It doesn’t get the attention that LDL “bad” cholesterol does, but another cholesterol-related particle called lipoprotein(a) can be an important signal of cardiovascular trouble down the road.
That’s the conclusion of a large study recently published in JAMA Cardiology. Researchers found that among nearly 28,000 initially healthy women, those with elevated levels of lipoprotein(a) were at increased risk of developing heart disease over the next 30 years. Meanwhile, women at the extreme end of the lipoprotein(a) spectrum—in the top 1 percent—were at heightened risk of not only developing heart disease but also suffering a stroke or dying of cardiovascular causes.
Those excess risks were seen regardless of whether the women had any of the better-known risk factors for cardiovascular disease, including high levels of LDL cholesterol. The findings, the researchers say, bolster the argument that most everyone should have their lipoprotein(a) level measured.
The lesser-known risk factor
Lipoproteins are tiny particles composed of different kinds of proteins and fat, and their main job is to transport cholesterol through the bloodstream to body cells. LDL (low-density lipoprotein) and HDL (high-density lipoprotein) are the two lipoproteins most people have heard of, since doctors routinely test for them. Most blood cholesterol is of the LDL variety.
LDL cholesterol is the “bad” form, because when you have too many LDL particles traveling through your blood, cholesterol can start to build up in the walls of the arteries, contributing to plaques that narrow and harden the vessels. HDL particles, in contrast, carry cholesterol to the liver to be removed from the body, which is why higher HDL is heart-healthy.
Lipoprotein(a), or Lp(a)—pronounced L-p-little a—looks very similar to an LDL particle, except that it contains a protein called apolipoprotein(a). But researchers have found that the effects of high Lp(a) may be even worse than those of high LDL: Too much Lp(a) can not only contribute to artery-clogging plaques, but also make blood more prone to clotting and increase inflammation in the blood vessels.
Considering all of that, it might seem like a no-brainer that doctors should test everyone’s Lp(a) levels. The main reason they don’t? There’s not much you can do if it’s elevated. A person’s Lp(a) blood level is almost entirely dictated by genetics, specifically the LPA gene that determines the precise makeup of apolipoprotein(a). So the Lp(a) level you had as a young child is probably the level you have now, and it’s unlikely to change much no matter how conscientious you are about diet and exercise.
That thinking around Lp(a) is changing, however. Recent studies have been clarifying the importance of Lp(a) as a unique cardiovascular risk factor, and several clinical trials are underway to test new Lp(a)-lowering treatments, as well.
What the new study adds
The findings are based on data from the Women’s Health Study, an ongoing research project that has tracked the health of a large group of U.S. women since 1993. All were age 45 or older and free of cardiovascular disease when they entered the study, at which point they had blood samples taken. Lp(a) was among the health metrics the researchers measured.
Over the next 30 years, just over 3,700 study participants developed heart disease, suffered a stroke, or died of a cardiovascular cause. And on average, those risks began to climb—in a stepwise manner—among women whose blood Lp(a) levels were 30 mg/dL or higher, or above the 75th percentile for the study group. Note: Lp(a) can be quantified in two different ways; see box below.
Among women with Lp(a) levels in the 30 to 60 range, the likelihood of developing cardiovascular disease was 16 percent higher compared to women with the lowest Lp(a) levels (less than 10). And when the researchers broke the data down further, women with Lp(a) in the 30 to 60 range were at somewhat higher risk of developing heart disease, but not of dying from it. Nor did they have an increased stroke risk.
The picture was different for women with very high Lp(a) levels (above 120), who showed a marked elevation in their likelihood of cardiovascular trouble. Compared to women with Lp(a) levels below 10, their risk of heart disease was 80 percent higher and their risk of stroke 41 percent higher. Meanwhile, their risk of dying from cardiovascular disease was nearly doubled.
Of course, many factors affect a person’s risk of cardiovascular disease. But the researchers took as many of those variables into account as they could, including the women’s LDL levels, blood pressure, smoking and alcohol habits, and whether they had a history of diabetes or ever used menopausal hormone therapy.
Even then, elevated Lp(a), itself, appeared to raise the long-term risk of cardiovascular disease.
The study did have limitations. It included only women, most of whom were white, so it’s unclear how well the findings might apply to men and people of other races. However, the overall pattern—high Lp(a) correlates with higher risks of cardiovascular disease—has been shown before in more diverse studies.
Who should be tested?
At the moment, there’s no universal definition for a concerning Lp(a) level. But the American College of Cardiology/American Heart Association (ACC/AHA) guidelines consider a level above 50 mg/dL (or ≥125 nmol/L) to be high. An estimated 20 percent of adults fall in that range.
While that’s a significant number of people, Lp(a) testing is often recommended only for certain groups, including people with a personal or family history of premature heart disease or stroke (before age 55 for men and before age 65 for women); those with a known family history of high Lp(a); those who have an inherited condition called familial hypercholesterolemia; and anyone who has high LDL cholesterol that does not respond to standard medication.
However, some guidelines call for broad Lp(a) testing. As of 2024, the National Lipid Association has been recommending a one-time Lp(a) blood test for all adults. (Because levels are generally stable throughout life, one-and-done would be enough.) The NLA considers Lp(a) levels above 50 to be “high risk,” and levels between 30 and 50 to be “intermediate risk.”
The takeaway. If you’ve never had an Lp(a) test, talk to your doctor about whether you should. Even though there are no specific medications for high Lp(a) just yet, knowing your number is still important. If it’s high, that might give you extra motivation to maintain heart-healthy habits like eating a largely plant-based diet and getting regular exercise.
In addition, your doctor might suggest more aggressive management of any other cardiovascular risk factors you have, like high blood pressure or diabetes. They might also recommend a statin, if you’re not already on one, to get your LDL cholesterol below 70. Although statins do not put a dent in Lp(a) levels, these drugs do lower the overall risk of heart disease and stroke.
At the very least, knowing your Lp(a) level arms you with information.
Lipoprotein(a) is measured either in milligrams per deciliter (mg/dL) or in nanomoles per liter (nmol/L). The JAMA Cardiology study reported values in mg/dL, which is also used by many labs. If you have had your Lp(a) tested, you may have received the results in nmol/L, however, and may wonder how your number compares to those in the study.
Because Lp(a) particle size varies among individuals, there is no exact universal conversion. But a commonly used approximation is that 1 mg/dL is about 2.5 nmol/L, so to convert from mg/dL to nmol/L, you multiply by 2.5 (conversely, to convert from nmol/L to mg/dL, divide by 2.5).
For example, 50 mg/dL—the level above which is considered “high” by the ACC/AHA—is approximately 125 nmol/L, while 120 mg/dL—the level at which risk started to markedly increase in the study—is approximately 300 nmol/L.




