Abstract 1021: High Cholesteryl Ester Transfer Protein Mass Predicts Accelerated Progression of Coronary Atherosclerosis in Abdominally Obese Patients
Background: Cholesteryl ester transfer protein (CETP) facilitates exchange of esterified cholesterol from high-density lipoprotein (HDL) to atherogenic lipoproteins. While some groups have reported that CETP deficiency is associated with elevated HDL cholesterol levels and protection from coronary heart disease, the impact of CETP on atherosclerosis progression is unknown.
Methods: 676 abdominally obese patients with coronary artery disease underwent serial intravascular ultrasound evaluation in the STRADIVARIUS study. The relationship between baseline levels of CETP mass and clinical characteristics and atheroma progression was investigated.
Results: Compared with the lowest quartile (mass <1.64 μg/L), patients with the highest quartile of CETP mass (>2.71 μg/L) were more likely to be female (50.2 v. 18.9%, p<0.001) and less likely to be treated with a statin (77.0 v. 89.3%, p<0.001) and have diabetes (30.1 v. 46.1%, p=0.009). The highest CETP levels were associated with higher levels of LDL cholesterol (103.5±34.8 v. 78.6±23.9 mg/dL, p<0.001), CRP (4.5 v. 3.0 mg/L, p<0.001) and leptin (30.9 v. 18.8 ng/mL, p<0.001). Of interest, there was no significant difference in HDL cholesterol levels between those with the highest and lowest CETP mass (38.2±10.4 v. 36.9±9.7 mg/dL, p=0.14) respectively. On serial evaluation higher CETP levels were associated with more progression of percent atheroma volume (+0.83±0.21 v. +0.03±0.21%, p=0.01) and total atheroma volume (+3.2±1.4 v. −2.9±1.4 mm3, p=0.001). Multivariable analysis revealed that CETP mass remained an independent predictor of change in percent atheroma volume (p=0.03) and total atheroma volume (p=0.03) after controlling for clinical characteristics.
Conclusion: High levels of CETP mass predict accelerated atheroma progression in abdominally obese patients. These results are consistent with the notion that a high CETP phenotype may remain a relevant and novel target for treatment with anti-atherosclerotic therapies.