What arterial plaque actually is

Atherosclerosis isn't 'pipes furring up from the inside' — it's a disease of the artery wall itself, driven by cholesterol particles getting trapped inside it. Get the mechanism and the rest of this guide follows: why soft plaque matters more than a tight narrowing, and why a 'clean' stress test can miss the plaque that causes a heart attack.

How plaque forms

The retention model

The artery is lined by a thin active layer, the endothelium. Where blood flow is turbulent (branch points, curves) it becomes leaky and inflamed, and ApoB-carrying particles (LDL and its relatives) pass into the wall and get trapped — the 'response-to-retention' model, the initiating step. Trapped particles are oxidised, which the body reads as danger.

The inflammatory loop

Oxidised particles recruit immune cells (monocytes) that become macrophages, which gorge on the trapped cholesterol and turn into foam cells — the earliest visible lesion (a 'fatty streak', present in many people by their 20s). Foam cells die, spilling a soft lipid/necrotic core; smooth-muscle cells lay a fibrous cap over it. The whole thing is self-amplifying: more particles in the blood means more retained, more inflammation, more plaque. Evidence ●●●●●

Soft vs. calcified

Two very different things

Soft (non-calcified) plaque is lipid-rich, inflamed, thin-capped — the young, dangerous, rupture-prone form (it shows as 'low-attenuation' plaque on a CT scan). Dense calcified plaque is older and largely a healing/stabilising signature — mineralised, quieter, less likely to rupture. A key nuance: spotty micro-calcification flags active instability, while large confluent dense calcium marks stability. This distinction runs through the whole imaging story.

Why most heart attacks come from small plaques

The vulnerable plaque

The lesion that kills is usually not the tightest narrowing. It's the thin-cap fibroatheroma — a large soft lipid core under a fibrous cap thinner than 65 microns, riddled with inflammation. Under stress the cap tears, the core hits flowing blood, and a clot forms in minutes. Because these plaques are soft rather than bulky, they are often non-obstructive — they barely narrow the artery, so they look reassuring on an angiogram or stress test. Evidence ●●●●●

Burden beats stenosis

Roughly 60–70% of heart attacks arise from lesions narrowing the artery less than 50%. The landmark PROSPECT study found future events were predicted by total plaque burden, a small lumen, and a thin-cap fibroatheroma — not by the tightest stenosis. This is the single most important reframing in the field: how much plaque you have, and how soft it is, matters more than the 'percent narrowing' — and it's exactly why a calcium score of zero can miss risk (covered in the scans section).

How to read the evidence dots

A five-dot mark grades how solid a claim is. ●●●●● overwhelming (many trials / meta-analyses agree) · ●●●●○ strong · ●●●○○ moderate or genuinely mixed · ●●○○○ weak or short-term only · ●○○○○ mechanism or marketing, not outcomes. Figures are group averages; individuals vary.