Lowering “bad” cholesterol substantially reduces the risk of a heart attack. Yet many people still develop coronary heart disease even after treatment brings their LDL cholesterol down to a recommended level. According to the World Health Organization (WHO), cardiovascular diseases kill nearly 17.9 million people worldwide each year.
Heart attacks and strokes account for more than four out of five of those deaths. Coronary heart disease develops when cholesterol accumulates in the blood vessels supplying the heart. If untreated, it can lead to a heart attack. Researchers now believe other fat-carrying particles explain much of the risk that remains after LDL is controlled.
Not All Cholesterol Carriers Are Equally Harmful
Researchers at Chalmers University of Technology in Sweden have identified blood protein patterns that offer clues to what happens beyond cholesterol buildup. They studied three types of particles that carry fats through the blood: LDL (low-density lipoprotein), triglyceride-rich lipoproteins (TRL), and lipoprotein(a), or Lp(a). All three can deposit cholesterol in artery walls, and LDL is the most abundant.
But abundance does not tell the whole story. A previous study by the same group found that counting these harmful particles was the best way to predict future heart disease. It also showed that TRL and Lp(a) were more harmful per particle than LDL.
“For this study, we wanted to understand what happens beyond the accumulation of cholesterol in artery walls, whether different fat-carrying particles can damage the blood vessels differently and why the remaining risk of heart disease still occurs,” says Jakub Morze, lead author and postdoctoral fellow at Chalmers.
Protein Patterns Point to Shared Inflammation
To understand the difference, the team used proteomics — the large-scale study of proteins. Proteins carry out essential functions in the body, and their levels change with diet, stress, aging, and disease. The researchers combined measurements of almost 3,000 blood proteins with genetic data and long-term health records. They found two very distinct patterns.
The pattern linked to LDL was mainly associated with cholesterol simply accumulating in artery walls. In contrast, TRL and Lp(a) shared many protein patterns and signs of more harmful biological effects. These particles contained proteins that attract immune cells, which could trigger inflammation and change the structure of blood vessel walls.
“The overlap for TRL and Lp(a) is one of the most interesting findings. 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,” says Morze.
What This Means for Heart Disease Prevention
The findings do not change the importance of lowering LDL. LDL reduction remains the foundation of prevention. However, the study points to biological processes that explain the remaining risk that persists even when LDL reaches a healthy level. “Lowering LDL cholesterol remains a cornerstone of prevention. Our findings point to biological processes that may help explain some of the risk that remains beyond LDL.
The next step is to establish whether measuring or targeting these processes can improve prevention alongside existing treatments,” says Clemens Wittenbecher, who led the study and is Assistant Professor of Precision Medicine and Diagnostics at Chalmers. This could pave the way for more precise prevention strategies that target inflammation and vascular changes caused by TRL and Lp(a), not just cholesterol buildup.
Q&A
Q: If my LDL is low, why am I still at risk for heart disease?
A: LDL is the most abundant cholesterol carrier, but TRL and Lp(a) are more harmful per particle. They cause inflammation and attract immune cells to vessel walls, creating risk that remains even after LDL is lowered.
Q: What is the difference between LDL, TRL, and Lp(a)?
A: All three are apolipoprotein B-containing lipoproteins that carry fats. LDL mainly deposits cholesterol. TRL and Lp(a) share protein patterns linked to inflammation and structural damage to blood vessels.
Q: Will there be new treatments targeting TRL and Lp(a)?
A: Researchers believe these findings could help identify new targets for prevention. Measuring these inflammatory processes may improve risk prediction beyond standard cholesterol tests.
FAQ
1. What did the Chalmers study do?
Researchers at Chalmers University analyzed nearly 3,000 blood proteins, combined with genetic and health records, to see how LDL, TRL, and Lp(a) damage blood vessels differently.
2. Which particles are most dangerous per particle?
TRL and Lp(a) were found to be more harmful per particle than LDL, despite LDL being more numerous in the blood.
3. Where was the study published?
The study titled “Apolipoprotein B-containing lipoproteins: distinct roles in atherosclerosis revealed by plasma proteomic profiling” was published on August 31, 2026, in the European Heart Journal. DOI: 10.1093/eurheartj/ehag718
4. Should I stop worrying about LDL cholesterol?
No. The authors stress that lowering LDL remains the cornerstone of prevention. This research explains additional risk that persists and points to future prevention strategies.
Disclaimer: This article is for informational purposes only and summarizes peer-reviewed research from Chalmers University of Technology published in the European Heart Journal. It does not constitute medical advice, diagnosis, or treatment. Always consult a qualified healthcare professional for advice regarding cholesterol, heart disease risk, and prevention strategies.
