Key result
Serum Lp(a) levels fail to correlate with cardiac allograft vasculopathy severity after heart transplant.
Why the study?
Do elevated Lipoprotein (a) levels correlate with the presence and severity of cardiac allograft vasculopathy in heart transplant recipients?
Observational (n=271)
No
Do elevated Lipoprotein (a) levels correlate with the presence and severity of cardiac allograft vasculopathy in heart transplant recipients?
p-value: p=0.408
Elevated Lipoprotein (a) levels are common in heart transplant recipients but do not appear to be significantly associated with the presence or severity of cardiac allograft vasculopathy.
Background Serum lipoprotein (a) [Lp (a)] level is an independent, genetic causal risk factor for atherosclerotic cardiovascular disease in general population. Cardiac allograft vasculopathy (CAV) is a major cause of morbidity and mortality after heart transplantation (HT). The association of Lp (a) serum levels and CAV development has not been firmly established. Purpose To assess the distribution of Lp (a) levels in HT recipients and evaluate the possible correlation between Lp(a) levels and the presence and severity of CAV. Methods A retrospective observational study including adult HT recipients on regular outpatient follow up in a tertiary centre. Lp (a), lipid profile, prevalence of statin and other lipid lowering drugs prescription were assessed during the last follow-up visit. Routine coronary angiography had been performed one year after HT. Subsequently, CAV was assessed every 24-36 months with either coronary angiography or coronary computer tomography angiography. CAV was graded as 0, 1, 2 or 3 using the International Society For Heart And Lung Transplantation [ISHLT] Grading Scheme. We divided the cohort between patients with no CAV or mild CAV (ISHLT 0-1) and patients with moderate or severe CAV (ISHLT 2-3) Results Two hundred seventy-one HT patients were included. All patients underwent Lp (a) assessment at least one year after undergoing HT. Median time after HT for Lp (a) determination was 8 years (interquartile range 5-15 years). Basal characteristics of the study population are displayed in Table 1. Median serum Lp (a) concentrations were 40 nmol/l (interquartile range 14-107 nmol/l); 94 (35%) patients had Lp (a)>75 nmol/l, while 62 (23%) had Lp (a)>125 nmol/l (Figure 1). Out of the 271 patients, eleven had incomplete CAV surveillance data due to chronic kidney damage. Thirty-nine patients (15%) had developed CAV grade2 or 3 during follow up. Median time from HT to CAV 2-3 detection was 12 years (interquartile range 6-17 years). Mean Lp (a) levels did not differ between patients with CAV 0-1 (median 37 nmol/l, interquartile range 13-106 nmol/l) and patients with CAV 2-3 (median 55 nmol/l, interquartile range 20-102 nmol/l, p value 0.408). Patients with CAV 2-3 showed significantly lower LDL and total cholesterol levels, and more aggressive lipid lowering treatment at the last follow-up assessment. They were also more frequently treated with everolimus, due to therapy adjustments following CAV disclosure. No statistically significant differences in recipients pretransplant clinical characteristics were observed between the two groups. Conclusions Elevated Lp(a) levels (≥125 nmol/l) are common finding in HT patients (23%). In this cohort higher serum Lp (a) levels were not associated with the presence and severity of CAV during follow up. Further study in larger HT populations is warranted to verify these results.Serum Lp (a) concentrations
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Bacich et al. (2025) conducted an observational in Heart transplant (n=271). Serum Lipoprotein (a) levels was evaluated on Presence and severity of cardiac allograft vasculopathy (CAV) (p=0.408). Serum Lipoprotein (a) levels did not significantly differ between heart transplant recipients with moderate/severe versus none/mild cardiac allograft vasculopathy (55 vs 37 nmol/l; P=0.408).
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