Atherosclerosis Drivers (Part 2) - How Plaques Grow, Change, and Lead to Cardiovascular Events
In Part 1, we explored how atherosclerosis begins: the early injuries to the arterial lining, the role of the glycocalyx, and why apoB-containing particles are the necessary ingredient for plaque formation. Now we follow the rest of the story — how plaques evolve over time, why some remain stable, and why others rupture and cause heart attacks or strokes.
Understanding this progression is crucial. Atherosclerosis is not a straight line. It moves through stages, and each stage presents opportunities to slow, halt, or even reverse risk.
From Fatty Streak to Fibrous Plaque: Early Atherosclerosis Progression
Once apoB-containing particles — including LDL, VLDL, IDL, and Lp(a), all of which carry cholesterol — slip beneath the artery’s thin inner lining, immune cells move in to clean them up. These immune cells ingest these apoB particles and become “foam cells,” the earliest visible sign of plaque.
Over time, repeated particle entry and inflammation create a more complex structure:
a lipid-rich core
a surrounding layer of inflammatory cells
a thin fibrous cap — a collagen layer that attempts to stabilize the plaque
This is the classic atherosclerotic plaque — the foundation of most heart disease.
Plaques like these can sit quietly for decades without causing blockage. The danger comes from how they change.
Soft vs. Hard Plaques: Understanding Plaque Stability
Plaques are not all the same — and their behavior depends on their composition.
Soft plaques (non-calcified plaques)
These early-stage plaques are lipid-rich and inflamed. They tend to:
have thinner caps
be more vulnerable to rupture (a tear in the plaque that triggers clot formation)
Soft plaque causes most heart attacks — not because it blocks the artery severely, but because it is unstable.
Hard plaques (calcified plaques)
Over years or decades, the body attempts to stabilize soft plaque by laying down calcium. This turns the plaque into a “hard,” more stable structure.
Calcified plaque:
is less likely to rupture
is more structurally stable
shows up well on imaging (like coronary calcium scoring)
Hard plaque is less likely to rupture, but it can still narrow the artery enough to limit blood flow. When that happens, exercise tolerance drops — a key marker of healthy aging — making these plaques clinically important even if they’re more stable.
How Plaques Narrow Arteries and Limit Blood Flow
As plaques grow, they begin pushing into the lumen — the open channel where blood flows. At first, the artery expands outward to make room. Eventually, it can’t keep up, and the plaque begins encroaching inward, narrowing the artery.
When blood flow becomes restricted, people may experience:
shortness of breath with exertion
reduced exercise capacity
chest tightness, pressure, or discomfort
fatigue during activities that previously felt easy
This is why stable angina — predictable symptoms with exertion — usually reflects flow limitation, not plaque rupture.
Plaque Rupture: The Real Cause of Most Heart Attacks and Strokes
A heart attack usually doesn’t happen because an artery slowly narrowed over time.
It happens because a vulnerable plaque ruptures.
A simple analogy
A plaque is like a scab inside your artery. If it tears open, the body thinks there is bleeding — and rushes to form a clot. But when that clot forms inside a fixed-diameter blood vessel, it can suddenly stop blood flow.
If the vessel supplies the heart → heart attack.
If the vessel supplies the brain → stroke.
What makes a plaque likely to rupture?
high inflammation
a thin fibrous cap
ongoing apoB particle entry
smoking
high blood pressure
high blood sugar or insulin resistance
stress and surges of stress hormones
This is why reducing cardiovascular risk is never about a single metric. Plaque stability — not just plaque size — determines consequences.
How Fast Atherosclerosis Progresses (and Why It Varies)
Plaque progression varies dramatically between individuals.
Some people accumulate plaque slowly, developing mild, stable disease well into old age. Others develop high-risk plaque earlier because of:
genetics (including Lp(a))
metabolic dysfunction
hypertension
chronic inflammation
smoking
high apoB levels over many years
The duration of exposure matters just as much as the degree. A slightly elevated apoB level over 30 years can be more harmful than a very high level for a short time.
Plaques are dynamic — they can grow, shrink, stabilize, or become inflamed depending on long-term risk factors. This is why ongoing monitoring, imaging, and risk assessment are so important in preventing heart disease.
How Plaque Behavior Can Be Changed: Key Levers to Reduce Cardiovascular Risk
Even after plaques form, you can still influence what happens next. The major levers that stabilize plaques and reduce cardiovascular events include:
Lowering apoB particle number
Statins, ezetimibe, PCSK9 inhibitors, bempedoic acid, and lifestyle changes all reduce the number of apoB particles entering the artery.
Improving metabolic health
Reducing insulin resistance, supporting glucose control, and decreasing visceral fat directly reduce inflammatory signaling within plaque.
Lowering blood pressure
Healthy vascular tone protects the arterial lining from ongoing injury.
Improving diet quality
Mediterranean and whole-food eating patterns reduce inflammation and support plaque stability.
Exercise
Regular aerobic activity improves artery flexibility and function while minimizing inflammation.
Smoking cessation
One of the most powerful interventions for plaque stabilization.
Addressing chronic stress and sleep quality
Stress hormones and poor sleep both worsen endothelial injury and inflammation.
Takeaway: Atherosclerosis Is Dynamic, and Its Consequences Are Modifiable
Atherosclerosis is common — nearly universal with advancing age — but its consequences are not inevitable. Mild plaque that stays stable may never cause a problem. Unstable plaque with ongoing inflammation is where risk lies.
Your daily actions — and your medical team’s strategy — profoundly influence which direction plaque moves.
If you’d like to better understand your risk and how to mitigate it, contact us to discuss options.
