Elevated lipoprotein(a) levels—a known driver of arterial disease—are also consistently associated with an increased risk of venous thromboembolism (VTE), according to a retrospective cohort study from the Mayo Clinic.
Mayo Clinic Study Connects Lipoprotein(a) to Venous Clots
Researchers found that patients with Lp(a) levels of 50 mg/dL or higher faced a higher incidence of deep vein thrombosis and pulmonary embolism, suggesting that this lipid particle may play a more significant role in venous health than previously recognized.
Analyzing Data From Nearly 70,000 Patients
The study, published in JAMA Cardiology, analyzed data from the Mayo Clinic Enterprise between 1997 and 2026 to determine if elevated Lp(a) tracks with venous events.
Out of 69,214 patients included in the cohort, 19,553 individuals—or 28.3%—had Lp(a) levels at or above the 50 mg/dL threshold.
During the follow-up period, 1,492 patients (2.2%) experienced incident VTE. The crude VTE rate was 2.8% for those with elevated Lp(a), compared to 1.9% for those with lower levels.
Adjusted Odds Reveal Clear Association With DVT and PE
After adjusting for variables, the research team identified a clear association between higher Lp(a) levels and both deep vein thrombosis (DVT) and pulmonary embolism (PE).
Specifically, the adjusted odds ratio for VTE was 1.36, with similar findings for DVT (1.33) and PE (1.33).
Risk Scales With Higher Concentrations
The investigation revealed that risk scales with the concentration of the lipoprotein.
For every 10 mg/dL increase in Lp(a), the adjusted odds ratio for VTE rose by 1.05. This trend remained consistent even after researchers excluded patients with active cancer or major thrombophilia, suggesting the risk is not exclusively driven by conditions already known to cause hypercoagulability.
When researchers examined higher thresholds, the effect sizes grew more pronounced. Patients with Lp(a) levels of 100 mg/dL or higher showed an adjusted odds ratio of 1.74, while those with levels of 150 mg/dL or higher reached an adjusted odds ratio of 2.66.
Methodological Limits and Clinical Implications
Luke Dreher, an internal medicine resident in the department of cardiovascular medicine at Mayo Clinic Arizona, and his colleagues acknowledged several limitations in their research.
The study relied on a retrospective design and data from a tertiary care setting where Lp(a) testing was clinically triggered rather than standardized. The cohort was predominantly white, and outcomes were identified through text-based documentation rather than direct clinical adjudication.
Despite these constraints, the investigators concluded that the association is distinct. The researchers suggest that as new Lp(a)-lowering therapies move toward clinical application, future trials should consider tracking venous outcomes alongside traditional arterial events to better understand the full spectrum of risk associated with this lipoprotein.