A prospective natural history study of coronary atherosclerosis following liver transplantation.

Autor: Koshy AN; Department of Cardiology, Austin Health, Melbourne, Victoria, Australia; The University of Melbourne, Parkville, Victoria, Australia., Nerlekar N; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Gow PJ; The University of Melbourne, Parkville, Victoria, Australia; Victorian Liver Transplant Unit, Austin Hospital, Melbourne, Victoria, Australia., Lim R; The University of Melbourne, Parkville, Victoria, Australia; Department of Radiology, Austin Health, Melbourne, Victoria, Australia., Smith G; The University of Melbourne, Parkville, Victoria, Australia; Department of Radiology, Austin Health, Melbourne, Victoria, Australia., Galea M; Department of Radiology, Austin Health, Melbourne, Victoria, Australia., Rodrigues TS; Department of Cardiology, Austin Health, Melbourne, Victoria, Australia., Lim HS; Department of Cardiology, Austin Health, Melbourne, Victoria, Australia; The University of Melbourne, Parkville, Victoria, Australia., Teh AW; Department of Cardiology, Austin Health, Melbourne, Victoria, Australia; The University of Melbourne, Parkville, Victoria, Australia., Farouque O; Department of Cardiology, Austin Health, Melbourne, Victoria, Australia; The University of Melbourne, Parkville, Victoria, Australia. Electronic address: omar.farouque@austin.org.au.
Jazyk: angličtina
Zdroj: Atherosclerosis [Atherosclerosis] 2022 Mar; Vol. 344, pp. 40-48. Date of Electronic Publication: 2022 Jan 30.
DOI: 10.1016/j.atherosclerosis.2022.01.020
Abstrakt: Background & Aims: Cardiovascular disease remains a leading cause of mortality following liver transplantation (LT). Whether it may be partially attributable to accelerated development of subclinical coronary artery disease is unclear. We sought to assess the longitudinal effect of LT on coronary plaque burden.
Methods: A prospective observational study was conducted in 30 asymptomatic patients who underwent computed tomographic coronary angiography (CTCA) pre- and a median 4-years following LT. Serial changes were quantified using coronary artery calcium score (CACS) and semi-quantitative CTCA scores, in a blinded fashion. High-risk plaque (HRP) characteristics were also assessed. Plaque progression was defined using prognostically significant cut-offs.
Results: In the study population (age 59.8 ± 8 years, 80% male), 93 of 459 coronary segments had plaque at baseline. On follow-up CTCA, 68 (+73.1%) new lesions appeared in segments without plaque initially. Nineteen (63.3%) patients demonstrated a clinically significant rise in plaque burden on CACS and semi-quantitative indices on CTCA (all p<0.001). CAD-RADS score rose to ≥4 (≥70% stenosis) in 9 (30%) patients, necessitating ischemia-guided revascularization in 3 (10%) patients. While the absence of coronary calcification or plaque pre-LT was protective, presence of HRP and development of post-transplant metabolic syndrome were both strong independent predictors of atherosclerosis progression.
Conclusions: Our findings suggest that LT is associated with early progression of coronary atherosclerosis. Accelerated progression was noted particularly in those with HRP and post-transplant metabolic syndrome. Understanding the mechanisms of this novel observation and the potential role of preventive cardiovascular therapies in this population merit further study.
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Databáze: MEDLINE