In path-breaking research, scientists have discovered how the good cholesterol in the body becomes dysfunctional and loses its cardio-protective properties - leading to clogging and hardening of the arteries.
"In the artery wall during atherosclerosis, a large proportion of apolipoprotein A1 (apoA1) - a primary protein present in high-density lipoprotein (HDL) - becomes oxidised and contributes to the development of coronary artery disease," said Stanley Hazen, head of preventive cardiology and rehabilitation at Cleveland Clinic in Ohio.
ApoA1 is the primary protein present in HDL - or good cholesterol - providing the structure of the molecule that allows it to transfer cholesterol out of the artery wall and deliver it to liver, from which cholesterol is excreted.
For over five years, Stanley Hazen and his team developed a method for identifying dysfunctional apoA1/HDL and discovered the process by which it is oxidised and turned dysfunctional in the artery wall.
The scientists then examined 627 cardiology patients for the dysfunctional HDL and found that higher levels raised the patient's risk for cardiovascular disease, said the study published in the journal Nature Medicine.
"This research is the first step in creating new tests and treatments for cardiovascular disease," Hazen said.
"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 added.