Mechanisms
Lp(a) does not predict cardiac allograft vasculopathy in 385 heart transplant recipients, unlike graft rejection history (J Clin Lipidol 2025)
Original title: The association between lipoprotein(a) levels and the development of cardiac allograft vasculopathy
In a retrospective cohort of 385 patients who underwent heart transplantation between 2001 and 2023, preoperative Lp(a) concentration did not differ significantly between those who developed clinically significant cardiac allograft vasculopathy (CAV, grade 2-3) and those who did not (grade 0-1) (14.0 vs. 12.0 mg/dL, P = .42). High Lp(a) (50 mg/dL or above) was not associated with CAV development on either univariable or multivariable analysis (hazard ratio 1.009, 95% CI 0.47-2.14, P = .9). A history of graft rejection was the only independent predictor of CAV identified (hazard ratio 2.88, 95% CI 1.50-5.52, P = .001). The absence of an Lp(a)-CAV association, in contrast to Lp(a)'s established role in native-vessel atherosclerosis, supports the view that CAV is driven by distinct, largely immune-mediated pathophysiological mechanisms rather than classic atherogenic lipid pathways.
Original abstract
Lipoprotein(a) [Lp(a)] has been established as an independent risk factor for cardiovascular diseases. However, its role in cardiac allograft vasculopathy (CAV) development remains controversial. In a retrospective cohort study of 385 patients who underwent heart transplant between 2001 and 2023, Lp(a) concentrations were compared between patients with and without clinically significant CAV (grade 0-1 vs 2-3). Preoperative Lp(a) concentrations were not significantly different between patients with and without CAV (14.0 vs 12.0 mg/dL, P = .42). High (≥50 mg/dL) Lp(a) values were not associated with CAV development on univariable or multivariable analysis (hazard ratio [HR] 1.009, 95% CI: 0.47-2.14, P = .9). A history of graft rejection was the only independent factor associated with CAV (HR 2.88, 95 % CI: 1.50-5.52, P = .001). Elevated Lp(a) levels were not associated with increased risk of CAV. The lack of a significant association between traditional risk factors and CAV underscores that CAV is not purely an atherosclerotic process and different pathophysiological mechanisms are involved.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.