Abstract:
Introduction. Cardiovascular disease remains the leading cause of long-term mortality after heart
transplantation, largely driven by cardiac allograft vasculopathy (CAV) and accelerated
atherosclerosis. Dyslipidemia develops frequently in this population as a consequence of
immunosuppressive therapy and metabolic alterations. Glucocorticoids, calcineurin inhibitors
(especially cyclosporine), and mTOR inhibitors significantly disrupt lipid metabolism, promoting
elevations in total cholesterol, LDL-cholesterol (LDL-C), and triglycerides. Given this high-risk
profile, lipid management is a central component of post-transplant care. The aim of this review is to
synthesize recent evidence on the mechanisms, clinical implications, and management of dyslipidemia
after heart transplantation.
Materials and Methods: A narrative literature search was performed in the Hinari database, limited
to publications from the last 5 years. Search keywords included: statins after heart transplantation,
cardiac transplant dyslipidemia, statin-immunosuppressant interactions, statin safety in transplant.
Emphasis was placed on mechanisms of post-transplant hyperlipidemia, efficacy of statin therapy,
comparative safety profiles, and clinically relevant drug-drug interactions between statins and
immunosuppressive agents.
Results: Post-transplant dyslipidemia is multifactorial. Corticosteroids increase hepatic lipoprotein
synthesis and insulin resistance, while cyclosporine impairs LDL receptor activity, leading to
hypercholesterolemia. mTOR inhibitors (sirolimus, everolimus) elevate triglycerides, whereas
tacrolimus shows a more favorable lipid profile. According to the 2019 ESC/EAS guidelines,
transplant recipients are managed according to overall cardiovascular risk. Early initiation of statins
after heart transplantation improves survival and reduces the incidence and progression of cardiac
allograft vasculopathy (CAV), independent of baseline LDL-C levels. Statins are first-line therapy and
also provide pleiotropic endothelial and anti-inflammatory effects that may protect the graft. However,
significant pharmacokinetic interactions occur with CYP3A4-metabolized statins when combined with
cyclosporine or mTOR inhibitors, increasing myopathy risk. Therefore, pravastatin and rosuvastatin
are generally preferred, with careful dose titration and monitoring of liver enzymes and creatine kinase.
Conclusions: Dyslipidemia after heart transplantation requires proactive and individualized
management. Statins remain the therapeutic cornerstone, providing both cardiovascular and graftprotective benefits. Careful drug selection and monitoring are essential to balance efficacy with safety
in the context of complex immunosuppressive regimens.
