Swedish researchers have identified hidden inflammatory mechanisms that damage blood vessels even after levels of "bad" cholesterol have been brought back to normal, the website infohub.kz reports.
Lowering low-density lipoprotein, known as "bad" cholesterol, significantly reduces the risk of a heart attack. Yet in some patients cardiovascular disease continues to progress even when their test results are ideal. A team from Chalmers University of Technology examined nearly 3,000 proteins in blood samples from about 35,000 people in the UK Biobank database to understand the nature of this hidden threat.
The analysis showed that two other types of fat particles are responsible for damaging the arteries: triglyceride-rich lipoproteins and lipoprotein, or Lp(a). Unlike ordinary "bad" cholesterol, which simply settles on the vessel walls, these particles carry proteins that attract immune cells. As a result, general chronic inflammation is triggered in the vascular walls, altering their structure.
Per particle, TRL and Lp(a) act far more destructively than conventional low-density lipoprotein. The authors stress that cholesterol control remains a key preventive measure, but the discovery of shared inflammatory pathways could help create new drugs for targeted protection of the blood vessels.