Heart Disease Question

Hi,

I joined this forum a while ago as I was going to start with Rapamycin but it is all on hold for now. I am 61 year old living in Bay Area and in Jan 2023, got 4 stents (2 in LAD, 1 each in LCx and RCA). Had 50-60% blockage in distal RCA and D2 of LAD. Before the stents:

LDL-C was in 70s, ApoB and LP(a) were never measured.

Meds were Metoprolol 50mg and Atorvastatin 40mg

After the stents:

LDL-C has been around 53, ApoB 64

A1C 5.4

Blood Pressure 110/70 (around this)

Meds were Metoprolol 50mg Extended Release, Rosuvastatin 20mg, Losartan 12.5mg, Aspirin 81mg, Effient was given for a year

Exercise - strength training 3 days a week, 50 minute run on treadmill (zone 2 for 40 min and 10 min zone 5)

Diet - mostly vegetarian, except chicken and fish

I got tested for LP(a) and got into Olpasiran double blind study. LP(a) dropped from 285 to 179 but not below 75 :frowning:

So on April 3, felt having a heart attack, went to hospital and distal RCA blockage was 99% and got another stent. The 4 stents were clear and did not show any plaque build up.

Now medicine is Metoprolol 50mg Extended Release, Rosuvastatin 20mg, Ezetimibe 10mg, Aspirin 81mg and Brilinta 90mg (twice a day for year).

The questions I have is:

  1. Why did plaque grow from 60% to 99% when my Medicine, Exercise, Diet was all on track? Any theories?
  2. What tests can I do to catch the progress of plaque proactively?
  3. What else should I be considering?

Thank you

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As a 63 yo male with a bad CAC, low carb is proven to reduce lp(a) by 15%. Vitamin C is supposed to help as well, I’ve switched to the expensive stuff after reading things and listening to Chris Masterjohn. I use Acerola powder.

Heavy metals cause heart disease. Chelation reduces calcium and ties up and gets rid of heavy metals. I did a chelation challenge and discovered I’ve been living with high levels of lead and uranium. DMSA is an oral chelator, could solve the problem for $250. I had to buy it on ebay and put the powder in capsules myself. It makes me sleep really well. Be sure to supplement copper and go slow…for several reasons:

That’s my post on chelation.

I think beta cyclodextrin works as well. No proof yet, but you can search the site and it has been discussed here. I’ve been using RemChol, or CholRem I don’t know which. They have a new version that is more potent and more quickly absorbed. I haven’t tried it yet.

Your numbers look really good, and your exercise is good. Crazy good, my LDL is usually more like 160.

Colchicine is another thing I’m trying. You can search for that here too. Very cheap from India. If I have no adverse effects I’ll stick with it.

Good Luck,

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Consider getting your DNA sequenced (genetic information). I did mine and it helped explain why I have some cardio disease and ongoing risk even though my lipids and diet/exercise/BMI/BP all indicate I should be fine.

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The problems is clearly Lp(a), there is a member of this forum that sees an excellent doctor that is treating them for that very problem. Maybe someone else can point them out.

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There is limited evidence that Glisodin may help to reverse atherosclerosis and it’s generally very well-tolerated with no known risks or drug interactions. From LEF: “Remarkably, the physicians found that two years of supplementation with GliSODin® actually reversed the buildup of atherosclerotic plaque in the carotid arteries, as determined by ultrasound measurements of carotid intima-media thickness.”

Vitacost is one of the most affordable sources. About $16 per month. Not all SOD sold as a supplement is the same formulation. I would suggest only using a product containing actual Glisodin.

More info:

GliSODin, a vegetal sod with gliadin, as preventative agent vs. atherosclerosis, as confirmed with carotid ultrasound-B imaging

M Cloarec et al. Eur Ann Allergy Clin Immunol. 2007 Feb.

Abstract

Prevention of cardiovascular disease should target high-risk subjects based on genetic/familial factors, blood chemistry, blood pressure, body mass index (BMI), and a history of/or current cigarette smoking. We selected active adults (n=76) aged 30-60 and investigated these risk factors, in order to recommend preventive measures. Another interesting variable is the preclinical status or atheroma of the arterial (carotid) wall or lumen. We also investigated the presence of oxidative stress in, and the anti-oxidant status of these subjects. We studied the anti-oxidative efficacy of superoxide dismutase (SOD) and variations of malondialdehyde (MDA). Supplementation with GliSODin, a vegetal SOD associated with gliadin, was effective in controlling the thickness of the carotid artery intima and media layers as measured uby ultrasonography-B. We could demonstrate the preventive efficacy of GliSODin at a preclinical stage in subjects with risk factors of cardiovascular disease.

PubMed Abstract

Additional information from a citing study:

”A research study on individuals at risk for developing atherosclerosis demonstrated a striking difference between the control and the protected SOD–supplemented group when examining carotid thickness. Individuals receiving SOD–gliadin daily (500 U SOD activity) or placebo for a period of 2 y were subjected to B-scan ultrasonography to measure the intima media thickness (IMT), a standard detection method for atherosclerotic lesions. Decreased carotid IMT measurements were seen in patients after 365 d of treatment with SOD–gliadin. Moreover, the supplemented group registered an increase in SOD and CAT levels in the blood compared with the placebo group. Additionally, lipid peroxidation, used as a measurement of oxidative stress, was reduced after SOD–gliadin intake. Together, these data suggest a potential role for SOD–gliadin supplementation in the prevention of atherosclerotic lesions, possibly through its general antioxidant action.”

Reference
Romao S. Therapeutic value of oral supplementation with melon superoxide dismutase and wheat gliadin combination. Nutrition. 2015 Mar;31(3):430-6. doi: 10.1016/j.nut.2014.10.006. Epub 2014 Nov 5. Erratum in: Nutrition. 2015 Sep;31(9):1187. PMID: 25701330.

