Modifiable cardiovascular risk factors may be linked more closely to rupture-prone coronary plaques than to higher plaque count. Digest
The tendency of an atherosclerotic plaque to rupture is a part of heart disease risk that a simple count of plaques cannot capture. A new study examined how cardiovascular risk factors that can and cannot be changed relate to both plaque number and structure across the coronary arteries, the main vessels supplying the heart with blood.
Researchers used optical coherence tomography, a technique that reveals near-microscopic details of plaque structure, to examine images from all three major coronary arteries in 131 patients. They assessed five plaque features associated with higher rupture risk: thinner protective caps, high lipid content, immune cells involved in inflammation, tiny blood vessels within plaques, and cholesterol crystals. The analysis compared plaque number and these features with counts of five modifiable risks: high blood pressure, abnormal blood lipids, diabetes, obesity, and smoking. Three nonmodifiable risks were assessed separately: an age 62 or older, being a male, and a family history of coronary artery disease.
- Each additional modifiable risk factor was associated with a 36% higher total count of plaque vulnerability features. Each additional nonmodifiable factor was linked to an approximately 20% increase, but this association was statistically uncertain.
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Each additional modifiable risk factor was also linked to 48% more lipid-rich plaques with thinner protective caps—an established high-risk plaque type. Nonmodifiable risk factors showed no clear association.
- More stable, fibrous plaques were 22% less common per additional modifiable risk factor.
- In contrast to modifiable risk factors, each additional nonmodifiable factor was associated with 12% more plaques overall and 108% more calcium-containing plaques.
Calcium can accumulate as plaques develop and change over many years, which may help explain why these plaques were more strongly linked to nonmodifiable risk factors such as older age. By contrast, smoking, diabetes, and other modifiable risk factors can affect ongoing processes within plaques by sustaining inflammation. Immune cells can release enzymes that break down collagen, weakening the plaque's tissue cap over its fatty core. This makes it more likely to rupture. If that happens, the exposed contents can trigger a blood clot that blocks blood flow to the heart. The modifiable risk factors could therefore make existing plaques more dangerous even without increasing their number.
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Age and family history cannot be changed, but they do not determine everything that happens within diseased arteries. This leaves meaningful room for prevention even after atherosclerosis has already developed.