Association of non-HDL cholesterol with plaque burden and composition of culprit lesion in acute coronary syndrome. An intravascular ultrasound-virtual histology study.

OBJECTIVE

Lipids play key role in coronary atherosclerosis. The role of non-high-density lipoprotein cholesterol (non-HDL-C) in atherosclerotic plaques using intravascular imaging remains unclear. This study aimed to assess its relationship with coronary plaque features using intravascular ultrasound (IVUS) in acute coronary syndrome (ACS).

METHODS

A total of 601 patients divided into two groups: normal non-HDL-C≤130 mg/dl (n = 410) and high non-HDL cholesterol >130 mg/dl (n = 191). IVUS performed before coronary intervention.

RESULTS

Mean age 53.18 ± 12.29 years. No significant differences in hypertension, diabetes, and smoking between groups. Plaque burden was significantly higher among normal versus high non-HDL-C groups (79.59 ± 9.98 % vs. 81.61 ± 5.39 %; p = 0.001). At minimal luminal site, fibrofatty percentage was higher in normal non-HDL-C group (p = 0.027), while necrotic core greater in high non-HDL-C group (p = 0.033). Segmental analysis, necrotic core was significantly higher in percentage (p = 0.006) and volumes (p = 0.011) in normal versus high non-HDL-C groups. Total cholesterol (r = 0.099, p = 0.015), LDL-C (r = 0.081, p = 0.046), triglycerides (r = 0.083, p = 0.041),and non-HDL-C (r = 0.099, p = 0.015) positively correlated with plaque burden. Total cholesterol (r = 0.115, p = 0.005), LDL-C (r = 0.107, p = 0.009), and non-HDL-C (r = 0.105, p = 0.010) positively correlated with necrotic core volume. Linear regression analysis showed age and non-HDL-C as predictors of higher plaque burden. Multiple linear regression analysis; age, body mass index, and non-HDL-C were predictors of larger necrotic core volume.

CONCLUSION

Non-HDL-C levels were positively associated with plaque burden, measure of extent of atherosclerosis. It is closely associated with and is a predictor of necrotic core volume; a marker of plaque vulnerability. This IVUS study demonstrates potential role of non-HDL-C in causation of plaque in ACS.