Cholesterol homeostasis, defined as the balance between absorption and synthesis, influences the progression of coronary atherosclerosis.
Consecutive stable angina pectoris patients (N?= 80) not receiving any lipid-lowering therapy were divided into 2 groups based on the presence of in vivo thin cap fibroatheroma (TCFA) in?de novo target vessels assessed by the combined use of virtual histology intravascular ultrasound and optical coherence tomography.
Patients with in vivo TCFA (n?= 42) showed a higher campesterol-to-lathosterol ratio (3.36 [interquartile range, 2.10 to 4.26] vs. 1.50 [1.20 to 2.50], p < 0.0001). The campesterol-to-lathosterol ratio, low-density lipoprotein (LDL) cholesterol, and high-sensitivity C-reactive protein (hsCRP) were positively correlated with the percentage of necrotic core volume (r?= 0.520, p < 0.0001; r?= 0.520, p?<?0.0001; and r?= 0.539, p < 0.0001, respectively) and negatively correlated with thinnest fibrous cap thickness (r?=??0.566, p < 0.0001; r?=??0.530, p < 0.0001; and r?=??0.358, p?= 0.007, respectively) . The independent predictors of the incidence of TCFA were the campesterol-to-lathosterol ratio (odds ratio: 3.989, 95 % confidence interval: 1.688 to 9.428; p?= 0.002), LDL cholesterol (odds ratio: 1.425, 95 % confidence interval: 1.023 to 1.985; p?= 0.03), hsCRP (odds ratio: 1.025, 95 % confidence interval: 1.003 to 1.047; p?= 0.02), and the percentage of necrotic core volume (odds ratio:1.084, 95 % confidence interval: 1.012 to 1.161; p?= 0.02).
Enhanced absorption and reduced synthesis of cholesterol may be related to coronary plaque vulnerability.