Five-year longitudinal assessment of cardiac allograft vasculopathy after heart transplantation using optical coherence tomography

Introduction The American Heart Association (AHA) has described the progression of atherosclerosis; however, cardiac allograft vasculopathy (CAV) after heart transplantation (HTx) develops through a distinct process influenced by immune-mediated inflammation. Unlike the gradual lipid-driven changes seen in atherosclerosis, CAV often progresses diffusely and rapidly. Long-term studies are valuable for understanding these unique morphological changes. Optical coherence tomography (OCT) enables both quantitative and qualitative assessments of coronary vessel morphology, providing detailed insights beyond those offered by conventional imaging modalities. Features such as layered fibrotic plaque (LFP), superficial macrophage infiltration (bright spot), and vasa vasorum can be visualized with high resolution, enabling a comprehensive evaluation of CAV progression. Purpose This study aimed to evaluate long-term morphological changes of CAV using serial OCT imaging over 5 years post-HTx. Methods In this single-center longitudinal study, ten HTx recipients (8 males, 2 females; mean age: 42 years) underwent OCT imaging beginning at 1-year post-HTx and were followed annually for 5 years. Patients were stratified by their 1-year post-HTx angiographic CAV grade: no-CAV group (grade 0; N=5) and CAV group (grades 1–3; N=5). Serial cross-sectional OCT images of the left anterior descending artery were analyzed at 1-mm intervals. Coronary lesions were categorized as mild intimal thickening (IT) (<500 µm), severe IT (≥500 µm), fibrous plaque, calcification, or fibroatheroma. Qualitative features of inflammation and vascular remodeling, including LFP, bright spots, and vasa vasorum, were also assessed. Results Although the number of coronary risk factors did not significantly differ between the groups, the median donor age was higher in the CAV group (no-CAV: 35 years vs. CAV: 50 years, P=0.03). At 1 year post-HTx, the no-CAV group predominantly exhibited mild IT, whereas the CAV group showed a higher prevalence of fibroatheroma and inflammatory features, including LFP and bright spots. During the 5-year follow-up, patients in the no-CAV group showed minimal morphological progression. In the CAV group, plaque burden did not significantly increase with optimal clinical management, including controlled lipid levels (median LDL-cholesterol at 5 years: no-CAV: 51 mg/dL vs. CAV: 26 mg/dL; P=0.55) and immunosuppressant therapy. Nevertheless, the persistence of LFP and bright spots indicated ongoing inflammatory activity despite clinical interventions. Conclusion The present 5-year longitudinal OCT study demonstrated that CAV progresses through an early inflammatory process with lesions that may persist over time. However, CAV lesion progression appeared to be minimized when considering the initial atherosclerotic burden, suggesting that clinical management may contribute to stabilizing vascular changes after HTx.