When I meet heart patients and families across India, I see one pattern repeat again and again:
People underestimate cholesterol… until it becomes the reason they land in an ICU.
And after a heart attack, they often look at their blood tests and say —
“But my cholesterol is normal now. How can cholesterol be the reason?”
This misunderstanding is one of the deadliest myths in heart health.
Because cholesterol behaves very differently after a heart attack, and if patients don’t know this, they end up ignoring a major risk factor. Let’s break this down — simply, honestly and scientifically.
Myth 1: “My cholesterol was normal during my heart attack, so cholesterol wasn’t the cause.”
Truth: Cholesterol DROPS after a heart attack — because of the heart attack.
This is one of the biggest blind spots in patient awareness.
What actually happens inside the body?
When a heart attack occurs, your heart muscle undergoes acute injury. In response, the body releases a storm of inflammatory signals called cytokines.
These cytokines:
- Suppress the liver’s ability to produce cholesterol
- Increase the clearance of LDL from the blood
- Change lipid metabolism for days
So within 24–48 hours, your LDL-C and total cholesterol fall sharply.
Scientific evidence
- LDL-C drops 20–30% after an acute myocardial infarction (AMI), i.e., heart attack.
- Cholesterol continues falling until Day 4 of hospital stay while Troponin rises.
- The drop correlates directly with troponin levels — meaning bigger heart attack = deeper cholesterol drop.
- Diabetes makes this fall even more dramatic.
This fall has nothing major to do with statins given in the hospital. It is a stress response of the body.
Why this myth is dangerous
Because patients assume:
“Cholesterol is fine — that means cholesterol is not my problem.”
But the truth is:
Your cholesterol was high BEFORE the heart attack,
and it dropped BECAUSE of the heart attack.
Myth 2: “If cholesterol drops naturally after a heart attack, maybe my body doesn’t need medications to reduce it.”
Truth: The drop is temporary — and dangerous to misinterpret.
How long until cholesterol rises again?
Without treatment, cholesterol slowly climbs back to its original levels:
- LDL and total cholesterol return to baseline in ~3 months
- But most patients are placed on high-intensity statins, so the levels stay low (for protection).
Guideline recommendation: Measure cholesterol on admission and then again at 12 weeks post-discharge — that’s when you get the real picture.
Myth 3: “Cholesterol is just a number.”
Truth: Cholesterol is a biological weapon when it enters your arteries.
LDL-C (“bad cholesterol”) is not just a lab value. It is one of the top 5 risk factors for heart attacks in both men and women, along with:
- Diabetes
- High blood pressure
- Smoking
- Family history
What LDL actually does inside your arteries
- LDL enters the artery wall.
- It becomes oxidised (damaged).
- The immune system reacts as if it’s a threat.
- White blood cells eat oxidised LDL — becoming foam cells.
- Foam cells form the lipid core of a plaque.
- The plaque grows silently for years.
This process is called atherosclerosis — a slow, predictable, dangerous disease.
What is plaque actually made of? (Most patients don’t know this)
Scientific studies examining coronary plaque show it contains:
- 87% fibrous tissue (collagen + elastin)
- 7% calcium
- 5% necrotic debris
- 1% foam cells
- Cholesterol crystals throughout
What is fibrous tissue?
Fibrous tissue is a mix of:
- Collagen fibers (strength)
- Elastin fibers (elasticity)
- Water + polysaccharides
- Fibroblast cells
- Matrix proteins (fibronectin, fibrillin, laminin)
This “fibrous cap” covers the dangerous lipid core.
How cholesterol damages the fibrous cap
- Excess LDL in plaque forms cholesterol crystals.
- These crystals expand and tear the fibrous cap.
- Inflammation around cholesterol weakens collagen.
- Smooth muscle cells stop producing protective matrix.
- Matrix metalloproteinases (MMPs) — enzymes released due to inflammation — start dissolving the cap.
This makes the plaque vulnerable.
And when a vulnerable cap ruptures, blood clots form instantly — triggering a sudden heart attack.
This is not opinion. This is well-documented cardiology science.
