Imaging is great for detecting calcified plaque in your coronary arteries. But before you have calcified plaque, the above risk factors tell you about the buildup of soft plaque. And 4 out of 5 of them are modifiable through lifestyle, exercise, and medication.
- If you made a dietary change (e.g., more fiber and less saturated fat), the tests tell you whether it actually worked.
- Statins are dosed based on the LDL or ApoB reduction you need. The most powerful statins cut cholesterol by 50%, but at higher doses the risk of side effects does go up.
- Other medications like PCSK9 inhibitors and ezetimibe exist, and whether to use them depends on the other numbers. For example, PCSK9 inhibitors have a secondary benefit of lowering Lipoprotein(a), and statins and GLP-1s have a secondary benefit of lowering inflammation.
- If blood pressure, HbA1c, etc is high, then there's a slightly different set of diet advice and a very different set of medications. For example, lowering blood pressure through diet is mostly about reducing sodium and increasing potassium.
Behavioral changes can only do so much to lower ApoB. It is a meaningful marker and may trigger additional workup. It may also signal that you should at least consider a statin.
ApoA is completely out of your control and will not change with behavioral modification.
So, no, you're incorrect that these tests are superfluous and all you need to say is "diet and exercise". Besides, even if that was always the answer to these results, you should still have a baseline to see if behavioral modification is doing anything.
"Why not just skip the HbA1c tests? After all, you know they'll give you insulin. Just start taking it."
Do you think everyone with poor blood test indicators is aware of how unhealthy they are? How quickly they need to reverse course? Or do think there might be some possible validity to discussing your results with an actual doctor and understanding how acute your symptoms actually are? Do you think there are no side effects to statins and everyone should just be on one at all times, forever? Do you think there might be some value, for those patients, in discussing GLP-1s? Or nah, everyone can just like, go run 10 miles tomorrow because some 20 year old in SV said so?
I'm always deeply confused by people who think all medicine is "just repeat whatever ChatGPT said as if it's profound, like, duh - I'm smart and invincible and can't quite figure out that other people aren't me", in spite of them not knowing anything about medicine in the first place.
Because for the same behavior, risks are going to be very different on the other side. In my family, for instance, we need significant interventions to get a reasonable risk due to all the bad genetic factors. In my wife's family, not so much. So knowing how serious the risk seems much better than just handing statins to absolutely everyone.
IMO, one of the most interesting things about the new hematology guidelines is that they're likely to get people treatment for symptoms like fatigue or low energy. A lot of doctors consider these "vague" complaints that are hard to diagnose. For some fraction of those cases, low ferritin or iron might be low hanging fruit.
I'm curious-did you have any traditional risk factors (LDL/ApoB, blood pressure, HbA1c, hs-CRP, high PREVENT or ASCVD score)? Or put another way, did you ever find an underlying cause as to why you had a heart attack at age 29?
Family has all the traditional cardiac symptom clusters (hypertension, elevated lipids/triglycerides, diabetes) and family history of heart attacks.
My biomarkers were good, but combined with family history and a past history of drug abuse (primarily stimulants), it's sort of a wonder it didn't happen sooner.
The MI itself was unusual. When they placed the stent in my heart, the coronary angiogram was able to image my arteries. I had almost no measurable stenosis in my arteries: a minor 30% in one inferior artery.
I was at the gym when it happened, the prevailing theory is that I had the one artery with vulnerable plaque and it ruptured from arterial pressure.
So on the one hand, it sucks that it happened at all. But on the other hand, I'll take "you didn't die and the rest of your heart looks clear" with no complaints.
This particular study looked at inflammation through imaging (CT scans) as part of Biograph's $17,500 program. You can get at the underlying signal fairly cheaply through a simple blood test (hs-CRP).
Importantly, routine bloodwork and clinical tools – including ... hs-CRP [among other tests] ... – showed no correlation with the presence of coronary inflammation and failed to identify which patients had inflamed arteries.
This is one of the things that makes me a little skeptical of their score. If it's accurate, there should be a positive correlation with known biomarkers. (I see you made a similar observation elsewhere.)
In their paper they actually find an inverse correlation with hs-CRP, which disappeared when removing two patients who were sick. So I wonder if the sample size being small is partly driving this.
Inflammation is likely a marker, but not the cause of heart failures.
That doesn't contradict it being an independent risk factor, but up to recently, it was assumed be causal driver.
Same thing happened with the Lp(a) drugs recently. Practically speaking, statins reduce LDL cholesterol (~50% at the strongest dose) and hs-CRP (~37%) and have cardiovascular outcomes data, so that's likely the route a patient would go based on the medications that are approved today.
The 4th generation heart rate sensor is quite interesting -- Apple Watch used to sample every ~5 minutes, and now it's every 5 seconds (basically continuous). I think that'll enable a lot of interesting health & wellness use cases.
It's interesting because during workouts, the heart rate sensor samples every 5 seconds but besides that, it was either every 2 or 5 minutes. I'm guessing the battery drain is too much to have it sample every 5 seconds all the time!
Too bad Apple reserved the [training] Readiness feature only for the Ultra 4 - I'm pretty sure Ultra 3 and probably below are just as well equipped to provide such insight...
- ApoB - about 20% of people with normal cholesterol results will have abnormal ApoB, and be at risk of heart disease.
- Lp(a) - the strongest hereditary risk factor for heart disease.
- hs-CRP - inflammation roughly doubles your risk of heart disease
- HbA1c - insulin resistance is a risk factor for just about everything.
- eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
These are simple blood tests. You can get them for <$200 through my company or others:
https://empirical.health/product/comprehensive-health-panel
Imaging is great for detecting calcified plaque in your coronary arteries. But before you have calcified plaque, the above risk factors tell you about the buildup of soft plaque. And 4 out of 5 of them are modifiable through lifestyle, exercise, and medication.
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