Lipoprotein(a) Testing: Who

What is lipoprotein(a) and why does it matter for heart health?

Lipoprotein(a) resembles low-density lipoprotein (LDL) cholesterol but carries an additional protein, apolipoprotein(a), attached to its surface. Epidemiological and genetic studies over many years have linked elevated Lp(a) to atherosclerotic cardiovascular disease and to calcific aortic valve disease. The particle is thought to contribute through several routes: delivering cholesterol into artery walls, carrying pro-inflammatory oxidized phospholipids, and possibly interfering with the breakdown of clots.

Unlike LDL cholesterol, Lp(a) concentration is determined mostly by variation in the LPA gene and changes little with diet, exercise or weight. Estimates suggest that around one in five people worldwide have levels high enough to be considered a risk enhancer. Because the level is largely fixed from early life, a single well-performed measurement usually tells you where you stand for life, which is why expert groups such as the European Atherosclerosis Society have advocated measuring it at least once in adulthood.

Who should get an Lp(a) blood test?

Guidelines in Europe and Canada support a once-in-a-lifetime Lp(a) measurement for adults, while US guidance has so far been more selective, focusing on people with a family history of early heart disease, a personal history of cardiovascular events despite good risk-factor control, or suspected inherited lipid disorders. Cascade testing of relatives is also reasonable when someone in a family is found to have a very high level, because the trait is inherited in a dominant pattern.

Many guidelines treat levels above roughly 50 mg/dL, or about 125 nmol/L, as increased risk, though assay units differ between laboratories and results should be interpreted with the lab's reference ranges. Clinicians should ask which unit is reported, because mg/dL and nmol/L values are not directly interchangeable.

What can you do if your Lp(a) is high?

Statins do not meaningfully reduce Lp(a), but they remain important because lowering LDL cholesterol reduces cardiovascular risk, including in people with high Lp(a). PCSK9 inhibitors lower Lp(a) modestly as a side effect of their main action, and lipoprotein apheresis is used in selected high-risk patients in some countries. Clinicians typically respond to a high result by setting more intensive LDL targets, controlling blood pressure, addressing smoking, diabetes and weight, and in some cases lowering the threshold for starting preventive therapy.

Several drugs designed to cut Lp(a) sharply, including antisense and small-interfering-RNA therapies, are in late-stage development. Results reported at the American Heart Association meeting showed that one such drug lowered the Lp(a) marker without a corresponding reduction in heart attack or stroke, raising questions about the best way to test the idea. Other trials with different agents are still underway, so the question of whether lowering Lp(a) improves outcomes is not yet fully answered. Until then, testing remains valuable mainly for risk stratification.