Detection of early changes in the coronary artery microstructure after heart transplantation: A prospective optical coherence tomography study.

ABSTRACT

BACKGROUND: Optical coherence tomography (OCT) enables in-vivo cardiac allograft vasculopathy (CAV) microstructure characterization. Early coronary artery microstructure changes after heart transplantation (HTx) may provide valuable mechanistic information regarding CAV development. Our in this study was to describe and characterize changes in the coronary artery microstructure during the first year after HTx using serial OCT scans. METHODS: Twenty-six patients were enrolled at routine baseline coronary angiography 3 months after HTx. Coronary OCT scans were performed on all 3 major vessels at baseline and were repeated 12 months after HTx. We contoured the vessel layers for absolute and relative measurements. Lipid plaques, calcified plaques, layered fibrotic plaques (LFPs) and bright spots were analyzed by delineating circumferential borders and measuring angulation of total circumference. RESULTS: A total of 8,789 frames from 71 vessels were analyzed after 3 and 12 months (vessel length 79 ± 24 mm vs 82 ± 23 mm, respectively, p = 0.39). Mean intima area increased by 20% from 3 months to 12 months (1.6 [1.2 to 2.7] mm2 vs 1.9 [1.3 to 3.2] mm2, p < 0.0001). Mean lumen area decreased by 2% (9.1 [7.5 to 11.6] mm2 vs 8.9 [6.9 to 10.9] mm2, p < 0.01). LFPs showed an almost 5-fold increase at follow-up (1.0% [0% to 6.5%] vs 4.8% [0% to 24.5%], p < 0.0001). Bright spots were also detected more frequently at 12 months (0% [0% to 2.8%] vs 0.8% [0% to 6.8%], p < 0.001). We found no significant difference in extent of lipid plaque (p = 0.78) or calcified plaque (p = 0.37) during follow-up. The intima area change and LFP progression during follow-up correlated strongly (r2 = 0.51, p < 0.0001). CONCLUSIONS: Early CAV formation during the first year after HTx is characterized by a pronounced intima layer thickening strongly associated with LFP progression. In contrast, the extent of lipid plaque and calcifications remained stable. LFP formation may be a key mechanism in CAV.