Division of Internal Medicine, Nordland Hospital, Norway; Department of Clinical Medicine, University of Tromsø, Norway.
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway; Norwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Norway.
J Clin Lipidol. 2021 Jan-Feb;15(1):134-141. doi: 10.1016/j.jacl.2020.12.006. Epub 2020 Dec 16.
Reduction of the aortic valve area (AVA) may lead to aortic valve stenosis with considerable impact on morbidity and mortality if not identified and treated. Lipoprotein (a) [Lp(a)] and also inflammatory biomarkers, including platelet derived biomarkers, have been considered risk factor for aortic stenosis; however, the association between Lp(a), inflammatory biomarkers and AVA among patients with familial hypercholesterolemia (FH) is not clear.
We aimed to investigate the relation between concentration of Lp(a), measurements of the aortic valve including velocities and valve area and circulating inflammatory biomarkers in adult FH subjects and controls.
In this cross-sectional study aortic valve measures were examined by cardiac ultrasound and inflammatory markers were analyzed in non-fasting blood samples. The study participants were 64 FH subjects with high (n = 29) or low (n = 35) Lp(a), and 14 healthy controls.
Aortic valve peak velocity was higher (p = 0.02), and AVA was lower (p = 0.04) in the FH patients compared to controls; however, when performing multivariable linear regression, there were no significant differences. Furthermore, there were no significant differences between the high and low FH Lp(a) groups regarding the aortic valve. FH subjects had higher levels of platelet-derived markers CD40L, PF4, NAP2 and RANTES compared to controls (0.003 ≤ P ≤ 0.03). This result persisted after multiple linear regression.
Middle-aged, intensively treated FH subjects have higher aortic valve velocity, lower AVA, and higher levels of the platelet-derived markers CD40L, PF4, NAP2 and RANTES compared to healthy control subjects. The aortic valve findings were not significant after multiple linear regression, whereas the higher levels of platelet-derived markers were maintained.
如果未被识别和治疗，主动脉瓣面积（AVA）的减少可能导致主动脉瓣狭窄，这对发病率和死亡率有重大影响。脂蛋白（a）[Lp（a）]以及包括血小板衍生生物标志物在内的炎症生物标志物已被认为是主动脉狭窄的危险因素；然而，家族性高胆固醇血症（FH）患者中 Lp（a）、炎症生物标志物和 AVA 之间的关系尚不清楚。
我们旨在研究成年 FH 患者和对照组中 Lp（a）浓度、主动脉瓣测量值（包括速度和瓣口面积）和循环炎症生物标志物之间的关系。
在这项横断面研究中，通过心脏超声检查主动脉瓣测量值，并分析非禁食血液样本中的炎症标志物。研究参与者为 64 名 FH 患者，其中高（n=29）或低（n=35）Lp（a），以及 14 名健康对照者。
与对照组相比，FH 患者的主动脉瓣峰值速度较高（p=0.02），AVA 较低（p=0.04）；然而，在进行多元线性回归后，差异无统计学意义。此外，高 FH Lp（a）组和低 FH Lp（a）组的主动脉瓣无显著差异。FH 患者的血小板衍生标志物 CD40L、PF4、NAP2 和 RANTES 水平高于对照组（0.003≤P≤0.03）。该结果在多元线性回归后仍然存在。
与健康对照组相比，中年、强化治疗的 FH 患者的主动脉瓣速度较高、AVA 较低，以及血小板衍生标志物 CD40L、PF4、NAP2 和 RANTES 的水平较高。经多元线性回归后，主动脉瓣结果无显著差异，而血小板衍生标志物的水平仍保持较高。
