What Level of Lipoprotein(a) Relates to a High Risk of Heart Events?

There is growing discussion of the need to screen everyone at least once for the genetic lipoprotein called Lipoprotein(a) or Lp(a). Even children should be screened once.

At the KAHN CENTER, we specialize in the assessment and management of Lp(a) and see many patients from across the globe.

Many people panic when they learn they have inherited Lp(a) yet only some persons develop premature atherosclerosis and aortic valve calcific stenosis. Is there a level of Lp(a) in the blood that predicts a higher risk of cardiac events?

STUDY

For the study, the researchers analyzed blood samples from 20,070 adults ages 40 years and older who had participated in three large U.S. National Institutes of Health (NIH) trials: the ACCORD, PEACE, and SPRINTTrusted Source.

Researchers presented the findings at the Society for Cardiovascular Angiography & Interventions (SCAI) 2026 Scientific Sessions and Canadian Association of Interventional Cardiology/Association Canadienne de cardiologie d’intervention (CAIC-ACCI) Summit in Montreal.

The average age of participants was roughly 65 years, and about 65% were male. Individuals were grouped based on their Lp(a) levels, ranging from low (less than 75 nanomoles per liter) to very high (equal or more than 175 nmol/L), and whether or not they had existing heart disease.

Over a median follow-up period of nearly 4 years, the team tracked major adverse cardiovascular events (MACE), including heart attack, stroke, and cardiovascular death. Overall, about 7.3% of participants experienced a MACE during the study period.

Notably, they found that individuals with Lp(a) levels of 175 nmol/L or higher had a significantly higher risk of cardiovascular death and stroke. The increased risk was particularly pronounced in those who already had cardiovascular disease.

The MACE rate over a median follow-up of 4 years was 7.3% in the overall cohort. This rate was consistent across Lp(a) levels of < 75, 75-125, and 125-175 nmol/L. In the group with levels of ≥ 175 nmol/L, however, the MACE rate was 8.1%.

Adjusted Kaplan-Meier survival curves confirmed that at mean follow-up of 4 years, those with an Lp(a) of ≥ 175 nmol/L had lower MACE-free survival compared with the group with an Lp(a) of < 75 nmol/L, with a more pronounced effect in those with versus without existing CVD (HR 1.30; 95% CI 1.07-1.57 vs HR 1.18; 95% CI 0.91-1.54).

In multivariable analysis modeled for MACE over 7 years, an Lp(a) of ≥ 175 nmol/L was independently associated with higher risk, with a hazard ratio that approached that of current smokers after accounting for age, gender, history of MI, total cholesterol, antihypertensive and lipid-lowering therapies.

Another analysis of Lp(a) as a continuous variable showed a steep increase in MACE risk beginning at levels > 125 nmol/L and continuing to the highest degree of risk for Lp(a) of ≥ 175 nmol/L.

In subgroup analyses of patients with and without CVD, the association between Lp(a) and MACE was more robust, and it was statistically significant in the secondary prevention cohort (P = 0.008) but not in the primary prevention cohort (P = 0.210)

CONCLUSIONS

At the KAHN CENTER, patients with an elevated Lp(a) get vascular imaging consisting of a carotid IMT ultrasound and either a coronary artery calcium score (CACS) or a AI coronary CT angiogram (CCTA) or both. We do see many patients with no atherosclerosis or valve disease despite a very high level of Lp(a).

The approach to patients with Lp(a) should be individualized based on the extent of atherosclerosis and valvular disease. Many patients may need only lifestyle, aspirin 81 mg a day, and periodic follow-up and reassessment.

Author

Dr. Joel Kahn

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