Myth 4: “Statins or lipid lower therapies only lower cholesterol.”
Truth: Statins or lipid lowering therapies (LLT) prevent the next heart attack by stabilising plaque.
Patients often think statins or LLT are only for “lowering numbers.” But statins and LLTs are powerful disease-modifying medications.
How statins protect your heart
1. Reduce cholesterol synthesis in the liver → Lower LDL-C levels in blood. → Less cholesterol enters plaques.
2. Increase LDL receptors → More LDL is pulled out of blood.
3. Reduce inflammation (major benefit) → Inhibit NF-κB, IL-1β, TNF-α and other inflammatory pathways. → Reduce immune cell attack on the plaque.
4. Strengthen the fibrous cap (super important) → Increase collagen synthesis → Reduce matrix-degrading enzymes (MMP-9) → Make plaques harder, safer, more stable
5. Reduce the chance of plaque rupture → Directly reduce risk of future myocardial infarction.
Statins and LLDs save lives — that is why every guideline worldwide includes them for heart patients.
So, what does all this mean for heart patients?
Key takeaways you must remember:
- Normal cholesterol during or after a heart attack is NOT normal. It is a temporary fall caused by inflammation.
- Your real cholesterol level was BEFORE your heart attack.
- LDL cholesterol is a core ingredient of plaque — this is proven science.
- Cholesterol crystals weaken and tear plaque.
- Statins and LLTs do more than bring numbers down — they stabilise plaque and prevent future events.
- Cholesterol rises back to baseline within 3 months if left untreated.
- LDL-C is among the top 5 risk factors in BOTH men and women.
My message as a heart patient leader
I had my heart attack at 33. I didn’t know any of this when it happened. Most patients and families don’t.
That is why I write, speak, educate and build communities — so no patient and family has to navigate this journey in confusion or fear.
At Heart Health India Foundation, we bring real patients, families and cardiologists together to bust myths with science and lived experience.
Because knowledge is medicine. Awareness is prevention. Science saves lives.
Every week, thousands of patients and families tell us how much this community has helped them feel confident, informed, and less alone.If you’re seeking the same — or if you’re a doctor who wants to contribute — join the Heart Health India Foundation community today.
If you found this useful, share it with someone you care about. It may help them avoid the next heart attack.
Bibliography:
- The Role of Lipids and Lipoproteins in Atherosclerosis https://www.ncbi.nlm.nih.gov/books/NBK343489/
- Mechanisms of fibrous cap formation in atherosclerosis https://pmc.ncbi.nlm.nih.gov/articles/PMC10475556/
- Lipid Management in Patients Presenting With Acute Coronary Syndromes: A Review https://pmc.ncbi.nlm.nih.gov/articles/PMC7955383/
- The Modification of Serum Lipids after Acute Coronary Syndrome and Importance in Clinical Practice https://pmc.ncbi.nlm.nih.gov/articles/PMC3322446/
- Cholesterol in human atherosclerotic plaque is a marker for underlying disease state and plaque vulnerability https://pmc.ncbi.nlm.nih.gov/articles/PMC2890627/
- Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes https://pubmed.ncbi.nlm.nih.gov/19327423/
- Current concepts in cardiovascular pathology: the role of LDL cholesterol in plaque rupture and stabilization https://pubmed.ncbi.nlm.nih.gov/9550502/
- Cholesterol crystal induced arterial inflammation and destabilization of atherosclerotic plaque https://academic.oup.com/eurheartj/article-abstract/37/25/1959/1748880?redirectedFrom=fulltext&login=false
- Statin treatment reduces matrix degradation capacity of proinflammatory polarized macrophages https://pubmed.ncbi.nlm.nih.gov/30098417/
- Effects of statins in reducing thrombotic risk and modulating plaque vulnerability https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.4960261305
- Statins and the vascular endothelial inflammatory response https://pmc.ncbi.nlm.nih.gov/articles/PMC3839264/
- Statins as Anti-Inflammatory Agents in Atherogenesis: Molecular Mechanisms and Lessons from the Recent Clinical Trials https://pmc.ncbi.nlm.nih.gov/articles/PMC3394171/
