Mahabadi Amir Abbas, Kahlert Philipp, Kahlert Heike Annelie, Dykun Iryna, Balcer Bastian, Forsting Michael, Heusch Gerd, Rassaf Tienush
West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Am J Cardiol. 2018 Aug 15;122(4):645-649. doi: 10.1016/j.amjcard.2018.04.046. Epub 2018 May 11.
Although lipoprotein(a) (Lp[a]) is linked with aortic valve calcification and clinical aortic valve stenosis (AVS) in middle-aged cohorts, patients aged ≥70 years represent a majority of patients with AVS, in which mechanisms leading to AVS may differ. We sought to determine whether Lp(a) distinguishes patients ≥70 years with and without AVS. We matched 484 patients ≥70 years with AVS, scheduled for transcatheter aortic valve implantation with 484 patients without AVS by age group and gender. Lp(a) levels were compared in patients with and without AVS and stratified by presence and absence of clinical coronary artery disease (CAD) manifestation. A total of 968 patients (mean age 80 ± 5 years, 48% women) were included. When comparing patients with and without AVS, no difference in Lp(a) was observed (AVS: 17 [8; 56] mg/dl, no AVS: 18.5 [8.5; 57] mg/dl, p = 0.56). In contrast, patients with clinical CAD manifestation had higher Lp(a) levels than those without clinical CAD manifestation (coronary artery disease: 19 [9; 60] mg/dl, no coronary artery disease 15 [7; 44] mg/dl, p = 0.0006). In regression analysis, no significant association of Lp(a) with AVS was observed in unadjusted (OR [95% CI]: 0.98 [0.91 to 1.06], p = 0.59) and risk factor-adjusted models (0.98 [0.90 to 1.06], p = 0.57). However, Lp(a) was independently associated with clinical CAD manifestation (unadjusted: 1.14 [1.04 to 1.24], p = 0.003, risk factor adjusted: 1.17 [1.07 to 1.27], p = 0.0006). In conclusion, in a large cohort of patients ≥70 years, Lp(a) was associated with clinical CAD manifesation, but not with AVS. Our results suggest that in patients over 70 years, the development of AVS is not influenced by Lp(a).
尽管脂蛋白(a)[Lp(a)]与中年人群的主动脉瓣钙化及临床主动脉瓣狭窄(AVS)有关,但≥70岁的患者占AVS患者的大多数,导致AVS的机制可能有所不同。我们试图确定Lp(a)是否能区分≥70岁有和没有AVS的患者。我们将484例计划接受经导管主动脉瓣植入术的≥70岁AVS患者,按年龄组和性别与484例无AVS患者进行匹配。比较有和没有AVS患者的Lp(a)水平,并根据有无临床冠状动脉疾病(CAD)表现进行分层。共纳入968例患者(平均年龄80±5岁,48%为女性)。比较有和没有AVS的患者时,未观察到Lp(a)有差异(AVS:17[8;56]mg/dl,无AVS:18.5[8.5;57]mg/dl,p = 0.56)。相比之下,有临床CAD表现的患者Lp(a)水平高于无临床CAD表现的患者(冠状动脉疾病:19[9;60]mg/dl,无冠状动脉疾病:15[7;44]mg/dl,p = 0.0006)。在回归分析中,未调整模型(OR[95%CI]:0.98[0.91至1.06],p = 0.59)和危险因素调整模型(0.98[0.90至1.06],p = 0.57)中均未观察到Lp(a)与AVS有显著关联。然而,Lp(a)与临床CAD表现独立相关(未调整:1.14[1.04至1.24],p = 0.003,危险因素调整:1.17[1.07至1.27],p = 0.0006)。总之,在一大群≥70岁的患者中,Lp(a)与临床CAD表现相关,但与AVS无关。我们的结果表明,在70岁以上的患者中,AVS的发生不受Lp(a)的影响。