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In-Stent Restenosis and Remote Coronary Lesion Progression Are Coupled in Cardiac Transplant Vasculopathy But Not in Native Coronary Artery Disease

Michael Jonas, MD^_*,,,_*, James C. Fang, MD^_*, John C. Wang, MD^_*, Satyendra Giri, MD^_*, Dan Elian, MD, Yedael Har-Zahav, MD, Hung Ly, MD^_*, Philip A. Seifert, MS, Jeffrey J. Popma, MD^_* and Campbell Rogers, MD^_*,

^_* Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
Heart Institute, Sheba Medical Center, Tel Hashomer, Israel
Harvard–MIT Division of Health Sciences and Technology, Cambridge, Massachusetts

View larger version (25K): [in a new window]   Figure 1 Cumulative frequency of minimal luminal diameters (MLDs). The cumulative frequency distribution curve of MLDs of: (A) stented segment, immediately after stent implantation and at follow-up; (B) reference, non-stented segment at baseline and at follow-up angiogram.

View larger version (18K): [in a new window]   Figure 2 Scatter plot shows correlation between in-stent late loss and non-intervened, reference segment late loss: (A) heart transplant patients and (B) native atherosclerosis patients. For each individual post-transplant patient, in-stent late lumen loss was closely coupled to late lumen loss of the individual matched non-intervened segment, in both the Sheba Medical Center and Brigham and Women’s Hospital (BWH) patient populations. In contrast, no such coupling of in-stent and reference vessel late loss was found in native atherosclerosis patients.

View larger version (105K): [in a new window]   Figure 3 Stenting and follow-up angiograms of Case 1: (A) angiogram showing significant stenosis of the ramus intermedius (arrow) and minimal irregularities of the reference left anterior descending artery segment (arrowhead); (B) post-stent angiogram showing good angiographic result after deployment of a bare-metal stent (arrow); (C) repeat angiogram, 6 months after stenting, showing focal in-stent restenosis of the ramus (arrow) with significant disease progression in the non-intervened mid- and distal portions of the left anterior descending artery (arrowhead).

View larger version (96K): [in a new window]   Figure 4 Photomicrographs show: (A) Ramus intermedius stent; (B) non-intervened, diagonal branch of Case 1 patient. 1) Verhoeff tissue elastin stain, 2) Carstair’s fibrin stain, and 3) Sirius red collagen stain demonstrate: in A, severe in-stent restenosis and in B, diffuse cardiac allograft vasculopathy with similar-appearing intimal thickening consisting of fibrotic, collagen-rich, hypocellular matrix with adventitial thickening and fibrosis in both the stented and the non-intervened artery. 4) Immunohistochemical CD-68 staining (positive reaction color is brown) showing macrophage infiltration in both stented segment neointima (A) and non-intervened allograft vasculopathy (B). Photomicrographs (Verhoeff tissue elastin stain) of the circumflex artery stent (C) and non-intervened, marginal branch (D) of Case 2, and high-power view of the in-stent restenosis neointima (C’); both in-stent restenosis and marginal branch transplant vasculopathy demonstrate similar fibrotic hypocellular neointima proliferation.