Coronary Plaque: What It Is, Why It Matters, and How We Actually See It
What’s in this article?
The Biological Process: Why plaque is living tissue, not a clogged pipe.
Plaque Types: The critical differences between soft, calcified, and mixed plaque.
The Rupture Myth: Why most heart attacks happen in arteries with only moderate narrowing.
Advanced Imaging: How CCTA and Fractional Flow Reserve (FFR) provide a 3D view of your risk.
The Ikigai Playbook: Moving from reactionary testing to proactive biological protection.
Coronary plaque is the underlying cause of most heart attacks. Understanding how plaque forms, how it behaves, and how we visualize it with tools like coronary CT angiography (CCTA) and fractional flow reserve (FFR) is central to modern preventive cardiology.
When we talk about “plaque,” it’s easy to picture a clogged pipe. But your arteries are living tissue. They respond to stress, injury, inflammation, blood pressure, and metabolic strain. Plaque is a biological process unfolding inside the wall of the artery itself.
How does coronary plaque form?
Plaque begins when cholesterol-carrying particles in the bloodstream slip beneath the inner lining of the artery and become trapped. All of these particles carry a protein called ApoB, which is the primary driver of this process.
The body interprets this trapped cholesterol as an injury. Immune cells arrive, inflammation follows, and over time, a structure forms inside the artery wall made up of fatty material, inflammatory cells, fibrous tissue, and eventually calcium.
Soft vs. Calcified vs. Mixed: What are the types of plaque?
Plaque exists along a spectrum, and the type of plaque you have matters more than the amount of narrowing it causes.
1. Soft (Non-Calcified) Plaque
This is early-stage, "active" plaque. It contains a large amount of fatty material and inflammatory cells. Soft plaque is inherently unstable and does not show up on standard calcium scans. Because it is prone to tearing (rupture), it is the type most likely to cause a sudden heart attack.
2. Calcified Plaque
Over time, the body attempts to stabilize plaque by laying down calcium—essentially a "scar." Calcified plaque is generally more stable, but it represents cumulative exposure to arterial injury. This is what a Coronary Artery Calcium (CAC) scan detects.
3. Mixed Plaque
Most arteries contain a mixture of both components. On advanced imaging, we look for "high-risk" features like outward expansion of the artery wall (positive remodeling) or "spotty" calcifications, which suggest the disease is still biologically active.
Why is narrowing (stenosis) not the whole story?
Most people picture heart disease as a pipe slowly clogging until it closes. However, the American College of Cardiology notes that most heart attacks occur in arteries that were only moderately narrowed (30–50% stenosis) beforehand.
The issue isn't gradual blockage; it's a sudden tear in unstable plaque. When a tear occurs, the body forms a clot to "heal" the site, and it is that clot that abruptly blocks blood flow. Waiting for severe narrowing to appear misses the biology that actually causes acute events.
How do we image coronary plaque at Ikigai?
We use imaging to understand the structure, stage, and physiological impact of disease.
Coronary CT Angiography (CCTA)
Unlike a basic calcium scan, CCTA is contrast-enhanced, allowing us to see the artery wall itself. It detects soft, calcified, and mixed plaque, as well as the exact degree of stenosis.
Fractional Flow Reserve (FFR)
Using advanced quantitative analysis, we can derive CT-based FFR. This is an estimate of whether a specific narrowing is actually limiting blood flow to the heart muscle.
A Call to Action for Your Future Self
Waiting for symptoms isn't prevention—it's reaction. Modern preventive cardiology asks a different question: If disease develops quietly over decades, when would you want to know about it? We image not to create fear, but to create precision. By understanding your unique plaque biology today, we can tailor a strategy to protect your heart for the decades to come.
Key Takeaways: Plaque and Prevention
- Plaque is Biological: It is an evolving process within the artery wall, not just a lump of fat.
- Stability Over Stenosis: A 30% soft plaque can be more dangerous than a 70% calcified plaque due to the risk of rupture.
- Beyond the Calcium Score: While a CAC score of zero is reassuring, it does not exclude high-risk soft plaque.
- Precision Imaging: CCTA and FFR provide a comprehensive view of total plaque burden and its impact on blood flow.
Recommended Reading
ApoB: The Particle That Matters: Why your ApoB count is a better predictor of plaque than LDL alone. [Internal Link Placeholder]
Why a Calcium Score of Zero Isn't a Free Pass: Understanding the "hidden" risk of non-calcified plaque.
Lp(a): The Genetic Heart Risk: How this specific particle accelerates plaque calcification.
Frequently Asked Questions
Is a calcium score of zero good?
Yes. A CAC score of zero is associated with very low short-term event rates. However, it does not exclude soft plaque, which is why we often recommend CCTA for a more complete baseline.
What is the difference between CCTA and FFR?
CCTA shows us the anatomy (what the plaque looks like), while FFR shows us the physiology (whether that plaque is actually blocking oxygen-rich blood flow).
Can plaque be reversed?
While "reversal" is complex, we can stabilize soft plaque and turn it into calcified (stable) plaque through aggressive ApoB lowering and lifestyle optimization, significantly reducing the risk of a rupture.
