Related Experiment Video
Updated: Aug 10, 2026

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment
Published on: August 2, 2024
Association between lipoprotein (a) levels and cardiac allograft vasculopathy among heart transplant recipients:
Daniela Bacich1, Enrico Giuseppe Italiano1, Marika Faggioli1
1Cardiac Surgery Unit, Department of Cardio-Thoracic-Vascular Sciences and Public Health, Padova University Hospital, Padova, Italy.
Insights
Serum lipoprotein (a) [Lp(a)] levels were not linked to cardiac allograft vasculopathy (CAV) in heart transplant recipients. Further research is needed to understand the relationship between Lp(a) and CAV in this population.
Area of Science:
- Cardiology
- Transplantation Immunology
- Clinical Biochemistry
Background:
- Serum lipoprotein (a) [Lp(a)] is a known risk factor for atherosclerotic cardiovascular disease.
- The association between Lp(a) and cardiac allograft vasculopathy (CAV) in heart transplant (HT) recipients is not well-established.
Purpose of the Study:
- To determine Lp(a) levels in HT recipients.
- To evaluate the correlation between Lp(a) levels and the presence/severity of CAV.
Main Methods:
- Retrospective observational cohort study of 271 adult HT recipients.
- Lp(a) concentration measured at follow-up.
- Comparison of Lp(a) levels between patients with and without CAV (grades 0-1 vs. 2-3).
Main Results:
- Median Lp(a) was 40 nmol/L; 23% had Lp(a) >125 nmol/L.
- No significant difference in median Lp(a) between CAV grades (37 vs. 55 nmol/L, P=.408).
- High Lp(a) levels were not associated with CAV 2-3 (multivariate HR 1.02, P=.977); older donor age was linked to CAV (P=.009).
Conclusions:
- Elevated serum Lp(a) levels are not associated with CAV presence or severity in HT recipients.
- The role of Lp(a) in CAV requires further investigation due to the study's sample size.
Background:
Serum lipoprotein (a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease in the general population, but its association with cardiac allograft vasculopathy (CAV) development has not been firmly established.
Objective:
To assess the distribution of Lp(a) levels in heart transplant (HT) recipients and evaluate the correlation between Lp(a) levels and the presence and severity of CAV.
Methods:
A retrospective observational cohort study encompassing 271 adult HT recipients on regular outpatient follow-up in a tertiary center. Lp(a) concentration was assessed during the last follow-up visit and compared between patients with and without clinically significant CAV, International Society for Heart and Lung Transplantation (grade 2-3 vs 0-1).
Results:
Median serum Lp(a) concentration was 40 nmol/L; 62 patients (23%) had Lp(a) >125 nmol/L. Median Lp(a) levels did not significantly differ between patients with CAV 0-1 and patients with CAV 2-3 (median 37 vs 55 nmol/L, P = .408). High (>125 nmol/L) Lp(a) levels were not associated with CAV 2-3, neither on univariable nor on multivariable analysis (hazard ratio multivariate 1.02, 95% CI: 0.35-2.95, P = .977). Elevated Lp(a) concentrations (>75, >125, >200 nmol/L) did not show significant correlation with either CAV 2-3 nor with CAV 1-2-3. Older donor age was significantly related to CAV development (+1.018% increase of CAV for every year of increase of donor age, P value .009).
Conclusion:
Elevated serum Lp(a) levels were not associated with the presence and severity of CAV in patients with HT with long post-transplant follow-up. The relationship between Lp(a) and CAV warrants further investigation, given the small sample of the current study.