A 70-year-old morbidly obese woman with severe emphysema presented with unstable angina. Coronary angiography revealed high-grade, calcified, ostial left circumflex (LCX) and distal right coronary artery (RCA) lesions. She was deemed a high-risk surgical candidate and underwent stenting of the left main coronary artery into the LCX with a 3.5 × 18-mm Xience V stent (Abbott Vascular, Santa Clara, California). A second 3.5 × 18-mm Xience V stent was overlapped distally to cover a mid LCX lesion, and both stents were post-dilated to 16 atm with a 3.5-mm noncompliant balloon. The RCA lesion was stented with a 3.0 × 12-mm Xience V and post-dilated to 16 atm with a 3.0-mm noncompliant balloon (Fig. 1). The patient did well for 6 months until she returned with unstable angina. Angiography revealed restenosis at the ostium of the stented LCX and within the distal RCA stent (Fig. 1). During repeat intervention, wiring of the LCX resulted in abrupt closure. The patient developed refractory ventricular fibrillation and died.
Angiography of the left coronary system at the index procedure demonstrating high-grade ostial and proximal circumflex coronary artery (LCX) lesions (A), post-intervention (B), and 6 months later, revealing severe in-stent restenosis (C). Angiography of the right coronary artery (RCA) demonstrating a distal stenosis (D), post-intervention (E), and 6 months later with in-stent restenosis (F).
A post-mortem examination was performed in which the coronary arteries were pressure flushed, formalin fixed, perfused with a lead-based contrast agent (Microfil MV-120, FlowTech, Carver, Massachusetts), and the stented segments were resected under fluoroscopic guidance. The explanted arterial segments were then scanned using a GE eXplore SP MicroCT scanner (GE Healthcare, London, Ontario, Canada) (1). Three-dimensional reconstructions at 23-μm resolution demonstrated heavy calcification and stent fracture at the sites of maximal restenosis. Both Xience V stents fractured in the middle of the hairpin bend in the connecting element and along the crown at the base of the connecting element. Histology of both stents revealed underlying heavy fibrocalcific plaque and extensive neointimal hyperplasia at the fracture site without thrombus (Figs. 2 and 3).⇓⇓ The histology of the RCA stent demonstrates inflammation and fibrin accumulation, possibly related to sloughed polymer at the site of fracture (Fig. 4). Autopsy studies have suggested a correlation between severe first-generation stent fracture and restenosis (2). In this case of clinical everolimus drug-eluting stent restenosis at 6 months, it is unclear whether stent fracture induced restenosis, or vessel pathoanatomic characteristics such as calcium, tortuosity, torsion, and local plaque composition lead to restenosis with coincidental stent fracture.
(A) MicroCT 3-dimensional reconstruction of the left main (LM) and left circumflex (LCX) coronary artery stents with a magnified image of the fractured segment to the right. The red dots highlight fracture points, with the dotted lines indicating the original connection. The calcified plaque is colored yellow, and residual intraluminal contrast is red. (B) Corresponding histological cross sections of LM/LCX stents demonstrating focal restenosis at the area of fracture. LAD = left anterior descending coronary artery.
(A) Micro-computed tomography (microCT) 3-dimensional reconstruction of the right coronary artery (RCA) stent with a magnified image of the fractured segment to the right. The red dots highlight fracture points, with the dotted line indicating the original connection. The calcified plaque is colored yellow, and residual intraluminal contrast is red. (B) Corresponding histological cross sections of the RCA stent demonstrating focal restenosis at the area of fracture, with inflammation and fibrin accumulation at areas of polymer displacement.
(A) Histological cross sections at the LCX stent fracture site demonstrating heavy underlying fibrocalcific plaque (bordered by yellow) and extensive neointimal hyperplasia (Movat stain, original magnification: 12.5×). (B) RCA stent fracture site on the left demonstrating underlying fibrocalcific plaque (hematoxylin and eosin stain, original magnification: 20×). The right image is a higher magnification of an area of sloughed drug-eluting stent polymer with surrounding inflammation (original magnification: 200×). Abbreviations as in Figure 1.
Dr. Virmani is a consultant for Medtronic AVE, Abbott Vascular, Arsenal Medical, Atrium Medical Corporation, Biosensors International, GlaxoSmithKline, Lutonix, and W. L. Gore. Dr. Kaplan has significant equity interest in Tryton Medical, Inc., a venture-backed company developing bifurcation stents. Dr. Kaplan also receives funding from Cordis/Johnson & Johnson, Medtronic, Boston Scientific, Edwards Lifesciences, and Abbott Vascular. All other authors have stated that they have no relationships relevant to the contents of this paper to disclose.
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