Title: “When Numbers Mislead:
Atherosclerosis Progression, Mathematical Illusions, and Clinical Reality in the Elderly”
by this blogger - lim ju boo, alias lin ru wu (林 如 武)
A close doctor friend of mine wrote this letter (in inverted comma) to me:
"Thank you very much Prof. Lim for your article here:
https://scientificlogic.blogspot.com/2026/01/can-atherosclerosis-and-stable-angina.html
Very informative. For your information, my LDL was 80mg/dl, crp 3.5mg and the rest of the parameters were normal. Had a ECG & Stress Test and was normal. The cardiologist suggested a CT Angio in view of my age 78yrs. It took me 1 year to decide to do it after consulting 2 other cardiologists. It showed about 25% blockage. The cardiologist suggested only low dose Atorvastatin or Rosuvastatin and both caused muscle pain, so I stopped it after 10 days. I now restrict my vegan diet further. If LDL is still raised after one month, I may want to try Pravastin or Ezetimibe. Please advice and comment Prof Lim. Thanks".
Here is my answer for my beloved friend.
Thank you doctor for your interesting question. I thought instead of answering your question as an individual, I should share out my answer and opinion to a much wider audience - without your name disclosed - for general educational purpose, since coronary heart disease affects almost every one irrespective of age, and is the Number One Killer in most countries. It should benefit everyone at risk who may be interested in reading my explanation. It took me some time to think over your question, analyze what you wrote, before I could write and answer here:
Here are my opinion:
Atherosclerosis is commonly perceived as a progressive, age-dependent, and eventually obstructive disease. However, clinical observations, particularly in elderly individuals, often contradict this simplistic model. This article examines a real-world scenario of mild coronary atherosclerosis detected at an advanced age and explores, through a deliberately artificial mathematical extrapolation, why linear models of disease progression are fundamentally flawed. This discussion then reconciles mathematical intuition with biological reality, emphasizing plaque stability, inflammation, and clinical context over luminal narrowing alone. Therapeutic implications, particularly regarding lipid-lowering strategies in statin-intolerant elderly patients, are also addressed.
Let me Introduce this subject just a little bit more, although not 100 % complete yet. This will take me a longer time to answer and you may lose your patience with me. But I am very patient looking at the stars and galaxies which is my real hobby in astronomy - not all these medical stuff.
Let me briefly answer:
Coronary atherosclerosis is frequently framed, both in public discourse and in some clinical thinking, as a slow but relentless accumulation of plaque that inevitably worsens with age. This narrative encourages a numerical mindset: percentage stenosis, LDL targets, and chronological age are often interpreted as predictors of future obstruction and cardiovascular events.
Yet, daily clinical practice tells a more mixed story. Many elderly individuals harbour coronary plaques that remain stable for decades, especially among vegans and stanched vegetarians, while acute coronary syndromes often arise more among animal fat eaters and sugar consumers from lesions that were previously considered “non-significant.” This discrepancy invites deeper reflection on how we conceptualize disease progression.
Since I was a medical researcher with a love for mathematics and statistics, let me give my mathematical thought on experiment using linear progression (with age).
To illustrate the danger of oversimplification, consider this following hypothetical model.
Given the age of 78 years with coronary stenosis on CT angiography at 25%. Let us assume (intentionally unrealistic) that we have zero plaque at birth. Using statistical linear progression with age with no biological acceleration, regression, rupture, or healing, then this calculation would mean this:
Annual progression rate =
25% / 78 years is approximately 0.32 % per year.
To reach 100% stenosis:
100 % / 0.32 % would approximately be 312 years.
By then, we would have long died from other causes.
However, please note this result I present here is purely mathematical, and not biological. Under a purely linear, age-driven model, complete coronary occlusion would occur at approximately 300+ years of age.
This interpretation is absurd, I am afraid. Please note this result is purely mathematical based purely on a straight-line linear correlation, and is not biological as we age. This result is biologically impossible, and that is precisely the point.
The calculation exposes a fundamental truth in that atherosclerosis is not a linear function of time or age.
Age alone is a poor predictor of plaque behavior. The human arterial system is not a pipe that slowly fills with debris; it is a living, adaptive, inflammatory, and sometimes self-stabilizing organ.
The biological reality is, how atherosclerosis actually behaves
Let me explain this in three steps:
1. Progression Is Non-Linear
Plaque accumulation occurs in fits and starts. Long periods of quiescence
Episodic acceleration during systemic inflammation, metabolic stress, infection, or oxidative injury. Possible stabilization or calcification over time. Many plaques stop progressing or become biologically inert - probably in your case at age 78?
2. Degree of Stenosis ≠ Cardiovascular Risk
Large clinical and pathological studies have shown that most myocardial infractions arise from plaques causing 30–50% stenosis, not severe obstruction as in your case. The dominant determinant of risk is plaque vulnerability, not lumen narrowing
Key factors include, inflammatory activity, fibrous cap thickness and lipid core composition. Thus, a stable 25% lesion in an elderly individual may represent vascular success, not failure.
