Researchers have pinpointed why "good" cholesterol goes "bad."
High-density lipoprotein (HDL) which is considered to be "good" cholesterol, can become "dysfunctional"; when this happens the cholesterol loses its heart-healthy properties, instead it clogs arteries and promotes inflammation, a Cleveland Clinic news release reported.
Clinical trials on pharmaceuticals that work to raise HDL levels have failed to show they can effectively improve cardiovascular health.
Recent studies have found a protein found in HDL is also present in an "oxidized form in diseased artery walls," the news release reported.
The main protein found in HDL is Apolipoprotein A1 (apoA1); this protein allows molecules to remove cholesterol from the artery walls and deposit it in the liver.
apoA1 is also believed to be responsible for giving HDL the ability to protect cardiovascular health. The researchers discovered that during atherosclerosis a chunk of the apoA1 becomes oxidized and can no longer protect the heart; instead it contributes to dangerous artery clogging.
The researchers came up with a plan for identifying dysfunctional apoA1/HDL. The research team analyzed the blood of 627 Cleveland Clinic cardiology patients and found higher levels of dysfunctional HDL increased the study subjects' risk of heart disease.
"Identifying the structure of dysfunctional apoA1 and the process by which it becomes disease-promoting instead of disease-preventing is the first step in creating new tests and treatments for cardiovascular disease," Doctor Stanley Hazen, M.D., Ph.D., Vice Chair of Translational Research for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic, said in the news release.
"Now that we know what this dysfunctional protein looks like, we are developing a clinical test to measure its levels in the bloodstream, which will be a valuable tool for both assessing cardiovascular disease risk in patients and for guiding development of HDL-targeted therapies to prevent disease," he said.
