Global Genomics Group, LLC, Richmond, VA.
J Am Heart Assoc. 2013 Nov 19;2(6):e000344. doi: 10.1161/JAHA.113.000344.
Apoprotein B-containing lipoproteins are atherogenic, but atheroprotective functions of apoprotein A-containing high-density lipoprotein (HDL) particles are poorly understood. The association between lipoproteins and plaque components by coronary computed tomography angiography (CTA) and intravascular ultrasound with radiofrequency backscatter (IVUS/VH) has not been evaluated.
Quantitative, 3-dimensional plaque measurements were performed in 60 patients with CTA and IVUS/VH. Apoproteins, lipids, and HDL subpopulations were measured with 2-dimensional (2D) gel electrophoresis, and correlation was assessed with univariate and multivariable models. ApoB particles were associated with a higher proportion of noncalcified plaque (NCP) and a lower proportion of calcified plaque (small, dense low-density lipoprotein cholesterol and high-density NCP: r=0.3, P=0.03; triglycerides and low-density NCP: r=0.34, P=0.01). Smaller, dense, lipid-poor HDL particles were associated with a shift from calcified plaque to NCP on CTA (α3-HDL% and low-density NCP: r=0.32, P=0.02) and with larger plaque volume on IVUS/VH (α4-HDL%: r=0.41, P=0.01; α3-HDL%: r=0.37, P=0.03), because of larger dense calcium (α4-HDL%: r=0.37, P=0.03), larger fibrous tissue (α4-HDL%: r=0.34, P=0.04), and larger necrotic core (α4-HDL%: r=0.46, P<0.01; α3-HDL%: r=0.37, P=0.03). Larger lipid-rich HDL particles were associated with less low-density NCP on CTA (α2-HDL%: r=-0.34, P=0.02; α1-HDL%: r=-0.28, P=0.05), with smaller plaque volume on IVUS/VH (pre-α2-HDL: r=-0.33, P=0.05; α1-HDL%: r=-0.41, P=0.01; pre-α2-HDL: r=-0.33, P=0.05) and with less necrotic core (α1-HDL: r=-0.42, P<0.01; pre-α2-HDL: r=-0.38, P=0.02; α2-HDL: r=-0.35, P=0.03; pre-α1-HDL: r=-0.34, P=0.04). Pre-β2-HDL was associated with less calcification and less stenosis by both modalities.
ApoB and small HDL particles are associated with larger plaque burden and more noncalcified plaque, whereas larger HDL and pre-β2-HDL particles are associated with plaque burden and less noncalcified plaque by both CTA and IVUS/VH.
载脂蛋白 B 脂蛋白是动脉粥样硬化的,但载脂蛋白 A 载脂蛋白高密度脂蛋白(HDL)颗粒的动脉粥样保护功能知之甚少。通过冠状动脉计算机断层血管造影术(CTA)和血管内超声与射频背向散射(IVUS/VH)评估脂蛋白与斑块成分之间的关系尚未得到评估。
对 60 例接受 CTA 和 IVUS/VH 的患者进行定量、三维斑块测量。用二维(2D)凝胶电泳测量载脂蛋白、脂质和 HDL 亚群,并通过单变量和多变量模型评估相关性。载脂蛋白 B 颗粒与非钙化斑块(NCP)比例较高和钙化斑块比例较低相关(小、密低密度脂蛋白胆固醇和高密度 NCP:r=0.3,P=0.03;甘油三酯和低密 NCP:r=0.34,P=0.01)。较小、致密、富含脂质的 HDL 颗粒与 CTA 上从钙化斑块向 NCP 的转变相关(α3-HDL%和低密 NCP:r=0.32,P=0.02),与 IVUS/VH 上更大的斑块体积相关(α4-HDL%:r=0.41,P=0.01;α3-HDL%:r=0.37,P=0.03),因为有更大的致密钙(α4-HDL%:r=0.37,P=0.03)、更大的纤维组织(α4-HDL%:r=0.34,P=0.04)和更大的坏死核心(α4-HDL%:r=0.46,P<0.01;α3-HDL%:r=0.37,P=0.03)。较大的富含脂质的 HDL 颗粒与 CTA 上较少的低密 NCP 相关(α2-HDL%:r=-0.34,P=0.02;α1-HDL%:r=-0.28,P=0.05),与 IVUS/VH 上较小的斑块体积相关(前-α2-HDL:r=-0.33,P=0.05;α1-HDL%:r=-0.41,P=0.01;前-α2-HDL:r=-0.33,P=0.05),与较少的坏死核心相关(α1-HDL:r=-0.42,P<0.01;前-α2-HDL:r=-0.38,P=0.02;α2-HDL:r=-0.35,P=0.03;前-α1-HDL:r=-0.34,P=0.04)。前-β2-HDL 与两种方式的钙化和狭窄程度减少有关。
载脂蛋白 B 和小的 HDL 颗粒与更大的斑块负担和更多的非钙化斑块相关,而更大的 HDL 和前-β2-HDL 颗粒与 CTA 和 IVUS/VH 的斑块负担和更少的非钙化斑块相关。