Author + information
- Received March 6, 2017
- Accepted March 9, 2017
- Published online June 5, 2017.
- Hiroyoshi Mori, MDa,
- Robert Kutys, MSa,
- Maria Romero, MDa,
- Renu Virmani, MDa and
- Aloke V. Finn, MDa,b,∗ ()
- aDepartment of Pathology, CVPath Institute, Gaithersburg, Maryland
- bDepartment of Cardiology, University of Maryland, School of Medicine, Baltimore, Maryland
- ↵∗Address for correspondence:
Dr. Aloke V. Finn, CVPath Institute, 19 Firstfield Road, Gaithersburg, Maryland 20878.
Pathologically verified hypersensitivity reactions following coronary stent implantation have been reported exclusively in first-generation drug-eluting stents secondary to the polymers used in devices (1). However, it is known that metals such as cobalt, chromium, tungsten, and nickel (all components of modern-day coronary stents) can provoke immune reactions, with the later thought to be the most immunogenic (2). A clinical study of patients receiving stainless steel bare-metal stents (BMS) demonstrated a higher frequency of angiographically determined in-stent restenosis in those with a metal allergy (positive patch-test reaction to nickel or molybdenum) versus patients without (negative patch-test reaction) (3). However, another clinical study of patients with a history of nickel or chromium allergy receiving coronary stents (drug-eluting stents or BMS) did not demonstrate increased early or late adverse outcomes after stenting (4). To our knowledge, there has been no pathologically confirmed case of local hypersensitivity reaction to BMS. Here, we present a very rare histological finding of hypersensitivity reaction in a contemporary cobalt chromium BMS (CoCr-BMS, MULTI-LINK VISION, Abbott Vascular, Santa Clara, California) associated with in-stent restenosis at a site of stent fracture.
A 58-year-old man with history of previous myocardial infarction had been treated with 3 BMS 4 years before sudden death (a 2.5 × 23-mm CoCr-BMS in the distal right coronary artery [RCA], a 2.5 × 18-mm CoCr-BMS in the middle left circumflex coronary artery, and a 3.0 × 20-mm Liberte stent [Boston Scientific, Natick, Massachusetts] in the obtuse marginal). Autopsy revealed in-stent restenosis in all BMS. The CoCr-BMS in the RCA showed focal hypersensitivity reaction only at a fracture site, whereas all other sections within the same stent showed mild inflammatory reactions (Figure 1). The section with the hypersensitivity reaction exhibited the highest degree of cross-sectional stenosis. The hypersensitivity reaction was characterized by marked chronic inflammation consisting of lymphocytes, eosinophils, plasma cells, and focal granulomatous inflammation.
Metal allergy is generally categorized as a delayed-type hypersensitivity reaction. Metal ions released from various alloys are thought to be potent allergens or haptens that can trigger inflammation. Thus, it is possible that in this case, stent fracture caused the accelerated release of metal ions leading to a focal hypersensitivity reaction in this lesion. Several studies have shown an association between stent fracture and higher rates of target lesion revascularization. However, it remains uncertain how fracture causes restenosis. This case suggests local hypersensitivity to metal needs to be considered in cases of restenosis associated with stent fracture. Moreover, because recent stent designs have emphasized thinner struts to improve deliverability, the fracture resistance of each should be carefully examined before their clinical adoption.
CVPath Institute has received research grants from Abbott Vascular, Atrium Medical, Boston Scientific, Biosensors International, Cordis (Johnson & Johnson), Medtronic CardioVascular, OrbusNeich Medical, and Terumo Corporation. Dr. Mori is a research fellow at CVPath Institute; and has received honoraria from Abbott Vascular Japan, Goodman, and Terumo Corporation. Dr. Virmani has speaking engagements with Merck; receives honoraria from Abbott Vascular, Boston Scientific, Lutonix, Medtronic, and Terumo Corporation; and is a consultant for 480 Biomedical, Abbott Vascular, Medtronic, and W.L. Gore. Dr. Finn has sponsored research agreements with Boston Scientific and Medtronic CardioVascular; and is an advisory board member to Medtronic CardioVascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 6, 2017.
- Accepted March 9, 2017.
- 2017 American College of Cardiology Foundation
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