In my last post, I suggested that, for high Lp(a) sufferers, a focus solely on Lp(a) volume and Lp(a) particle number was based on a specific concept of the mechanism by which Lp(a) does harm. That is, Lp(a) does harm to the cardiovascular system by being “sticky” and adhering ITSELF to injured artery walls.
But are there other ways that Lp(a), and perhaps even low Lp(a), does harm? Before we think about that question, some background is in order.
- Apo(a) and LDL attach to each other to form Lp(a). (See the graphic in the first post of this thread.)
- Lp(a) attaches itself to artery walls
One interesting question is this… Do these two attachments take place through the same mechanism? I believe the answer is no but I’m not 100% certain about this.
Notice, however, that there is nothing about these two attachment types that imply anything other than that Lp(a) volume and particle number need to be measured.
But suppose there was a 3rd type of attachment related to Lp(a) that was significant.
The main thrust of the article is stated in the abstract:
Lp(a), via its apo(a) moiety, is a ligand for the ?2-integrin Mac-1, thereby facilitating inflammatory cell recruitment to atherosclerotic plaques. These observations suggest a novel mechanism for the atherogenic properties of Lp(a).
To express in more accessible English, the study posits that Lp(a) is dangerous not just because it attaches to the artery wall itself. Instead, it may even be mostly dangerous because inflammatory cells get “recruited” or “attached” to Lp(a) such that when Lp(a) becomes attached to or penetrates an artery wall, these other inflammatory cells are dragged along with Lp(a) to make the atherosclerotic condition even worse.
Now stop and think about this for a moment and the implications for assessing our Lp(a) risk state.
The implication of this study is that merely measuring Lp(a) volume and Lp(a) particle number doesn’t get at what the additional danger of Lp(a) might be. Why? Well, because those two measures of Lp(a) don’t include a measure of the volume of inflammatory material that has been “recruited” by Lp(a) and is then dragged into the artery wall along with Lp(a).
Get it? Believe me I understand that this is hard to get your head around the first time. I’ve pasted in a diagram below that is taken from the study that makes it all a bit clearer.
In some future posts, I’ll continue to explore some of the findings of the study as well as some implications of this 3rd sort of “stickiness” that Lp(a) seems to have. The 3rd sort of “stickiness” being it’s “recruitment” of inflammatory cells.
– cross posted at TrackYourPlaque.com