Researchers at Chalmers University of Technology in Sweden used proteomics analysis to examine why some people develop heart disease even after reducing their bad cholesterol to recommended levels. The team analyzed nearly 3,000 proteins in blood samples and compared results with genetic information and long-term health records.
The study examined three types of fat-carrying particles: LDL, TRL (triglyceride-rich lipoproteins), and Lp(a) (lipoprotein(a)). All three contain apolipoprotein B and can contribute to atherosclerosis, but through different mechanisms.
LDL primarily deposits cholesterol in artery walls. TRL and Lp(a) showed a striking overlap in their associated protein patterns. These overlapping patterns linked to the later development of heart disease and appeared to involve proteins capable of attracting immune cells, suggesting these particles may promote inflammation and changes in blood vessel wall structure.
"The overlap for TRL and Lp(a) is one of the most interesting findings," says Jakub Morze, lead author and postdoctoral fellow at Chalmers. "It suggests that these particles may affect some of the same inflammatory and vascular processes. This could help identify targets for more precisely directed prevention in the future."
The findings suggest that TRL and Lp(a) individually pose greater cardiovascular risk than LDL particles, which explains why reducing LDL cholesterol alone does not eliminate heart disease risk in some patients.