup>2</sup> post-ACh, p=0.007) but had a vasodilatory response to NTG (5.96 ± 2.35 mm<sup>2</sup> at baseline vs 6.17 ± 2.55 mm<sup>2</sup> post-NTG, p&lt;0.001). In conclusion, complete ABSORB-BVS resorption was demonstrated at 5-year follow-up. However, this healing response was associated with endothelium-dependent vasomotor dysfunction within the BVS segment.

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