3. Imaging Shows Anatomy, Not Biology
CT coronary angiography provides valuable anatomical information on degree of luminal narrowing, calcification burden
However, it does not directly assess to inflammatory state, plaque stability and propensity for rupture. Clinical interpretation must therefore integrate imaging with functional testing, biomarkers, and symptoms.
The Central Role of Inflammation
In individuals with relatively low LDL levels, systemic inflammation becomes a dominant risk driver.
High-sensitivity C-reactive protein (hs-CRP) correlates strongly with cardiovascular events. Inflammation influences endothelial dysfunction, plaque destabilization, and thrombosis. In such cases, atherosclerosis behaves less like a lipid storage disease and more like a chronic inflammatory disorder.
Please read further my explanation on why the rate of atherosclerosis is not a linear progression, but an accelerated exponential scenario after middle age here:
The Progression of Atherosclerosis and Coronary Heart Disease with Age
https://scientificlogic.blogspot.com/2026/01/the-progression-of-atherosclerosis-and.html
Let me now talk a little about therapeutic implications in the elderly, namely statin intolerance - the question you asked and is worried about your muscular pain.
We know that statin-associated muscle symptoms are real, particularly in elderly patients, in individuals with low baseline LDL. Those with possible mitochondrial vulnerability. Discontinuation due to myalgia is clinically reasonable as in your case.
What then can we offer as alternative options for the elderly? My answer is, Pravastatin - as you correctly suggested yourself as a doctor, because this drug is hydrophilic with lower muscle penetration. It also has lower myopathy risk, and a modest LDL reduction
Ezetimibe has non-statin mechanism in pharmacological action. To the best of my knowledge its tolerability is excellent. However, it has limited benefit when LDL is already low
In patients with LDL of about 80 mg/dL, the absolute risk reduction from further LDL lowering is modest, and treatment should be individualized rather than target-driven.
Let me explain further
Thoughts on Pravastatin vs Ezetimibe - their challenges
A. Pravastatin
Pros. It is hydrophilic, causing less muscle penetration. It has lower myopathy risk, but a mild LDL reduction
Cons. It is still a statin. This drug may still provoke symptoms in sensitive individuals. If tried, it should be low-dose and symptom-led, not target-led.
B. Ezetimibe
The pros is this drug is a non-statin. It acts at gut cholesterol absorption. It has minimal muscle side effects. It is well tolerated in elderly patients. The cons are, it has modest LDL lowering (~15–20%). It has limited effect if LDL is already low. Given LDL = 80 mg/dL, the marginal benefit may be small, but tolerability is excellent.
The deeper question: what actually stabilizes plaques?
From both evidence and physiology. Stability depends on inflammation control (CRP ↓). It also depends on oxidative stress reduction. It depends on endothelial function. Plaque stabilization is not shrinkage
A vegan diet already addresses saturated fat, cholesterol intake. What remains are modifiable targets, such insulin resistance (even in “normal” glucose), chronic low-grade inflammation. Sleep, stress, micronutrients (e.g. magnesium, omega-3 balance even in vegans)
Having explained all that, let me now re-frame my earlier clinical question on total blockage once again because this is an important and misleading question. The key question is not:
“When will this patient reach 100% blockage?”
But rather, “Is the disease biologically active or clinically dangerous?”
In many elderly individuals like your good self, mild coronary atherosclerosis represents a stable, slow-burning process, like a charcoal fire, not an inevitable path to occlusion. It is not a petrol fire that suddenly burst into a big fire - I always like to give this analogy to doctors, scientists and patients alike.
Mathematical extrapolation, when stripped of biological context, leads to misleading conclusions. Atherosclerosis does not obey simple linear rules, nor does age dictate destiny. In elderly patients with mild disease, normal functional testing, and low LDL levels, emphasis should shift from numerical obsession to plaque stability, inflammation control, and overall vascular health.
In such cases, the presence of modest plaque burden at advanced age may be interpreted not as impending catastrophe, but as evidence of remarkable physiological resilience.
I hope I manage to answer your question dear friend using the best of my knowledge in medical research, in medicine, biochemistry, pharmacology, molecular biology and above all using my knowledge in medical nutrition which is the most important health-protective asset in preventive and curative medicine.
Let us all walk together in wisdom, not with acquired knowledge from universities or even through highly expensive and time honoured medical and scientific research.
I hope I have managed to answer
References for Further Reading
1. Libby P. Inflammation in atherosclerosis. Nature. 2002;420:868–874.
2. Ridker PM et al. Inflammation, C-reactive protein, and cardiovascular risk. Circulation. 2003;107:363–369.
3. Naghavi M et al. From vulnerable plaque to vulnerable patient. Circulation. 2003;108:1664–1672.
4. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657–671.
5. Puri R et al. Impact of statins on plaque progression. J Am Coll Cardiol. 2015;65:1273–1285.
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