Discoveries
The Case for Lp(a) Testing
Martha Gulati, MD, Anita Dann Friedman Chair in Women's Cardiovascular Medicine and Research
It’s time for a shift in how we assess cardiovascular risk. While hypertension, diabetes, smoking and high LDL cholesterol dominate clinical conversations, one equally important threat continues to be overlooked: lipoprotein(a), or Lp(a). This genetically inherited particle is a potent driver of heart disease—and yet most patients are never tested for it.
Lp(a), a unique and particularly dangerous form of cholesterol, acts as a carrier for inflammatory molecules, accelerates arterial plaque buildup and promotes clot formation, which can lead to plaque rupture and subsequent cardiovascular events. An estimated 20% of people worldwide have elevated Lp(a) levels, which are linked to increased risks of heart attack, stroke, aortic stenosis and peripheral artery disease.
Despite this clear connection, a recent study across six academic health systems in California found that fewer than 0.3% of adults undergo Lp(a) testing. Even among those with a family or personal history of heart disease, testing rates were less than 3.3% and 4%, respectively, which represents a massive gap in prevention efforts.
U.S. guidelines currently recommend Lp(a) screening only for individuals with a family history of early heart disease or those with established heart disease. Until recently, scientists measured Lp(a) in milligrams per deciliter (mg/dL), with normal levels falling below 30 mg/dL. Now, scientists view the number of Lp(a) particles in the blood, measured in nanomoles per liter (nmol/L), as a more accurate measurement. Normal levels of Lp(a) fall at or below 75 nmol/L.
Since 90% of Lp(a) is genetically determined, measuring Lp(a) is usually a one-time test. While it’s true that Lp(a) can’t be modified through diet and exercise, levels may fluctuate in response to menopause, chronic disease or certain medications. Women should be retested after menopause, when Lp(a) levels may increase, particularly if levels prior to menopause were borderline.
Currently, the only U.S. Food and Drug Administration-approved treatment for Lp(a) is apheresis, which is expensive, intensive and in short supply. But despite the lack of treatment options, assessing Lp(a) levels can help guide patient care. Patients with elevated Lp(a) may benefit from more aggressive LDL-lowering strategies, including statins, PCSK9 inhibitors and lifestyle modifications.
Promising therapies targeting Lp(a) are currently in clinical trials, including pelacarsen and olsparin, which aim to decrease Lp(a) production at the RNA level. If these therapies prove effective at reducing cardiovascular events, they will strengthen the case for Lp(a) testing.
While we don’t yet know if lowering Lp(a) translates to fewer cardiovascular events, we do know that identifying high-risk patients allows us to intervene earlier.”
— Martha Gulati, MD
Measuring Lp(a) is simple. It’s covered by insurance. And most importantly, Lp(a) test results help guide important conversations around lifestyle and risk-factor modifications.
While we don’t yet know if lowering Lp(a) translates to fewer cardiovascular events, we do know that identifying high-risk patients allows us to intervene earlier by tightening LDL control, adjusting treatment plans and empowering patients to make informed decisions about their health.
Cardiologists and primary care providers alike need to make Lp(a) testing a priority, not an afterthought. If we’re serious about cardiovascular prevention, we need to use all the tools in our toolbox.
