Lp(a)

Lipoprotein(a), Lp(a) for short, is an LDL particle with an extra protein attached to it, apolipoprotein(a). That protein closely resembles plasminogen, a protein that dissolves blood clots, and it gets in the way of that dissolving. As a result an Lp(a) particle does two things at once: it carries cholesterol into the artery wall, like any LDL particle, and it promotes inflammation and clotting at the spot where it lodges. How much Lp(a) you produce is set for more than 90 percent by a single gene. The value is largely fixed in early childhood and barely changes afterwards, not with diet, weight or exercise either. Because Lp(a) is an LDL particle, the cholesterol it carries counts in your total cholesterol and in your non-HDL, without appearing separately. A raised Lp(a) therefore stays invisible in an ordinary fat profile: it sometimes explains why someone with a tidy LDL still develops cardiovascular disease young, or why it runs strikingly often in a family. Your report shows Lp(a) as one number, in nmol/L or in g/L depending on your lab, and those units cannot be converted exactly; so read your result beside your own lab's threshold. The table further down sets those thresholds side by side.

A high Lp(a) raises the risk of a heart attack, a stroke and of narrowing of the aortic valve, and that link is causal: people with an inherited high Lp(a) get those diseases more often, independently of all their other risk factors. It is one of the few inherited risk factors you can see with a single blood test, and because the value is stable for life, that in principle needs doing only once. For anyone who wants to stay healthy that is the value of this test: knowing once whether you carry this trait, so that for the rest of your life you know how strict to be with the other risk factors. What you can do about the number itself is limited, and that is the honest side of this story. Lifestyle barely moves Lp(a), and there is no approved drug yet that lowers it specifically; drugs for that are being studied. What you can do, and what demonstrably reduces the risk, is tackle the rest of your risk more strictly: keep LDL low with food and exercise, a healthy blood pressure, no smoking, a healthy weight. That is why the European expert panel advises measuring Lp(a) once in every adult, while the Dutch guideline for now considers it only at moderately increased risk, in unexplained early vascular disease and with early cardiovascular disease in the family.

A high Lp(a) is almost always inheritance. Anyone who inherits a small variant of the apo(a) protein makes a lot of it; a large variant gives a low value. On top of that, an underactive thyroid, a pregnancy and kidney disease can raise the value temporarily or lastingly, and hormone therapy after the menopause or a liver disease can lower it. A low Lp(a) is not a problem and asks nothing of you. The European panel works with three bands: below 75 nmol/L (0.30 g/L) a raised Lp(a) is ruled out, above 125 nmol/L (0.50 g/L) it is established, and in between it counts alongside your other risk factors. Do not convert between nmol/L and g/L yourself; the factor differs from test to test. If your Lp(a) is high, the question shifts from this one number to the rest. Every bit of LDL you remove with food and exercise counts for more with a high Lp(a), because your artery wall already has more to bear; the same goes for blood pressure, smoking and weight. Statins do not lower Lp(a) and can even raise it slightly; that is no reason to stop them, because the benefit for your arteries far outweighs that. With a high Lp(a) the useful question is therefore not how to bring this one number down, but how low you keep the rest. And tell your family: the trait is inherited, and one test in a parent, brother or sister says a lot.