Development of a model for prediction of coronary atherosclerotic regression: evaluation of high-density lipoprotein cholesterol level and peripheral blood monocyte count
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Shigemasa Tani Michiaki Matsumoto Takeo Anazawa Hirofumi Kawamata Shingo Furuya Hiroshi Takahashi Kiyoshi Iida Takehiko Washio Narim
- چاپ و سال / کشور: 2011
Description
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 (b -0.56, p\0.0001) and the decrease in monocyte count (b 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 (D) monocyte count and DHDL-C were above or below the median values was prepared. Among the four groups, the group with DHDL-C C8.8% and Dmonocyte count B -8.6% showed the largest plaque regression (-20.4%), and the group with DHDL-C\8.8%and Dmonocyte count[ -8.6% showed the increase of the plaque volume (2.6%). In viewof the inflammatory nature of atherosclerosis, the model constructed using the two predictors may be a useful model for the prediction of plaque regression
Heart Vessels DOI 10.1007/s00380-011-0130-8 Received: 28 October 2010 / Accepted: 25 February 2011
