1.
Fibrinogen and the Severity of Coronary Atherosclerosis among Adults with and without Statin Treatment: Lipid as a mediator.
Zhang, Y, Zhu, CG, Guo, YL, Li, S, Xu, RX, Dong, Q, Li, JJ
Heart, lung & circulation. 2016;(6):558-67
Abstract
BACKGROUND It has been proposed that plasma fibrinogen is associated with lipid levels and increased cardiovascular risk. However, the interrelationship has not been well-elucidated. We hypothesise that lipids may be potential mediators. METHODS We enrolled 4748 consecutive subjects scheduled for coronary angiography in this study. The severity of coronary atherosclerosis was assessed by Gensini score (GS). By principle component analysis, a multi-marker lipid index was extracted weighting the coefficients of six atherogenic lipid parameters: total cholesterol (TC), low-density lipoprotein-cholesterol, non-high-density lipoprotein-cholesterol (non-HDL-C), apolipoprotein (apo) B, apoB/apoA1, and TC/HDL-C ratio. Moreover, using mediation analysis, the relationship between fibrinogen and lipids with high GS was evaluated. RESULTS Fibrinogen was positively associated with GS after adjustment (β=0.100, p<0.001). We stratified our analyses by statin use status and found that subjects in the upper fibrinogen tertiles had higher levels of atherogenic lipid parameters irrespective of statin status (p<0.001, all). Significantly, we observed a synergistic effect of fibrinogen and concurrent elevated lipid index for high GS. The adjusted odds ratios were greater in participants who had high fibrinogen levels and also high lipid index compared to those with low lipid index [on statin: 1.725(1.258-2.364) vs. 1.261(0.962-1.652); not on statin: 2.197(1.450-3.328) vs. 1.166(0.417-3.258)]. Specifically, mediation analysis indicated that around 24% of the effect of fibrinogen on high GS was mediated by lipid index, which was attenuated to 13% by statin status. CONCLUSIONS The increased risk of fibrinogen on coronary atherosclerosis appeared to be enhanced by the high atherogenic lipid levels, which mediated around 24% of this effect.
2.
Non-HDL-C is a Better Predictor for the Severity of Coronary Atherosclerosis Compared with LDL-C.
Zhang, Y, Wu, NQ, Li, S, Zhu, CG, Guo, YL, Qing, P, Gao, Y, Li, XL, Liu, G, Dong, Q, et al
Heart, lung & circulation. 2016;(10):975-81
Abstract
BACKGROUND Recent guidelines recommended both low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) are the primary target of lipid modulating therapy. However, which lipid measure is most closely related to the severity of coronary atherosclerosis has not yet been assessed. METHODS We studied 1757 consecutive subjects undergoing coronary angiography who were not receiving any lipid-lowering therapy. Low-density lipoprotein cholesterol was measured directly, and non-HDL-C was calculated. The severity of coronary stenosis was determined using the Gensini Score (GS) system. RESULTS In the overall population, LDL-C and non-HDL-C were all dramatically increased according to the quartiles of GS (p<0.001, both). In patients with coronary atherosclerosis (n=1097), non-HDL-C (r=0.138, p<0.001) was more closely related to GS than LDL-C (r=0.113, p<0.001) tested by Spearman correlation analysis. Multivariate logistic regression analysis suggested that non-HDL-C (OR=1.326, 95% CI 1.165-1.508, p<0.001) was slightly superior to LDL-C (OR=1.286, 95% CI 1.130-1.463, p<0.001) in predicting high GS after adjusting for potential confounders. Among patients with LDL-C less than the median, discordant non-HDL-C could not provide extra value in predicting high GS (OR=0.759, 95% CI 0.480-1.201). However, among patients with LDL-C greater than or equal to the median, the cardiovascular risk was overestimated for patients with discordant non-HDL-C (OR=0.458, 95% CI 0.285-0.736). CONCLUSIONS Our data support the use of non-HDL-C ahead of LDL-C in predicting the severity of coronary atherosclerosis, especially among patients with LDL-C greater than or equal to the median.
3.
Use of low tube voltage and low contrast agent concentration yields good image quality for aortic CT angiography.
Wei, L, Li, S, Gao, Q, Liu, Y, Ma, X
Clinical radiology. 2016;(12):1313.e5-1313.e10
Abstract
AIM: To evaluate the impact of a "double-low" imaging protocol (low tube voltage and low contrast agent concentration) on image quality and radiation dose for aortic computed tomography (CT) angiography (CTA). MATERIALS AND METHODS This was a prospective study of 72 patients undergoing aortic CTA. They were randomised to the double-low and conventional CT (control) groups (n=36/group). Axial imaging was performed in the study group, and control patients were scanned with the conventional protocol. Double-low parameters were: 80-100 kV, 200 mAs, 128×0.625 collimation, 1-mm section thickness, 0.5-mm increments, 300 mm field of view (FOV), iohexol (300 mg iodine/ml, 1-1.5 ml/kg, injected at 4-5 ml/s). Control CT parameters were: 120 kV, 200-300 mAs, iopamidol (370 mg iodine/ml; 1-1.5 ml/kg, injected at 4-5 ml/s); the remaining parameters were the same as in the double-low group. RESULTS Image noise and quality scores of the double-low and control groups were 15.05±1.53 versus 14.67±1.53 and 3.52±0.51 versus 3.44±0.5 (both p>0.05), respectively. Radiation dose was 56% lower in the double-low group compared to control patients (6.76±1.08 versus 15.48±1.01 mSv, p<0.001). Iodine intake per-capita in the double-low group was 18% lower compared to the control group (300.25±7.2 versus 367.86±5.54 mgI/kg, p<0.001). CONCLUSIONS The "double-low" technique for aortic CTA significantly reduced the doses of radiation and iodine contrast agent, while maintaining good image quality.
4.
Impact of short-term low-dose atorvastatin on low-density lipoprotein and high-density lipoprotein subfraction phenotype.
Xu, RX, Guo, YL, Li, XL, Li, S, Li, JJ
Clinical and experimental pharmacology & physiology. 2014;(7):475-81
Abstract
Statins can significantly reduce low-density lipoprotein-cholesterol (LDL-C) and modestly raise or not alter high-density lipoprotein-cholesterol (HDL-C). However, their impact on high-density lipoprotein (HDL) and low-density lipoprotein (LDL) subfractions has been less examined. The aim of the present study was to investigate the short-term impact of low-dose atorvastatin on HDL and LDL subfractions in humans. In this randomized study, data from 52 subjects were analysed. Thirty-seven patients with atherosclerosis were randomized to treatment with atorvastatin 10 mg/day (n = 17) or 20 mg/day (n = 20) for 8 weeks, with 15 healthy subjects without therapy used as a control group. The lipid profile and lipoprotein subfractions were determined using the Lipoprint system at baseline and at 8 weeks. The data suggest that atorvastatin treatment (10 and 20 mg/day) for 8 weeks significantly decreases LDL-C levels and reduces the cholesterol concentration of all LDL subfractions, which is accompanied by an increase of the mean LDL particle size. Although 10 mg/day atorvastatin treatment for 8 weeks had no impact on the HDL subfraction, 20 mg/day atorvastatin for 8 weeks significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles without changing serum HDL-C levels in patients with atherosclerosis. Therefore, the results suggest that 20 mg/day atorvastatin treatment for 8 weeks may result in a favourable modification of the HDL subfraction phenotype in addition to its effects on the cholesterol concentration of all LDL subfractions and mean LDL particle size.