Key result
Elevated Lp(a) ≥/dL is linked to ~27% higher risk of incident carotid plaque.
Why the study?
The long-term association between lipoprotein(a) levels and the continuum of carotid atherosclerosis from plaque initiation to stenosis in a general population was unclear.
Do elevated lipoprotein(a) levels associate with incident carotid plaque and progression to carotid stenosis in a general population free of cardiovascular disease at baseline?
Cohort (n=3,272)
Do elevated lipoprotein(a) levels associate with incident carotid plaque and progression to carotid stenosis in a general population free of cardiovascular disease at baseline?
Elevated lipoprotein(a) ≥ 50 mg/dL serves as a robust marker for long-term cardiovascular risk, strongly associating with the continuum of carotid atherosclerosis from plaque initiation to severe stenosis.
Answers are grounded in this paper and cite their sources.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Our findings suggest that elevated Lp(a) is associated with the continuum of carotid atherosclerosis, from plaque initiation to luminal stenosis. Measuring Lp(a) may help identify individuals at an increased lifetime risk of atherosclerosis beyond conventional cardiovascular risk factors.”
Lp(a) was associated with carotid plaque progression; leaves open whether Lp(a) lowering alters stenosis risk in Japanese adults.
AIMS: The aim of this study was to investigate the long-term association between lipoprotein(a) [Lp(a)] and the longitudinal continuum of carotid atherosclerosis, from initial plaque formation to progression to carotid stenosis, in a prospective study of a general Japanese population. METHODS AND RESULTS: We studied 3272 participants in the Suita Study (mean age: 58.0 ± 11.5 years; 57.9% women) who were free of cardiovascular disease and carotid plaque at baseline (1995-2004). Follow-up carotid ultrasonography was performed biennially until June 2016. Incident carotid plaque was defined as a maximal intima-media thickness (IMT) ≥ 1.7 mm in the entire carotid artery. Progression from plaque to stenosis was defined as ≥50% stenosis in participants who developed plaques. We employed Cox proportional hazards models for incident plaques, linear mixed-effects models for annual IMT changes, and logistic regression for progression to stenosis. During a median follow-up of 11.5 years, 1432 participants developed carotid plaques. Compared with Lp(a) < 15 mg/dL, the multivariable-adjusted hazard ratio for incident plaque was 1.27 [95% confidence interval (CI), 1.01-1.61] for Lp(a) ≥ 50 mg/dL. Participants with Lp(a) ≥ 50 mg/dL had significantly accelerated annual progression of maximal IMT (β = 0.014 mm/year; 95% CI, 0.003-0.025) compared with those with Lp(a) < 15 mg/dL. Furthermore, high Lp(a) levels were associated with progression to ≥50% carotid stenosis (multivariable-adjusted odds ratio, 2.29; 95% CI, 1.15-4.57). CONCLUSION: Elevated Lp(a) levels (≥ 50 mg/dL) were associated with the longitudinal continuum of carotid atherosclerosis, from plaque initiation to advanced stenosis. These findings suggest that high Lp(a) levels serve as a robust marker for long-term cardiovascular risk accumulation, highlighting the importance of screening and potential targeted interventions in individuals with Lp(a) ≥ 50 mg/dL.
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Teramoto et al. (2026) conducted a cohort in Carotid atherosclerosis (n=3,272). Elevated Lipoprotein(a) [Lp(a) ≥ 50 mg/dL] vs. Lp(a) < 15 mg/dL was evaluated on Incident carotid plaque (HR 1.27, 95% CI 1.01-1.61). Elevated lipoprotein(a) ≥/dL was associated with increased risk of incident carotid plaque and progression to stenosis.
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