A game: see if you can identify my cardio risk

gregtay · September 5, 2022, 4:30pm

Here is a little fun game :). Below are my latest numbers from the doc. I am at high-risk for a MI, stroke, and heart valve issues. I discovered this 18 months ago when I went into cardiac arrest due to an MI(you can read about it in my other thread.) So here is the game, take a look at my numbers below, try to identify which one identity’s the risk. Why is this important? Because many people have asked me if there was any testing/data that would have identified my risk prior to my MI. At the time the doctors seemed to tell me “not really, at least not a test we would have performed on you because your risk would have been identified as ‘low’, no further testing needed”… but now I know more and there certainly was something that we missed… something that EVERYONE (in my opinion) should get checked. So here ya go, these are my numbers and data:

Age: 48 (male)
Heart Rate (resting: 38bpm
Blood pressure: 112/61 mmHg
Weight: 172 pounds (typical race weight is 162-165)
Height 5’9"

Blood results:
Total Cholesterol: 140mg/dL
LDL: 61mg/dL
LDL Particles 725 nmol/L
HDH: 68 mg/dL
HDL Particles 38 mcmol/L
Trig: 50mg/dL
Lipoprotein (a): 287 nmol/L
Apoliporotein B: 64 mg/dL

ECG Results:
Ventricular Rate (HR): 30BPM (this set off alarms on the machine… opps!)
PR int: 176 ms
QRSD int: 116ms
QT int: 480ms
QTC Int: 339ms
P Axis -22deg
R Axis 43deg
tWave axis 60deg

Echo results:
Ejection factor: 61%
No significant valvular heart disease
Normal flow pattern
Normal left ventricular filling pressure
(I won’t post all the numbers from the echo… but all in the normal range)

History:
Previous heart disease/issues: None (prior to MI/CA in Feb 2021)
Family history of heart disease: None
Medications (prior to MI event) None (now they have me on a ton of stuff)
Other health issues: None
Smoker?: Never.
Alcohol: Some beer and red wine when not race season… but nothing noteworthy.

Diet: 90% vegan, low fat, low sodium, lots of fruits and veggies. (@synthetic will tell you that my diet must be crap because i don’t eat just kale and carrots)

Cardio Activity: Prior to MI in 2021: Competitive amateur triathlete, USAT All-American for 45-49AG, 12-14 hours of training a week, (these days I still train but not as much and not at the same intensity… but still very active.

Okay… So how does this compare to your numbers and lifestyle? And can you figure out why I am at high risk for a MI, stroke, and heart valve issues?

TBtri_CO · September 5, 2022, 6:09pm

The main lab that sticks out to me is your lipoprotein a level is ~10x normal level. Several meta-analyses showed increase in ASCVD risks even at levels >30. One trial (INTERHEART) showed an odds ratio of ~1.5 of MI for patients whose lipoprotein a levels were >50. There are plenty of problems with applying that data to a single person, but that lab does stand out on your results as rather abnormal.

ThisIsIt · September 5, 2022, 8:51pm

The main lab that sticks out to me is your lipoprotein a level is ~10x normal level. Several meta-analyses showed increase in ASCVD risks even at levels >30. One trial (INTERHEART) showed an odds ratio of ~1.5 of MI for patients whose lipoprotein a levels were >50. There are plenty of problems with applying that data to a single person, but that lab does stand out on your results as rather abnormal.

That was going to be my guess, even though I have no idea what normal values are. Then what? Do statins affect lipoprotein a, are there other drugs that do? Diet?

gregtay · September 5, 2022, 9:31pm

The main lab that sticks out to me is your lipoprotein a level is ~10x normal level. Several meta-analyses showed increase in ASCVD risks even at levels >30. One trial (INTERHEART) showed an odds ratio of ~1.5 of MI for patients whose lipoprotein a levels were >50. There are plenty of problems with applying that data to a single person, but that lab does stand out on your results as rather abnormal.

Exactly. And how few people have their LP(a) levels checked? I am guessing very very few.

gregtay · September 5, 2022, 10:00pm

The main lab that sticks out to me is your lipoprotein a level is ~10x normal level. Several meta-analyses showed increase in ASCVD risks even at levels >30. One trial (INTERHEART) showed an odds ratio of ~1.5 of MI for patients whose lipoprotein a levels were >50. There are plenty of problems with applying that data to a single person, but that lab does stand out on your results as rather abnormal.

That was going to be my guess, even though I have no idea what normal values are. Then what? Do statins affect lipoprotein a, are there other drugs that do? Diet?

Unfortunately, LP(a) is not lowered by diet, exercise, lifestyle or statin meds. LP(a) is created in your liver and the amount you create is hereditary/genetic. You cannot change your number… basically, you only need to get your level tested once in your lifetime because it isn’t going to change much. Niacin has been found to lower LP(a) by ~20%, but not enough to make a difference in risk and most cardiologist do not recommend this treatment path. PCSK9 inhibitors have been found to have a side effect of lowering LP(a) by a bit more, but still not enough to lower your risk level (and good luck getting insurance to pay for it, because Rapatha was not an approved treatment for high LP(a)). There is a new drug in trials now that is believed to lower LP(a) by ~80% (meaningful reduction that would lower risk) but it remains a few years out.

