Normal cholesterol, be careful of myocardial infarction! Doctors warn: These "two blood lipids" are the culprit of inflammation

Different lipid and protein profiles in blood are an important research direction for researchers to explore the risk of cardiovascular disease; schematic diagram. (Taken from Freepik)

[Compiled by Chen Chengliang/Comprehensive Report] Bad cholesterol is not the only clue in assessing the risk of heart disease. Swedish research has found that two other blood lipids linked to cardiovascular disease partially overlap with blood protein signatures associated with inflammation and blood vessel changes, providing new clues to understanding risks beyond cholesterol.

The science news website "SciTechDaily" reported that this study was published in the "European Heart Journal" on August 31. The research team analyzed data from 35,269 people with no previous cardiovascular disease in the UK Biobank, looked at nearly 3,000 blood proteins, and verified it with data from another group of 5,915 people.

The study compared three types of blood lipids, including low-density lipoprotein (LDL), commonly known as "bad cholesterol", triglyceride-rich lipoprotein (TRL), and lipoprotein (a) [Lp(a)]. The researchers found 471 blood protein signatures associated with TRL and 53 with Lp(a), 36 of which overlapped.

These common features are related to immune responses, inflammatory signals and changes in vascular tissue. In other words, the study found that TRL and Lp(a) are not only related to blood lipid values, but also exhibit some similar biological signals. However, this does not mean that the two blood lipids have exactly the same effect, nor can this study alone conclude that inflammation directly causes heart disease.

Risk clues beyond blood lipid numbers

The research team then tracked the participants' health records. Among the UK Biobank analysis cohort, 1,599 people developed coronary artery disease during the follow-up period. After adjusting for blood lipid concentration and other factors that may affect the results, the researchers found that TRL and Lp(a)-related protein signatures were still associated with a higher risk of coronary artery disease; LDL-related protein signatures did not show a statistically significant association.

Further statistical analysis estimated that protein signatures related to immune activation and vascular remodeling may explain 62% of the association between TRL and coronary artery disease risk, and 14% of the association with Lp(a)-related risk. This is an association proportion estimated by a statistical model and is not proof that these biological processes directly cause the disease.

The research does not negate the importance of controlling bad cholesterol, but suggests that other lipid-related biological signals may also help understand coronary artery disease risk. Whether these protein characteristics can further improve risk assessment remains to be confirmed by follow-up studies.