Plaque regression vs plaque stabilization
Heart disease is the leading killer of Americans. Heart attacks (MI) are currently thought by researchers to be caused primarily by vulnerable plaque which ruptures. This process of building plaque over time according to researchers is the result of endothelial dysfunction. The precise cause of endothelial dysfunction is unknown but researchers suspect that both lifestyle and genetics contribute to a process in the immune system which causes inflammation. This inflammation is ultimately what produces endothelial dysfunction as we age but in addition the ability of blood platelets to aggregate also is influenced by LP(a) which is genetically determined for the most part. High levels of LP(a) are associated with increased risk of cardiac events such as heart attack and stroke.
20% of individuals have an LP(a) level which is very high and would put them at an increased risk of early heart disease. This means that if you get your LP(a) tested and it's over 50 mg/dL then you're at risk of having a heart attack or stroke at an earlier than expected age. To reduce this risk there are two main strategies so far:
- Plaque regression
- Plaque stabilization
To achieve plaque regression according to studies it is required that LDL levels be kept very low. Under 70 is associated not only with the lowest cardiovascular risk according to studies but is also shown to cause plaque to regress over time. Plaque stabilization also can occur but it seems to be the result of lowered inflammation.
There are many risk factors and some may be beyond the control of most individuals. Poverty and stress are both risk factors (economic misfortune and a difficult life). Stress can be controlled or managed to a certain degree but because stress can raise blood pressure it can increase risk. Economic misfortune can put an individual at risk for exposure to pollutants in the air and or water which could create risk or cause inflammation.
To reduce LP(a) some researchers suggest using high dose Niacin but this presents systemic risk in exchange for lowering LP(a). Niacin is shown to cause insulin resistance. Insulin resistance may in fact be much worse of a risk factor than LP(a). LP(a) has to in essence ride LDL so it is shown so far that if LDL is kept low then the threat of high LP(a) is reduced along with the reduction of LDL in correlation.
A whole food plant based diet, certain supplements such as pomegranate, and beet root, have been shown to reduce cardiovascular risk. These dietary adaptations have been shown to promote both plaque regression and plaque stabilization if followed over a long enough period of time. This could take months or years of strict adherence and for this reason there are drug based approaches which may be more effective for the average person.
PSK9 inhibitors have the most promise for the drug approach. The problem with this treatment is the cost is around $14,000 per year and insurance doesn't usually cover it. In addition it is very new so doctors don't often prescribe it. As a preventative treatment it does seem to be the most promising. It works by way of an injection which causes a lasting decrease in LDL cholesterol and LP(a). In theory this injection combined with a statin is all most people would seem to need to reduce risk even with a bad diet. Of course because these treatments are not widely available it is wise for people to get their LP(a) tested and in my opinion consider a whole food plant based diet. Discuss it with your doctor.
References
Dave, T., Ezhilan, J., Vasnawala, H., & Somani, V. (2013). Plaque regression and plaque stabilisation in cardiovascular diseases. Indian journal of endocrinology and metabolism, 17(6), 983.
Heemskerk, M. M., van den Berg, S. A., Pronk, A. C., van Klinken, J. B., Boon, M. R., Havekes, L. M., ... & van Harmelen, V. (2014). Long-term niacin treatment induces insulin resistance and adrenergic responsiveness in adipocytes by adaptive downregulation of phosphodiesterase 3B. American Journal of Physiology-Endocrinology and Metabolism, 306(7), E808-E813.
Migrino, R. Q., Bowers, M., Harmann, L., Prost, R., & LaDisa, J. F. (2011). Carotid plaque regression following 6-month statin therapy assessed by 3T cardiovascular magnetic resonance: comparison with ultrasound intima media thickness. Journal of Cardiovascular Magnetic Resonance, 13(1), 37.
Tsimikas, S. (2017). A test in context: lipoprotein (a): diagnosis, prognosis, controversies, and emerging therapies. Journal of the American College of Cardiology, 69(6), 692-711.
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LPa also called lipoprotein a. This is not routinely checked in lipid profile.
I think this may be checked if there is familial hypercholesterolaemia.
The Bp reading in the picture is unrealistic. Diastolic which is the bottom bit of the reading of 134 indicates malignant hypertension and imminent haemorrhagic stroke.
Interesting article
I see you are either a medical researcher or a doctor? This is all true what you said. And yes LP(a) isn't regularly checked but you can get it checked privately by simply going through Quest Diagnostics. It's good to have this information because knowing your level of risk can help you make decisions regarding lifestyle modification. LP(a) being high is increased risk which means you have to reduce your risk elsewhere to avoid consequences. Just as getting a CT scan increases risk of cancer even though there is no proof it causes cancer.
Im a doctor.
Yes LPa can be checked privately but I don’t think it makes much difference as long as we control LDL and total cholesterol.
It is difficult to research the radiation associated cancer but there is a risk.
I agree with what you say above. What would you suggest is the appropriate range to keep LDL and total cholesterol?
These are in mmol/l
Total chol < 5, LDL<3.
In patients who already has ischaemic heart disease the targets are 4 and 2 respectively.
Now there is more emphasis on non HDL cholesterol which is total cholesterol minus HDL and this should be < 4
I aim to keep my total chol under 3.8 with ideal around 2.5. This is supposed to be around 150 max and 100 ideal total cholesterol in mg/dL. The reasoning behind these numbers are the result from the Framingham Study. From a risk perspective the 150 mg/dL and below seems to provide the most assurance. More specifically the ratio between LDL/HDL seems important from what I know about how HDL clears arteries.
This is achievable through a plant based diet for the most part but there are herbal supplements which can help as well. From what I could find there isn't really any harm in having extremely low LDL and only added risk if it's higher.
Reference
https://en.wikipedia.org/wiki/Framingham_Risk_Score
The evidence is contradictory
Heart disease is a killer disease and so many great minds have been lost to it
It's good to pointed out how organic food could help out