Monocytes and high-density lipoprotein cholesterol (HDL-C) play important roles in the process of coronary atherosclerosis. We hypothesized that a reasonable predictive model of coronary plaque regression might be constructed using the change in the peripheral monocyte count and the serum HDL-C level. The plaque volume, as assessed by volumetric intravascular ultrasound, was measured at the baseline and after 6 months of pravastatin therapy in 114 patients with coronary artery disease. After 6 months of pravastatin therapy, a significant decrease of the plaque volume by 9.9% (p < 0.0001, vs. baseline) was observed; furthermore, a corresponding increase of the serum HDL-C level and decrease of the peripheral blood monocyte count were also seen (12.5%, p < 0.01 and -7.3%, p < 0.0001). In a multivariate regression analysis using the serum lipids and traditional risk factors as the covariates, the increase in the serum HDL-C (β -0.56, p < 0.0001) and the decrease in monocyte count (β 0.23, p = 0.03) were identified as independent predictors of the plaque regression. A model for the prediction of plaque regression according to whether the achieved the change in (Δ) monocyte count and ΔHDL-C were above or below the median values was prepared. Among the four groups, the group with ΔHDL-C ≥8.8% and Δmonocyte count ≤-8.6% showed the largest plaque regression (-20.4%), and the group with ΔHDL-C <8.8% and Δmonocyte count >-8.6% showed the increase of the plaque volume (2.6%). In view of the inflammatory nature of atherosclerosis, the model constructed using the two predictors may be a useful model for the prediction of plaque regression.
SummaryLow density lipoproteins (LDLs) are heterogeneous aggregations of molecules of different particle sizes, and smallsize LDLs are more potent risk factors for atherosclerosis. We examined the qualitative characteristics of LDLs in patients with stable coronary artery disease (CAD) receiving statin therapy. LDL-particle size was estimated based on the LDL-cholesterol/apolipoprotein B ratio (LDL-C/apoB) in 214 age-adjusted men receiving statin therapy. The LDL-C/ apoB ratio was significantly lower in the CAD (+) group (n = 107) than in the CAD (-) group (n = 107) (median, 1.17 versus 1.19, P = 0.0095). LDL-C/apoB was significantly lower in patients with serum TG ≥ 150 mg/dL than in those with serum TG < 150 mg/dL, and in patients with serum HDL-C < 40 mg/dL than in those with serum HDL-C ≥ 40 mg/ dL (1.06 versus 1.18, P = 0.012; 1.08 versus 1.22, P = 0.0023). Stepwise logistic regression analysis revealed that elevated serum TG was an independent predictor for smaller sizes of LDLs, both in the overall subjects (β : -0.165, P = 0.02) as well as in the subset with serum LDL-C < 100 mg/dL (β : -0.252, P = 0.011). This study demonstrated that not only the absolute serum LDL-C level, but also the qualitative characteristics of LDL may be monitored for secondary prevention of CAD. Such monitoring is particularly important in patients with elevated serum TG levels, which is associated with smaller sizes of LDL-particles. (Int Heart J 2011; 52: 343-347) Key words: Coronary artery disease, Low-density lipoprotein particle size, Statins M any large clinical studies have demonstrated the efficacy of statins for coronary artery disease (CAD) prevention. However, it has been demonstrated that strict control of the serum low-density lipoprotein cholesterol (LDL-C) level by statin therapy is not sufficient by itself to completely prevent ischemic cardiac events, even when secondary prevention measures are undertaken to control coronary risk factors other than the serum LDL-C. 1,2)Atherosclerosis-inducing lipoproteins are produced in the liver, which is the major site of production of very low-density lipoprotein (VLDL). VLDLs are then metabolized to intermediated-density lipoprotein (IDLs) and LDLs, with a progressive decrease in particle size and an increase in particle specific gravity. LDLs, among other lipoproteins, are aggregations of molecules of different particle sizes. Those with small particle sizes are called small-dense (sd-) LDLs (pattern B phenotype), which have a potent atherosclerosis-inducing effect.3) For a given level of the serum LDL-C levels, the presence of molecules of smaller particle sizes has been demonstrated to be associated with higher ischemic cardiac events. 4,5) In current clinical practice, however, only the absolute serum level of LDL-C is measured, and no qualitative tests (eg, measurement of the particle size) of LDL are performed. Hence, we hypothesized that some patients with chronic stable CAD might have qualitatively abnormal LDL (LDL with a small particle size) despite statin therap...
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