Key result
Elevated Lp(a) is linked to plaque burden but not adverse events in CAD.
Why the study?
It remains unclear whether lipoprotein(a) contributes to increased risk of adverse cardiovascular events in patients with established ASCVD.
Does elevated Lipoprotein(a) increase atherosclerotic plaque burden and long-term adverse cardiovascular events in patients with established coronary artery disease?
Observational (n=798)
Yes
Does elevated Lipoprotein(a) increase atherosclerotic plaque burden and long-term adverse cardiovascular events in patients with established coronary artery disease?
In patients with established coronary artery disease, elevated Lp(a) is associated with increased coronary plaque burden but does not significantly increase the risk of long-term MACE or mortality.
BACKGROUND & AIMS: Although lipoprotein(a) [Lp(a)] is an established independent risk factor for atherosclerotic cardiovascular disease (ASCVD) in primary prevention settings, it remains unclear whether Lp(a) contributes to an increased risk of adverse cardiovascular events in patients with established ASCVD. METHODS: The current analysis combines the ATHEROREMO and IBIS-3 observational studies, which together enrolled 798 patients undergoing coronary angiography for stable angina pectoris or acute coronary syndrome. Intravascular ultrasound (IVUS) and near-infrared spectroscopy were performed to assess coronary plaque characteristics in a non-culprit study segment. Regression models were applied to relate Lp(a) to coronary plaque characteristics and long-term (up to 10 year) clinical outcomes. Lp(a) was analysed both as a continuous and categorical variable (using 75 nmol/L and 125 nmol/L as threshold). RESULTS: Mean age of the patients was 61.6 years (10.8); 75% were male; 19% had elevated Lp(a) levels (>125 nmol/L). Patients with Lp(a) > 125 nmol/L had a significantly higher prevalence of hypercholesterolemia and prior percutaneous coronary intervention. These patients demonstrated higher IVUS-derived plaque burden (40.7% (±11.5) vs. 38.6% (±10.7), p = 0.028), though no associations were found with other plaque characteristics, e.g. minimum lumen area, lipid core burden index and thin-cap fibroatheroroma. No association was found between Lp(a) and -5-year major adverse cardiac events (HR 1.06, 95% CI: 0.70-1.60, p = 0.78) and 10-year all-cause mortality (HR 0.63, 95% CI: 0.38-1.06, p = 0.78). CONCLUSIONS: Among patients with established ASCVD, Lp(a) was associated with plaque burden, supporting evidence that relates Lp(a) to atherosclerotic disease. However, Lp(a) was not associated with long-term mortality or cardiac adverse events in these patients.
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Mira et al. (2026) conducted an observational in Coronary Artery Disease (n=798). Elevated Lipoprotein(a) (>125 nmol/L) vs. Lipoprotein(a) ≤125 nmol/L was evaluated on 5-year major adverse cardiac events (HR 1.06, 95% CI 0.70-1.60, p=0.78). Elevated Lp(a) >125 nmol/L was associated with higher coronary plaque burden (40.7% vs 38.6%, p=0.028) but not with 5-year major adverse cardiac events (HR 1.06; 95% CI 0.70-1.60; p=0.78).
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