title: Comparison of drug-eluting versus bare metal stents in cardiac allograft vasculopathy.
abstract: Although not a definitive treatment, percutaneous coronary intervention offers a palliative benefit to patients with cardiac allograft vasculopathy. Given the superior outcomes with drug-eluting stents (DESs) over bare metal stents (BMSs) in native coronary artery disease, similar improvements might be expected in transplant patients; however, the results have been mixed. Consecutive cardiac transplantation recipients at a single center receiving a stent for de novo cardiac allograft vasculopathy from 1997 to 2009 were retrospectively analyzed according to receipt of a DES versus a BMS. The angiographic and clinical outcomes were subsequently evaluated at 1 year. The baseline clinical and procedural characteristics were similar among those receiving DESs (n = 18) and BMSs (n = 16). Quantitative coronary angiography revealed no difference in the reference diameter, lesion length, or pre-/postprocedural minimal luminal diameter. At the 12-month angiographic follow-up visit, the mean lumen loss was significantly lower in the DES group than in the BMS group (0.19 ± 0.73 mm vs 0.76 ± 0.97 mm, p = 0.02). The DES group also had a lower rate of in-stent restenosis (12.5% vs 33%, p = 0.18), as well as a significantly lower rate of target lesion revascularization (0% vs 19%, p = 0.03). At 1 year, DESs were associated with a lower composite rate of cardiac death and nonfatal myocardial infarction (12% vs 38%, p = 0.04). In conclusion, DESs are safe and effective in the suppression of neointimal hyperplasia after percutaneous coronary intervention for cardiac allograft vasculopathy, resulting in significantly lower rates of late lumen loss and target lesion revascularization, as well as a reduced combined rate of cardiac death and nonfatal myocardial infarction.
authors.affiliation: Division of Cardiovascular Medicine, Stanford University School of Medicine, California, USA. jtremmel@stanford.edu
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Tremmel
authors.forename: Martin K C
authors.initials: MK
authors.lastname: Ng
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Ikeno
authors.forename: Sharon A
authors.initials: SA
authors.lastname: Hunt
authors.forename: David P
authors.initials: DP
authors.lastname: Lee
authors.forename: Alan C
authors.initials: AC
authors.lastname: Yeung
authors.forename: William F
authors.initials: WF
authors.lastname: Fearon
mesh_terms: D001241:Aspirin / Q000008:administration & dosage; D016009:Chi-Square Distribution; D000077144:Clopidogrel; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000628:therapy*; D054855:Drug-Eluting Stents; D005260:Female; D016027:Heart Transplantation; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D008297:Male; D008670:Metals; D008875:Middle Aged; D017239:Paclitaxel / Q000008:administration & dosage; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D012189:Retrospective Studies; D012307:Risk Factors; D020123:Sirolimus / Q000008:administration & dosage; D015607:Stents; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D014184:Transplantation, Homologous; D016896:Treatment Outcome; D050257:Tubulin Modulators / Q000008:administration & dosage
chemical_list: D007166:Immunosuppressive Agents; D008670:Metals; D010975:Platelet Aggregation Inhibitors; D050257:Tubulin Modulators; D000077144:Clopidogrel; D013988:Ticlopidine; D017239:Paclitaxel; D001241:Aspirin; D020123:Sirolimus