Statins
Lp(a) does not predict coronary plaque progression during intensive statin therapy, a SATURN substudy of 915 patients (Atherosclerosis 2017)
Original title: Lipoprotein(a) and coronary atheroma progression rates during long-term high-intensity statin therapy: Insights from SATURN
This analysis of the SATURN trial (comparing rosuvastatin 40 mg with atorvastatin 80 mg over 24 months using serial intravascular ultrasound) measured baseline and follow-up Lp(a) in 915 of 1039 participants (mean age 57.7 years, 74% men, 96% Caucasian) to test its relationship with change in coronary atheroma volume. Baseline LDL cholesterol fell from a median 114 to 60 mg/dL (P<0.001), while Lp(a) barely changed (17.4 to 16.5 mg/dL, P=0.31). At baseline, 676 patients had Lp(a) below 50 mg/dL (median 10.9 mg/dL) and 239 had Lp(a) at or above 50 mg/dL (median 83.2 mg/dL). Neither baseline nor on-treatment Lp(a) quartiles, nor Lp(a) risers versus non-risers, were associated with change in percent atheroma volume, regardless of achieved LDL cholesterol. The findings show that in coronary artery disease patients on long-term maximally intensive statin therapy with low on-treatment LDL cholesterol, Lp(a) levels do not predict coronary atheroma progression.
Original abstract
Background & Aims: Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL)-like particle that associates with major adverse cardiovascular events (MACE). We examined relationships between Lp(a) measurements and changes in coronary atheroma volume following long-term maximally-intensive statin therapy in coronary artery disease patients.
Methods: Study of coronary atheroma by intravascular ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. Baseline and follow-up Lp(a) levels were measured in 915 of the 1039 SATURN participants, and were correlated with changes in percent atheroma volume (ΔPAV).
Results: Mean age was 57.7 ± 8.6 years, 74% were men, 96% were Caucasian, with statin use prior to study enrolment occurring in 59.3% of participants. Baseline [median (IQR)] LDL-cholesterol (LDL-C) and measured Lp(a) levels (mg/dL) were 114 (99, 137) and 17.4 (7.6, 52.9) respectively; follow-up measures were 60 (47, 77), and 16.5 (6.7, 57.7) (change from baseline: p < 0.001, p = 0.31 respectively). At baseline, there were 676 patients with Lp(a) levels <50 mg/dL [median Lp(a) of 10.9 mg/dL], and 239 patients with Lp(a) levels ≥ 50 mg/dL [median Lp(a) of 83.2 mg/dL]. Quartiles of baseline and follow-up Lp(a) did not associate with ΔPAV. Irrespective of the achieved LDL-C (<vs. ≥70 mg/dL), neither baseline nor on-treatment (<vs. ≥median) Lp(a) levels significantly associated with ΔPAV. No significant differences were observed in ΔPAV in Lp(a) risers versus non-risers, nor in those patients with baseline or on-treatment Lp(a) levels <vs. > 50 mg/dL.
Conclusions: In coronary artery disease patients prescribed long-term maximally intensive statin therapy with low on-treatment LDL-C levels, measured Lp(a) levels (predominantly below the 50 mg/dL threshold) do not associate with coronary atheroma progression. Alternative biomarkers may thus associate with residual cardiovascular risk in such patients.
plaque imagingrisk predictionstatins
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.