Abbreviations and Acronyms

BVS

bioresorbable vascular scaffold

HFrEF

heart failure with reduced ejection fraction

LAD

left anterior descending coronary artery

OCT

optical coherence tomography

Introduction

Acquired coronary stent fracture¹ resulting from unexpected vascular or cardiac remodeling is a rare but possible metallic stent–related long-term complication. This complication theoretically could be minimized if bioresorbable vascular scaffold (BVS) (Absorb; Abbott Vascular) is implanted and then allowed to degrade. Optical coherence tomography (OCT) evaluation of a patient 39 months after BVS treatment for heart failure with reduced ejection fraction (HFrEF) showed remaining discernible struts, with the evidence of coronary longitudinal remodeling not causing serious concern for stent fracture, which typically occurs in metallic stents.

Case Report

A 60-year-old man with hypertension, diabetes, and hyperlipidemia underwent coronary angioplasty for effort angina and documented severe stenosis in the proximal left anterior descending coronary artery (LAD) with reduced left ventricular EF (LVEF, 43%) and mild apical hypokinesia on coronary computed tomography angiography.

Technique

A diagnostic coronary angiogram produced the same finding (Fig. 1A and 1B), and a 3.0- × 18-mm BVS was implanted for the critically stenotic lesion. An angiogram of the LAD after dilatation with a 3.5- × 15-mm noncompliant balloon at 20 atm is shown in Figure 1C. The LV end-diastolic volume (LVEDV) decreased initially from 262 to 127 mL after BVS implantation, with the LVEF increasing from 43% to 56%.

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The patient developed recurrent chest tightness, however, with a positive stress test 39 months later. In addition, LVEDV increased to 158 mL, LVEF decreased to 37%, and severe apical hypokinesia was found. Therefore, he underwent another coronary angiography, which showed only severe stenosis at the distal LAD without significant restenosis at the stent site (Fig. 2A). The distal lesion was treated using a 2.5- × 28-mm drugeluting stent. The OCT demonstrated a degraded but discernible BVS within the vessel wall. Notably, the entire length of the visible scaffold, from distal (Fig. 2B) to proximal (Fig. 2C), was 20.5 mm, which represented 13.9% elongation compared with the original length of the BVS (Fig. 2). Nevertheless, there was no concern about permanent stent fracture because the BVS was designed to resorb completely.

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Discussion

For metallic stents, several factors, including stent overlap, longer stent length, right coronary artery location, calcified or tortuous lesions, lesions with high angulation, and stent overexpansion, are associated with the risk of stent fracture.¹ Acquired coronary stent fracture resulting from unexpected vascular or cardiac remodeling is rare but possible. Stent fracture has been reported to be associated with clinical events, as well.² One meta-analysis³ evaluating stent fractures from 8 studies with 108 cases suggested that lesions with stent fractures had higher rates of in-stent restenosis (38% vs 8.2%; P < .01) and target lesion revascularization (17% vs 5.6%; P < .01) than those without.

Fully bioresorbable scaffolds were fundamentally designed to minimize the potential long-term adverse effect of metallic stents. Results from large, randomized clinical trials, however, raised concerns that there could be a higher risk of device thrombosis with the BVS than with the cobalt-chromium everolimus-eluting stent, especially when bioresorption was ongoing.⁴ Because of safety issues, the manufacturer discontinued the device. In patients with HFrEF, LV chamber size was more vulnerable to fluid overload than in those with normal EF. Besides chronic remodeling, serial chest x-ray or echocardiography occasionally showed that the LV size of the population with HF could change significantly either during acute decompensation or because of diuretic use in clinical practice. This case report showed unexpected elongation of the BVS. With such vascular remodeling, the patient could have been at risk for potential stent fracture–related complications if a metallic stent had been implanted. As shown in this case with HFrEF, however, the BVS still has a favorable impact on reducing the longer-term risk of stent fracture because of unpredictable but possible HF-related cardiac remodeling.

The timing of the follow-up angiography and OCT is crucial in this case. During the process of BVS degradation, polymer is gradually replaced by an increasingly cellular matrix. Although the BVS polymer would be expected to dissolve completely within 3 years after implantation, the space left behind would gradually be occupied by cellular matrix within 5 years. At 5 years after implantation, the stented segment would become a “golden tube” on OCT imaging, with no visible box-shaped appearance.⁵ Thus, because of the visible, box-shaped space at 39 months after BVS implantation in the current case report, the authors could accurately measure the total length of the BVS based on its distal and proximal box-shaped appearance.

To the authors' knowledge, this report is the first to show vascular longitudinal remodeling more than 3 years after BVS implantation in a patient with HFrEF. The OCT images suggested that the patient was free from potential adverse events resulting from stent fracture, which can occur in metallic stents in the long term. The authors did not perform OCT to confirm the initial length of the BVS just after implantation, and the single case described here did not allow conclusions about the true clinical impact of the BVS; however, the findings imply a longer-term benefit of BVSs for patients with HF if the improved design of next-generation BVSs could reduce the risk of scaffold thrombosis during bioresorption.