Key result
Elevated Lp(a) ≥ 90 mg/dL linked to ~62% higher incidence of cardiac allograft vasculopathy.
Why the study?
It was unclear what role Lp(a) plays in cardiac allograft vasculopathy development and how it interacts with other lipids after heart transplantation.
Does elevated Lp(a) ≥ 90 mg/dL increase the risk of developing cardiac allograft vasculopathy in adult heart transplant recipients?
Cohort (n=504)
No
Does elevated Lp(a) ≥ 90 mg/dL increase the risk of developing cardiac allograft vasculopathy in adult heart transplant recipients?
Absolute Event Rate: 15.2% vs 9.4%
p-value: p=0.031
Elevated Lp(a) ≥ 90 mg/dL is associated with an increased risk of developing cardiac allograft vasculopathy in heart transplant recipients, particularly among those with well-controlled LDL levels (≤ 100 mg/dL).
May inform CAV risk stratification post-transplant; leaves open whether Lp(a) lowering modifies vasculopathy incidence.
Background Cardiac allograft vasculopathy (CAV) is the leading cause of late graft failure and mortality after heart transplantation (HT). Among non-HT patients, elevated Lp(a) levels are associated with increased atherosclerotic cardiovascular disease (ASCVD) risk. However, it is less clear what role Lp(a) may play in the development of CAV and how it interacts with other lipids post-transplant. Objectives We sought to examine the association between elevated Lp(a) and CAV among adult HT recipients at a single high-volume heart transplant center. Methods We performed a retrospective analysis of 504 adult HT recipients followed at the transplant center who had undergone coronary angiography for CAV evaluation within 5 years post-transplant. Maximum Lp(a) values and lipid panels obtained concurrently were collected. Patients were considered to have CAV if they had CAV 1 or higher by ISHLT grading on any coronary angiography obtained within 5 years post-transplant. Results In our cohort, 114 patients developed CAV. Among all patients who developed CAV, there was a significant difference in 5-year incidence rate of CAV when stratified by Lp(a) ≥ 90 mg/dL or < 90 mg/dL. The incidence of CAV was 9.4 per 100 person/years in the lower Lp(a) group versus 15.2 per 100 person/years in the higher Lp(a) group (p=0.031). Kaplan-Meier plots of CAV-free survival showed a significant association between CAV-free probability and Lp(a) ≥ 90 mg/dL (p=0.037). After stratifying Kaplan-Meier plots by LDL, the relationship between Lp(a) ≥ 90 mg/dL and CAV-free probability remained significant (p=0.012) among patients with LDL ≤ 100 mg/dL but was no longer significant (p=0.85 in patients with LDL > 100 mg/dL. Among patients with LDL ≤ 100 mg/dL, the Cox model results suggested higher Lp(a) levels increase the risk of developing CAV after HT (HR 1.35, 95% CI 1.03-1.76, p=0.03). Conclusions Among post-HT patients, Lp(a) ≥ 90 mg/dL was associated with increased risk for development of CAV, particularly at lower LDL levels. In patients with LDL ≤ 100 mg/dL, Lp(a) ≥ 90 mg/dL was associated with CAV-free survival. Lp(a) may be a useful biomarker for risk stratification in transplant patients and a potential future target for CAV prevention with emerging Lp(a) therapeutics.
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Cao et al. (2025) conducted a cohort in Cardiac allograft vasculopathy (n=504). Elevated Lipoprotein(a) (≥ 90 mg/dL) vs. Lipoprotein(a) < 90 mg/dL was evaluated on Incidence of cardiac allograft vasculopathy (CAV) per 100 person-years (p=0.031). Elevated Lp(a) ≥ 90 mg/dL was associated with a significantly higher incidence of cardiac allograft vasculopathy compared to Lp(a) < 90 mg/dL (15.2 vs 9.4 per 100 person-years).
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