Atherogenic Dyslipidemia After Liver Transplantation: Mechanisms and Clinical Implications

Cardiovascular disease (CVD), particularly atherosclerosis-associated CVD, is a major cause of long-term mortality after liver transplantation (LT). The liver is central in lipid homeostasis, and changes associated with insulin resistance, weight gain, adipose tissue inflammation, and development of nonalcoholic fatty liver disease (NAFLD) after LT promote atherogenesis. These factors synergistically alter lipid homeostasis, thereby leading to the production of proatherogenic lipoproteins, which contribute to the heighted risk of CVD-associated events observed in LT recipients. Although the exact mechanism promoting this shift of a proatherogenic lipoprotein profile is currently not known, the choice of immunosuppression and preexisting metabolic risk factors (ie, NAFLD) are likely contributors. This shift in proatherogenic lipoprotein subparticles presents clinical challenges as the traditional lipid profile employed in clinical practice may not fully capture this atherogenic risk. This review focuses on lipoprotein metabolism and atherogenesis in LT recipients.