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LP(a) and C-Reactive Protein appear to be joint predictors of cardiovascular health, suggesting that a systemic inflammatory process, not yet mechanistically well-defined, may be involved. Inflammatory processes tend to elevate both LP(a) and hsCRP. Have you been checked for hsCRP?

Bicep mentioned colchicine, and a pivotal study on colchicine effects on cardiovascular mortality was published in the NEJM.and was quite promising. It may be worth discussing it with your doctor. Because colchicine and rosuvastatin have the potential of causing a severe DDI, the colchicine dose would likely need to be adjusted lower than 0.5 mg/day as used in the aforementioned study.

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You pretty much have to quit colchicine when taking Rapa or Grapefruit too.

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I found the Bale and Doneen book, Beat the Heart Attack Gene, to be super helpful. So helpful, in fact, that I read it twice. And then actioned all the items they suggested in the book. They discuss the very question(s) you’re asking … why do you have plaque. And as you’ll discover, there are many variables that can contribute to atherosclerosis, including, but not limited to periodontal disease, glucose, levels of fibrinogen (very important), MPO (very important), levels of inflammation (including MPO), undiagnosed sleep apnea, genetics including 9P21, Omega 3, hemoglobin, Ox LDL, lipoprotein fractionation (very important), homocysteine, and easily 20 other important variables. For an alternate perspective, also take a look at the book “The Clot Thickens” by Malcolm Kendrick.

One more thing … you asked about measuring plaque progression. I found the Cleerly AI test to be, by far, the most helpful test I did.

Good luck.

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Herm - yes I have been checked for hsCRP… no inflammation… I am wondering why the plaque progressed in one place… the stents are clear… Is it just Lp(a)?

Deborah - Can you please let me know what specific DNA sequencing was done… and where did you get it done?

WHAT??? I’m on colchicine and just started rapa… can you fill me in, please?

Jeff… Thank you… Here are some of my numbers…

LP PLA2 58 nmol/min/mL
MPO 270 pmol/L
Glucose 92 mg/dL
hsCRP 0.3 mg/L
Homocysteine 13.9 umol/L
Insulin 18.8 ulU/mL
Apob 35 mg/dL

LDL PARTICLE NUMBER 432 nmol/L
LDL SMALL 62 nmol/L
LDL MEDIUM 69 nmol/L
HDL LARGE 4741 nmol/L
LDL PATTERN B Pattern
LDL PEAK SIZE 216.2 Angstrom
No Periodontal disease (but I am now getting tested for bacteria)

Haven’t been tested for 9P21, Omega 3, Fibrinogen

I will reread Beat the Heart Attack Gene… and will also read The Clot thickens…

Appreciate the guidance… Determining the cause is quite challenging…

As an FYI, I didn’t think I had periodontal disease but the Oral DNA test said otherwise. Also, it seems some of your lipoprotein fractionation results are high, in particular, HDL large, LDL peak size, and you’re also Pattern B. To be clear, I’m not a doctor.

WRT the lipoprotein fractionation test, Dr Mark Hyman considers this test to be one of the most important tests for ASCVD.

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I did 23&me many years ago to find out if i had the risk APOE allele (I dont). But then last year I asked them to send me the entire raw data. The entire genome. I then uploaded that to Promethease. Promethease is very inexpensive and easy to use.

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I think he’s talking about the grapefruit… you don’t want to be taking grapefruit with colchicine. I haven’t looked into it, but I suspect it could cause an overdose. Eating grapefruit with medications makes things very complex and more dangerous. Its not generally recommended. Be very, very careful if you, or anyone, is taking grapefruit / juice.

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Oh, I just saw it this morning. Somebody posted a link to the drug interactions with colchicine. It showed Rapa as being sort of intermediate, so it does actually keep the colchicine from breaking down. Not as bad as grapefruit. Rosuvastatin was the worst with colchicine. Can’t find it now.

Took my second dose today. Nothing.

I think what I will do is just stop the colchicine day before and a couple days after the Rapa. I’m biweekly so no big deal.

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Strange, the WebMD drug interaction checker shows no interaction for rapamycin (sirolimus) and colchicine…

but interestingly Drugs.com says there is a bit of interaction:

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Thank you to Rap Admin and @Bicep ! I never would have known!!!

Hmmm, I can definitely skip the day I take rapa. Do you feel I should do more? Is it just about more frequent blood tests for levels? I’ll also run it by my doc.

One of the side effects of too much is, you know, death, so there’s that. That might offset taking it to reduce heart attacks.

My life feels like whack-a-mole :slight_smile:

EDIT: here’s a question that I’m sure everyone here knows but me!… in light of this potential low risk, I ask…. Do you always consider someone’s weight when dosing? I know it’s been mentioned here with a rapa dose, but I know other things, like vaccines, are the same dose whether you are 100 or 300 pounds. I am aprox 109 pounds so wonder if I can get away with less colchicine. And on that note, I have planned to ramp up to 6mg of rapa this week or next. (I had 1gm, then 3gm, tomorrow I’m thinking of 5 because it’s going well so far)

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Yes, size does matter. It seems that people who cannot tolerate Rapamycin as well as others tend to be quite small in size. IMHO, doses are definitely size dependent.

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You might also want to check your insulin level. 18.8 µIU/ml seems rather high.
Combined with a glucose of 92mg/dl this gives an HOMA-IR of 4.3 which is way above the recommended max value of 2 and probably indicate insulin resistance.
BTW I’m the opposite, my glucose is high at 108 but my insulin is 4 so my HOMA-IR is 1.1 only.

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