Poor HDL functionality bears heightened risk of acute coronary syndromes

Several high-density lipoprotein (HDL) functionality parameters, which are linked to HDL roles on cholesterol metabolism, endothelial protection and antioxidant/anti-inflammatory defence, contribute to an increased risk of incident acute coronary syndromes (ACS) and its manifestations in individuals at high risk of cardiovascular disease, a study reports.

The current case-control study was nested within the PREDIMED cohort, a trial evaluating the effects of Mediterranean vs low-fat diet. The population comprised 167 patients with incident ACS and 333 non-ACS controls. ACS patients were more likely to use glucose-lowering drugs (p<0.001), be current smokers (p=0.013) and have greater systolic blood pressure levels (p<0.001).

Researchers measured the following HDL functional characteristics: HDL cholesterol concentration (in plasma); cholesterol efflux capacity; antioxidant ability measured by the HDL oxidative-inflammatory index; phospholipase A2 activity; and sphingosine-1-phosphate, apolipoproteins A-I and A-IV, serum amyloid A, and complement 3 protein (in apolipoprotein B-depleted plasma).

Multivariable conditional logistic regression models showed ACS risk to be associated with low values of cholesterol efflux capacity (odds ratio [OR], 0.58) and levels of sphingosine-1-phosphate (OR, 0.70) and apolipoprotein A-I (OR, 0.58). Higher HDL oxidative inflammatory index values had a marginal association with the risk (OR, 1.27).

On further analysis, low values of cholesterol efflux capacity (OR, 0.33), sphingosine-1-phosphate (OR, 0.60) and apolipoprotein A-I (OR, 0.59) were specifically related to myocardial infarction. On the other hand, high HDL oxidative-inflammatory index values (OR, 1.53) and low apolipoprotein A-I levels (OR, 0.52) were linked to unstable angina.

The findings may prove valuable for the discovery of novel prognostic biomarkers or potential therapeutic targets of cardiovascular disease related to HDL function, according to the researchers.