title: Frequency, mechanisms, and implications of late peri-stent contrast staining: analysis (from the HORIZONS-AMI Trial).
abstract: Previous studies have suggested that angiographically detected persistent contrast staining (PSS) at follow-up may predict subsequent very late stent thrombosis. The Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial was a dual-arm, factorial, randomized trial in patients with ST-segment elevation myocardial infarctions. All follow-up angiograms (1,330 lesions in 1,115 patients, median time 13.3 months) without major cardiovascular events before follow-up angiography were analyzed at a core laboratory blinded to clinical events for the presence of PSS (defined as contrast staining outside the stent contour extending to ≥20% of the stent diameter). Corresponding follow-up intravascular ultrasound (IVUS) data (275 lesions in 248 patients) were also evaluated to assess the mechanisms of PSS. PSS was present in 23 patients (2.1%) at follow-up and was not more common with paclitaxel-eluting than with bare-metal stents. All 6 PSS patients with follow-up IVUS had stent malapposition (vs 41.2% malapposition in the follow-up IVUS cohort). Comparing poststent and follow-up IVUS, 2 patients had late acquired and 4 had persistent malapposition; all 6 showed positive vessel remodeling from baseline to follow-up (mean vessel area 22.0 ± 8.0 to 32.4 ± 11.7 mm(2), p = 0.07). During 3-year follow-up, stent thrombosis developed in no patient with PSS compared with 8 PSS-negative patients (0% vs 0.8%, p = 0.68). The rates of revascularization and major adverse cardiovascular events were also not increased in PSS patients. In conclusion, in the large-scale HORIZONS-AMI trial, PSS at angiographic follow-up was infrequent and was associated with late stent malapposition and positive remodeling but was independent of stent type. Identification of PSS was not associated with subsequent stent thrombosis.
authors.affiliation: Columbia University Medical Center, New York, NY, USA.
authors.forename: Tadayuki
authors.initials: T
authors.lastname: Yakushiji
authors.forename: Shinji
authors.initials: S
authors.lastname: Inaba
authors.forename: Akiko
authors.initials: A
authors.lastname: Maehara
authors.forename: Sorin J
authors.initials: SJ
authors.lastname: Brener
authors.forename: Bernhard
authors.initials: B
authors.lastname: Witzenbichler
authors.forename: Giulio
authors.initials: G
authors.lastname: Guagliumi
authors.forename: Bruce R
authors.initials: BR
authors.lastname: Brodie
authors.forename: Mirle A
authors.initials: MA
authors.lastname: Kellett
authors.forename: Ke
authors.initials: K
authors.lastname: Xu
authors.forename: Roxana
authors.initials: R
authors.lastname: Mehran
authors.forename: Gary S
authors.initials: GS
authors.lastname: Mintz
authors.forename: Gregg W
authors.initials: GW
authors.lastname: Stone
mesh_terms: D000368:Aged; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D017023:Coronary Angiography; D004311:Double-Blind Method; D054855:Drug-Eluting Stents; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006083:Graft Occlusion, Vascular / Q000175:diagnosis* / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000628:therapy*; D017239:Paclitaxel / Q000494:pharmacology; D062645:Percutaneous Coronary Intervention / Q000379:methods*; D011446:Prospective Studies; D011475:Prosthesis Failure; D013997:Time Factors; D018084:Ultrasonography, Interventional; D014481:United States / Q000453:epidemiology
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D017239:Paclitaxel