Treating High Lp(a): A Risk Factor For Atherosclerosis

“Treatment for High Lp(a) Risk
Factor for Atherosclerosis” What could help 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%. 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 with 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. And 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% 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 were high then 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 1000-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%
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 progression 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. And we’ll explore the role
diet can play, next.
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