So, “Then what?”. Great question, because basically I have been told I am at high risk due to genetics, there is no way to reduce that risk today. But I believe having the knowledge is incredibly valuable. First off, I know I need to work with a cardiologist for the rest of my life to manage the risk (maybe that was an obvious thing after having an almost life-ending cardiac event). I wish I could have gone back in time and had my LP(a) tested before my event… doing so would have likely led me to have already been under the care of a cardiologist, maybe we would have done further testing even though my typical risk score was extremely low. The very high LP(a) was always there… I just never had anyone look for it.

So, my advice to everyone is: next time you have blood work done, have your LP(a) level checked (need to make sure you find a lab that can check it.) Have your APO B levels checked as well (which i think it just a normal thing they check in Canada… but not in the US.)

Knowing your LP(a) levels might reveal that you are at risk for an MI, stroke, or heart valve issues… even if you live a healthy lifestyle and all your other risk factors are low. And just in case you are wondering what percentage of the population has an elevated LP(a) level?.. studies show about 20%.

Amnesia · September 6, 2022, 4:06am

Do you mind putting up the reference ranges for your blood test data.
Even as an MD, because I practice in a different country, for some tests we have different units and different reference ranges. It always makes it easier when reference range data is included (although those reference ranges can also be a trap for unsuspecting people, medical included).

gregtay · September 6, 2022, 6:27pm

Do you mind putting up the reference ranges for your blood test data.
Even as an MD, because I practice in a different country, for some tests we have different units and different reference ranges. It always makes it easier when reference range data is included (although those reference ranges can also be a trap for unsuspecting people, medical included).

here ya go (these the reference ranges in my lab report. I believe a typical LP(a) is around 30-50, and 75 is where they start to see increased risk, but they research is ongoing.

(adding a capture of the chart since it didn’t paste very well.

My level Normal high very high
Total Cholesterol: 140mg/dL <200 240+
LDL: 61mg/dL <100 160-189 190+
LDL Particles 725 nmol/L <1000 1600-2k 2000+
HDH: 68 mg/dL 40+
HDL Particles 38 mcmol/L 30+
Trig: 50mg/dL <150 200-499 500+
Lipoprotein (a): 287 nmol/L <75 75-125 125+
Apoliporotein B: 64 mg/dL <90 100-139 140+

st_speedskater · September 8, 2022, 9:31pm

Gee, my panel only has these tests:

LIPID PANEL BASIC
Cholesterol, Total <200 mg/dL
Triglyceride <150 mg/dL
HDL Cholesterol >39 mg/dL
LDL Cholesterol <100 mg/dL
Non HDL Cholesterol <130 mg/dL
VLDL Cholesterol <30 mg/dL
TC:HDL Ratio <5.10
LDL:HDL Ratio <2.54

Fasting Time 12 hrs
.

gregtay · September 9, 2022, 2:20am

Gee, my panel only has these tests:

LIPID PANEL BASIC
Cholesterol, Total <200 mg/dL
Triglyceride <150 mg/dL
HDL Cholesterol >39 mg/dL
LDL Cholesterol <100 mg/dL
Non HDL Cholesterol <130 mg/dL
VLDL Cholesterol <30 mg/dL
TC:HDL Ratio <5.10
LDL:HDL Ratio <2.54

Fasting Time 12 hrs

LP(a) isn’t part of the normal lipid panel today… but it should be :-/

140triguy · September 9, 2022, 1:22pm

I saw your blood test results. Mine were all very good, EXCEPT LDL, which was 104. No LPa test was done. My follow-up CT-angiogram showed a Agatston estimate of 323, showing significant calcium buildup.

It seems then that the essential markers are LPa and maybe LDL. With a lifelong baseline of LPa, it seems that LPa sets the course for the possibility of heart disease, and LDL level is what indicates the amount of plaques and calcification that will occur under the LPa circumstances. Inflammation in the coronary arteries is a result of these measures. External factors such as lifestyle impact the speed of progression.

If you and I HADNâ€™T been so active and healthy, we would have had far worse blockages. BUT, we wouldnâ€™t have known because we wouldnâ€™t have created ischemic conditions (while exercising), and would not have felt the warning chest pain or had the MI. The disease would have galloped on with smoking or eating/drinking or inactivity until someday when we were 56 and pulling a lawnmower cord or helping our kids move their shit into their college dorms.

I guess weâ€™re lucky?

gregtay · September 12, 2022, 4:40am

I saw your blood test results. Mine were all very good, EXCEPT LDL, which was 104. No LPa test was done. My follow-up CT-angiogram showed a Agatston estimate of 323, showing significant calcium buildup.

