Abstract 13326: Multilayer Appearance as a Finding of Mural Thrombosis is Associated with Subsequent Plaque Progression in Cardiac Transplant Patients
Background: Cardiac allograft vasculopathy (CAV) is a major limitation to long-term survival following heart transplantation. The pathogenesis of CAV remains to be established although multiple mechanisms may play a role.
Method: We performed a retrospective serial analysis in 132 cardiac transplant recipients undergoing gray-scale and virtual histology intravascular ultrasound (VH-IVUS) imaging of left anterior descending artery during routine annual follow-up. All patients had at least two serial IVUS imaging, and the first (baseline) and last (follow-up) IVUS images were analyzed. The study subjects were divided into two groups based on the presence of multilayer appearance (Figure A) at baseline IVUS.
Results: At baseline, patients with multilayer appearance (ML [+] group, n=38) had a longer time elapsed since transplantation (6.5 [2.0, 9.2] vs. 2.0 [0.2, 5.3] years, p<0.01), larger external elastic membrane volume (p<0.01) and plaque volume (p<0.01) than those without ML (ML [-] group, n=94). Intraluminal thrombi (n=11) and plaque ruptures (n=5) were identified in ML (+) group, but not in ML (-) group (p<0.01). After median follow-up of 3.0 (2.0, 4.0) years, the positive changes of plaque volume (p=0.02, Figure B) and the negative changes of lumen volume were greater in ML (+) group compared with ML (-) group. The changes of necrotic core volume and dense calcium volume were greater in ML (+) group (p<0.01 for both). Subsequent multilayer formation (55% vs. 23%, p<0.01), intraluminal thrombus formation (16% vs. 4%, p=0.02), and subsequent plaque ruptures (16% vs. 1%, p<0.01) were more frequently observed in ML (+) group.
Conclusions: The observation of a multilayer appearance, which may be indicative of repeated episodes of mural thrombosis, was not infrequently identified in asymptomatic cardiac transplant recipients. This finding may be associated with morphological features of vulnerable plaques and possibly contributes to progression of CAV.
- © 2012 by American Heart Association, Inc.