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What could explain severe coronary disease in someone considered to be at low cardiovascular disease risk with a healthy lifestyle? A young man ends up in the ER with a heart attack; ultimately found to have severe coronary artery disease, yet given his age, blood pressure, and cholesterol, his 10-year risk of a heart attack should only be like 2 percent. But what he did have was a high lipoprotein(a) level, also known as Lp(a), markedly high at 80, which may help explain it. You can see the same thing in women. A 27-year old with a heart attack with a high Lp(a). What is this Lp(a), and what can we do about it?
Lp(a) is an underestimated cardiovascular risk factor. It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur even in people without high cholesterol, because it is cholesterol. It’s basically an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But it has yet to gain recognition by practicing physicians.
The main reason for the limited clinical use of Lp(a) is the traditional lack of effective and specific therapies to lower it. Lp(a) concentrations are approximately 90 percent genetically determined, so the conventional thinking has been that you’re just kind of born with higher or lower levels, and there’s not much you can do about it. Even if that were the case, you still might want to know about it, since if it was high, that would be all the more reason to make sure all the other risk factors that you do have more control over are absolutely as good as possible––like maybe help you quit smoking, and do everything you can do lower your LDL cholesterol as much as possible.
Lp(a) levels in the blood can vary a 1,000-fold between individuals (from less than 0.1 mg/dL to a hundred or more). Here’s the graph of odds of heart disease at different levels. Less than 20 is probably optimal, with greater than 30-50 considered elevated. Even when the more conservative threshold of greater than 50 is used, that describes about 10-30 percent of the global population, an estimated 1.4 billion people. So, if we’re like the 1 in 5 people with elevated levels, what can we do about it?
The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There’s something called apheresis, which is basically like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and then give your blood back to you. And when you do that, you can reverse the progress of disease. Atherosclerosis continues to get worse in the control group, but better in the apheresis group. This is great for proving the role of Lp(a), but has limited clinical application, given the cost, accessibility, and the time commitment required for biweekly sessions of two to four hours each. It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, costing more than $50,000 a year. There has to be a better way. We’ll explore the role diet can play, next.
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