What might cause Lp(A) to go from low 200s to low 300s over the course of a year? No real change in diet, exercise, weight, etc., but started on statins and ezetimibe. I had thought Lp(a) should be constant. Same lab.
Over the past nine months rosuvastin was increased from 20mg to 40mg, total C, HDL and APO A-1 went down a bit, LDL went up a bit and non-HDL C was essentially unchanged. This was two different labs, but same scales.
Statins can increase Lp (a), typically by ~ 10% though there’s a huge range. Not really sure of the value with repeat testing of Lp(a) even when elevated. Rather, it’s more of a one and done type test that is used to guide the decision making process. I’m assuming the units are nmol/L and not mg/dL, as I’d be thinking about some other possible contributing factors going on.
The units are nmol/L. The question was motivated by my understanding that it’s a one and done test, because it’s genetic and shouldn’t change by much over time. An increase from 232 to 330 with a standard range of <75 seems a massive change. My guesses of things to look at that might cause a change would be diet, exercise, weight, possibly other drugs. With the exception of starting statins and ezetimibe, none of those has changed. Both tests were at the same lab.
What other possible contributing factors going on might have caused the change?
You can find a table listing variables with their impact on Lp(a) levels in table 1 in this paper: Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement - PMC
Based on what you’ve said here, given that nothing else you can think of has changed, it may indeed be related to the statin. However, in these situations the risk reduction conferred by statin-mediated apoB reduction typically outweighs any increase in Lp(a) levels, simply due to the respective differences in overall particle burden. Until Lp(a)-directed therapies are available, the alternative option to a statin would be a PCSK9 inhibitor, which would require further discussions with your physician (or, more likely, a lipid specialist, as not many generalists are going to be familiar with these details).
The only thing listed in table 1 that has changed is statins, which the table notes “May slightly increase Lp(a) (but reports are heterogeneous)”. Very odd.
The statin increase was designed for risk reduction. However, since the increase numbers have gotten somewhat worse - LDL went up a bit, total C, HDL and APO A-1 went down a bit and non-HDL C was essentially unchanged. Also A1-C increased. Since you mentioned it, apoB was 60 (90 is borderline) in the latest test, but there was no prior test for comparison.
As you say, next step is a discussion with my cardiologist and I’m trying to be well informed and to be able to ask the right questions. A discussion regarding a PCSK9 inhibitor is clearly warranted.
Cardiologist can’t think of why Lp(a) would increase dramatically. “It shouldn’t happen”. Same lab as prior test. Very odd. None of the factors listed in the paper you linked are close to relevant. He said Lp(a) was a major topic at the recent AHA annual meeting.
I’ll cut rosuvastatin back to 20mg and continue ezetimibe. In January I’ll start the PCKS9 inhibitor Repatha (insurance issues) and discontinue ezetimibe. Repatha should help a bit with Lp(a) and significantly with LDL. More blood work after a few months to see if it helped. Then we’ll wait for new Lp(a) drugs to come out of clinical trials.
Sounds good - I’m glad your cardiologist is staying on top of things, including the recent AHA meeting.
This paper appears to stand for the proposition that high Lp(a) levels are not a serious risk if you have a CAC score that’s zero or low. Independent Association of Lipoprotein(a) and Coronary Artery Calcification With Atherosclerotic Cardiovascular Risk - ScienceDirect
What do you think?