Researchers at Chalmers University of Technology in Sweden have identified biological processes that may help explain why some people develop heart disease despite lowering their LDL cholesterol to recommended levels. The findings suggest that other particles transporting fats in the blood may contribute to arterial damage through inflammation and related changes.
The study, published in the European Heart Journal, examined three types of lipoproteins: low-density lipoprotein (LDL), triglyceride-rich lipoproteins (TRL), and lipoprotein(a), or Lp(a). All three contain apolipoprotein B, a structural protein, and can contribute to cholesterol deposits in artery walls. These deposits can restrict blood flow and increase cardiovascular risk.
Using proteomics, the large-scale study of proteins, researchers analyzed measurements of nearly 3,000 blood proteins alongside genetic information and long-term health records. This approach enabled them to examine biological patterns associated with different lipoproteins rather than focusing only on the amount of cholesterol these particles carry.
TRL and Lp(a) showed substantially overlapping protein patterns despite being distinct particle types. These patterns were also associated with subsequent heart disease. The findings pointed to proteins involved in attracting immune cells, potentially promoting inflammation and changes in blood vessel walls. LDL-associated proteins were more closely linked to cholesterol accumulation.
The results suggest that TRL and Lp(a) may influence some of the same inflammatory and vascular processes. These shared pathways could provide targets for further research into prevention strategies. However, the study did not test a new treatment or establish a protein-based blood test for routine clinical use.
Lowering LDL cholesterol remains an established component of heart disease prevention, the researchers emphasized. Additional studies are needed to determine whether measuring or targeting the newly identified processes improves outcomes alongside existing treatments. For now, the findings offer a potential explanation for some remaining cardiovascular risk rather than evidence supporting immediate changes to current clinical care.