Vascular Calcification The Real Story | Episode 51
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- Опубліковано 3 вер 2023
- We'll discuss the general process of vascular calcification and some common risk factors for this. How do smooth muscle cells in the blood vessel wall contribute to the process? And what about macrophages? How do statins affect calcification? What about CAC-scores? What would happen if you have a low score and started taking a statin? Which calcified plaques are at highest risk for rupture? Find out in this episode of vlmd rounds.
#atherosclerosis #ldl #cholesterol #calciumscore
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What you refers as micro calcification is commonly known as soft plaques, is that right? It is undetectable with CAC scans. But soft plaque may break off & form clots down stream, stroke, heart attack. Calcified plaque is more stable, so statin may raise CAC score but reduce risk. I can't take statin - bad painful cramps that go away as soon as I stop starins.
Because microcalcifications are very hard to see, they may be in soft plaques, yes. Macrocalcifications form from microcalcifications, so at least in the initial stages statins form microcalcifications 1st before stabilizing the plaque. Your complaint with statins is a fairly common one. Some people are now doing scans that can pick up soft plaques which would be useful in assessing risk.
What statin or what family of statins would you recommend instead of Pravastatin?
Hey Dr Loh! Greetings from London, England. I recently discovered you on LinkedIn and really enjoyed this presentation. What are your views on improving cardiovascular health and prevention of vascular calcification through occasional prolonged fasting (around 24 - 72 hours)?
@IflyUploaded Thank you for watching. As a clinician, I have to say that it depends. In a young, healthy person a prolonged fast may be fine. In aging patients (~age 35 and above), I have to worry about anabolic resistance. A 72 hour fast may accelerate muscle catabolism which may not be easy to reverse.
@@vlmdrounds interesting! Would a 24 hour fast be something you’d consider suggesting for the over 35s? And if someone is in their 40s and athletic would you still caution against 72 hours + fasts?
@@IfyUploaded I do caution against fasting for over 35s in general. If you are in energy balance then a prolonged fast will drive you towards catabolism...
Dear Dr. Loh, I have two questions: a) Several studies state that lp(a) exists almost exclusively in species that cannot independently produce vitamin c, and vitamin c has a key role in the formation of collagen (type 3 collagen for example is an essential component for blood vessel health, just see who is affected by veds (ehlers danlos of vascular type). What do you think of these studies that affirm this association between low ability to produce vitamin c and lp(a)? 2) You were talking about oxidized ldl as a response of the immune system. But are they a useful exam to do from a preventive point of view? Or are other tests to evaluate atherosclerosis better (cimt, mediated flow dilatation, etc...)? Kind regards from Rome, Italy.
@palandromarco5761 Wow, I am happy to have such good listeners on this podcast! Thank you for your question.
Re: your 1st question--as I mentioned in the episode, Lp(a) is a carrier of oxidized phospholipids (oxPL) and autotaxin. The autotaxin is able to convert oxPL to LPA (Lysophosphatidic Acid) which has many interesting functions in the body related to cell survival, proliferation and has many broad signalling functions. In relation to collagen, it is able to enhance ECM (extracellular matrix ) deposition without inducing fibrosis. It may play an important role in wound healing by antagonizing TGF-beta which can cause excessive ECM deposits. So it seems it may have s finely tuned role in wound healing and may have, as some people have suggested, evolved in humans to compensate for an inability to make vitamin C.
Re; your 2nd question--I do find it useful to see the load of oxLDL on patients and the advanced lipid panel I use does provide this. Because atherosclerosis is generally a slowly progressing condition getting a sense of the oxLDL load in "healthy"-appearing individuals can be useful for preventive purposes. CIMT is evaluation of disease progression since intimal hyperplasia has already happened. FMD is more useful in risk evaluation and for prevention.
Hi Dr Loh.
Thank you for another fascinating episode.
Do you have a recommended paper to read related to statins causing calcification?
Thank you, Conrad. There is actually a lot of data on this and it is "well-known" in the sense that I don't think anyone is arguing against the data. However, it doesn't seem to be well-known to practitioners who are prescribing. Most of them are surprised when I tell them.
Here is the article from AHA Journals that I referenced on the effects of Pravastatin. The 1st line of their abstract acknowledges that statins increase vascular calcification: www.ahajournals.org/doi/10.1161/ATVBAHA.120.315737
Here is a recent one: journals.plos.org/plosone/article?id=10.1371/journal.pone.0289111
Another: www.jacc.org/doi/abs/10.1016/j.jacc.2015.01.036
As per my episode, the explanation given is that the type of calcification caused by statins is "good", whereas all other types of calcification are "bad". (Right! 😏)
@@vlmdrounds Thank you very much. I appreciate you sharing the journal articles. Very interesting reading that I wasn't aware of.
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Why does this calcification form in the first place in some people given same diet and lifestyle? Isn’t it true that some people don’t get calcification of the arteries!
Calcification is part of the immune response to damage and fibrosis. Calcification is an attempt to stabilize the structure of the plaque/lesion. It may be argued that necrotic plaques without calcification may be in greater danger of rupture.
@@vlmdrounds Thanks. What statin if any is preferable to Pravastatin?
How do I stop damaging my arteries?
That's a good question. I wish more people realized that they can influence so much of their own health through their lifestyles. However, evidence-based practices in nutrition, sleep and exercise are hard to come by and should not be couched in simplistic terms ("eat healthy, exercise more!") If you are interested in structured, science-based approach to protecting your arteries, you can find out more by scheduling some time to talk here: calendly.com/tulaversity/free-program-information-session
@@vlmdrounds Thank you.