It seems then that the essential markers are LPa and maybe LDL. With a lifelong baseline of LPa, it seems that LPa sets the course for the possibility of heart disease, and LDL level is what indicates the amount of plaques and calcification that will occur under the LPa circumstances. Inflammation in the coronary arteries is a result of these measures. External factors such as lifestyle impact the speed of progression.

If you and I HADNâ€™T been so active and healthy, we would have had far worse blockages. BUT, we wouldnâ€™t have known because we wouldnâ€™t have created ischemic conditions (while exercising), and would not have felt the warning chest pain or had the MI. The disease would have galloped on with smoking or eating/drinking or inactivity until someday when we were 56 and pulling a lawnmower cord or helping our kids move their shit into their college dorms.

I guess weâ€™re lucky?

Hell yes we are the lucky ones! First off… the doctors told me repeatedly that without my fitness I would not be here… full stop. Heck… they still can’t believe I survived even with my fitness level. I am certain that if hadn’t pursued that life of an athlete… I would be dead. And you are right, it would have probably been something like mowing the lawn or walking up stairs that took me out.

In my case I don’t think there was any warning, at least nothing I can remember (but my brain is pretty much wiped from the day everything happened… so I can’t really answer if I felt anything before I went down.) Admittedly… if I had felt something, I am not sure I would have stopped, I just don’t think I would have accepted that something could be wrong.

Heard from my cardiologist at Mayo Clinic this morning, they results for my extensive genetic testing came back (Genetic Risk Score (GRS) for CHD), my results showed below average risk (my score was .82). So the doctors have come back and said they have high confidence that LP(a) is the main abnormality. All my other risk factors remain low.

Birdmantris · September 12, 2022, 1:34pm

Unfortunately, LP(a) is not lowered by diet, exercise, lifestyle or statin meds. LP(a) is created in your liver and the amount you create is hereditary/genetic. You cannot change your number… basically, you only need to get your level tested once in your lifetime because it isn’t going to change much.

Feel free to disregard all of this if you’d like, but I’d like to offer another perspective and/or give you something to think about. Apologies if anything comes off as overly blunt

Lp(a) levels definitely have a large genetic component. However, it is not entirely fixed and is, to some degree at least, clearly modifiable through diet.

Changes in lipoprotein(a), oxidized phospholipids, and LDL subclasses with a low-fat high-carbohydrate diet (jlr.org)
Healthy Dietary Interventions and Lipoprotein (a) Plasma Levels: Results from the Omni Heart Trial | PLOS ONE
Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the DELTA Study, protocol 1 - PubMed (nih.gov)
Changes in dietary fat intake alter plasma levels of oxidized low-density lipoprotein and lipoprotein(a) - PubMed (nih.gov)

Consuming more carbohydrates absolutely makes your lp(a) go up. Again, not necessarily to the degree that genetics do, but to some degree at least.

But the bigger point I want to make is that lp(a) may not even be much of an independent risk factor. It’s a primary carrier of oxidized phospholipids, and it seems once you account for oxPL lp(a) basically loses any predictive power.

Oxidized Phospholipids, Lipoprotein(a), Lipoprotein-Associated Phospholipase A2 Activity, and 10-Year Cardiovascular Outcomes | Arteriosclerosis, Thrombosis, and Vascular Biology (ahajournals.org)

There aren’t a ton of studies on this either, but pretty well demonstrated that decreasing the glycemic load will decrease oxPL

Effect of a Traditional Mediterranean Diet on Lipoprotein Oxidation: A Randomized Controlled Trial | Cardiology | JAMA Internal Medicine | JAMA Network
A monounsaturated fatty acid-rich diet reduces macrophage uptake of plasma oxidised low-density lipoprotein in healthy young men | British Journal of Nutrition | Cambridge Core
A Mediterranean-style low-glycemic-load diet increases plasma carotenoids and decreases LDL oxidation in women with metabolic syndrome - ScienceDirect
Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a) | Arteriosclerosis, Thrombosis, and Vascular Biology (ahajournals.org)
Foxo1 links hyperglycemia to LDL oxidation and endothelial nitric oxide synthase dysfunction in vascular endothelial cells - PubMed (nih.gov)

Also seed oil consumption - Impact of 8-week linoleic acid intake in soy oil on Lp-PLA 2 activity in healthy adults - PubMed (nih.gov)

It may be the case that reducing oxidative stress could significantly reduce lp(a), as it seems a major role of lp(a) is to accept those oxidized phospholipids

So obviously I don’t think you’re about to look at this and drastically cut carbs, but heavy consumption of carbs and/or seed oils (which are absurdly prone to oxidation) should absolutely be expected to increase oxidative stress. And that COULD play a big role in lp(a). Or, as alluded to above, it could be the factor that is actually driving disease even if lp(a) is elevated.

But anyway, I would encourage you to seek an oxidized phospholipid/oxLDL test because (here’s the blunt part, sorry), you definitely fit the profile of someone with high levels of oxidative stress and it would suck to be missing the real problem.

I also could be wrong! But take it under consideration anyway. Cheers

gregtay · September 14, 2022, 11:12pm