From Stable Plaque to Sudden Heart Attack: Understanding Plaque Rupture

The journey from high cholesterol to a heart attack often hinges on a single, dramatic event: plaque rupture. Understanding this process is key to appreciating why managing LDL cholesterol is not just about preventing plaque growth, but also about keeping existing plaques stable and less likely to cause a catastrophic blockage.
For years, a plaque can exist within an artery wall, growing slowly and not causing major problems. This is known as a stable plaque. It typically has a thick, fibrous cap that walls off its soft, fatty core from the bloodstream. While it may narrow the artery, it is less likely to break apart.
The danger arises when a plaque becomes unstable. These plaques often have a thin, fragile cap and a large, lipid-rich core with a lot of inflammatory cells. High levels of LDL cholesterol and chronic inflammation contribute to the thinning of this cap. Eventually, mechanical stress from blood flow or a surge in blood pressure can cause the weak cap to tear or rupture.
When the plaque ruptures, its fatty contents are exposed to the blood. The body’s clotting system immediately mistakes this for an injury and initiates a rapid response to “heal” the area by forming a blood clot (thrombus). This clot can grow so large that it completely blocks the artery within minutes, cutting off blood flow to the heart muscle. This is a heart attack.
This is why aggressive cholesterol management is so critical. Lowering LDL cholesterol, particularly with medications like statins, has been shown to not only slow plaque growth but also to stabilize existing plaques by reducing inflammation and helping to thicken their fibrous caps. This makes them less likely to rupture, directly preventing the final, tragic step in the progression of heart disease.