Retinal microvascular associations with cardiometabolic risk factors differ by diabetes status: results from the UK Biobank.
Retinal microvascular associations with cardiometabolic risk factors differ by diabetes status: results from the UK Biobank.
复制标题
DOI：
10.1007/s00125-022-05745-y
复制
发表时间：
2022-10
期刊：
影响因子：
8.2
通讯作者：
Rudnicka, Alicja R.
中科院分区：
文献类型：
--
作者：
Tapp, Robyn J.;Owen, Christopher G.;Barman, Sarah A.;Strachan, David P.;Welikala, Roshan A.;Foster, Paul J.;Whincup, Peter H.;Rudnicka, Alicja R.
关键词：
该研究的目的是检查视网膜血管形态测量与血压、身体成分和生物化学的关联，并确定这些关联是否因糖尿病状况而异。英国生物银行眼部评估包括 68,550 名 40-70 岁的参与者，他们接受了免散瞳视网膜摄影、血压和身体成分测量以及血液学分析。全自动图像分析程序提供了视网膜血管直径和弯曲度的测量。使用多级线性回归检查视网膜血管形态与糖尿病状态的心脏代谢危险因素之间的关联，以提供血管直径的绝对差异和弯曲度的百分比差异（允许人内聚类）。这些分析总共包括 50,233 名参与者（从 68,550 名减少）。总体而言，与没有糖尿病的人相比，患有糖尿病的人的小静脉更加弯曲，小动脉直径也更宽。静脉曲张与心脏代谢危险因素之间的关联因总脂肪指数、HbA1c、C反应蛋白、白细胞计数和粒细胞计数的糖尿病状态而异（p相互作用<0.01）。例如，对于非糖尿病患者，白细胞计数每增加一个单位，与静脉曲张度增加 0.18%（95% CI 0.05，0.32%）相关；对于糖尿病患者，白细胞计数单位增加与静脉曲张度增加 1.48%（95% CI 0.90，2.07%）相关。对于小动脉直径，收缩压、舒张压、平均动脉压 (MAP) 和低密度脂蛋白胆固醇之间存在明显的交互作用。例如，对于非糖尿病患者，收缩压升高10 mmHg与小动脉直径差异-0.92 μm（95% CI -0.96至-0.88 μm）相关，而对于糖尿病患者，则与小动脉直径差异-0.58 μm（95% CI -0.76至-0.41 μm）相关。没有观察到小动脉迂曲度或小静脉直径的相互作用。我们提供了明确的证据，证明糖尿病对与视网膜微血管结构相关的心脏代谢危险因素具有改变作用。这些观察结果表明临床前疾病过程的发生，并且可能是高血糖导致的自身调节受损的征兆，这被认为在糖尿病相关微血管并发症的发展中发挥着关键作用。支持此处报告结果的数据可通过英国生物银行 (https://www.ukbiobank.ac.uk/enable-your-research/apply-for-access) 获取。在线版本包含经过同行评审但未经编辑的补充材料，可在 10.1007/s00125-022-05745-y 获取。
The aim of the study was to examine the association of retinal vessel morphometry with BP, body composition and biochemistry, and to determine whether these associations differ by diabetes status. The UK Biobank ocular assessment included 68,550 participants aged 40-70 years who underwent non-mydriatic retinal photography, BP and body composition measurements, and haematological analysis. A fully automated image analysis program provided measurements of retinal vessel diameter and tortuosity. The associations between retinal vessel morphology and cardiometabolic risk factors by diabetes status were examined using multilevel linear regression, to provide absolute differences in vessel diameter and percentage differences in tortuosity (allowing for within-person clustering). A total of 50,233 participants (a reduction from 68,550) were included in these analyses. Overall, those with diabetes had significantly more tortuous venules and wider arteriolar diameters compared with those without. Associations between venular tortuosity and cardiometabolic risk factors differed according to diabetes status (p interaction <0.01) for total fat mass index, HbA1c, C-reactive protein, white cell count and granulocyte count. For example, a unit rise in white cell count was associated with a 0.18% increase (95% CI 0.05, 0.32%) in venular tortuosity for those without diabetes and a 1.48% increase (95% CI 0.90, 2.07%) among those with diabetes. For arteriolar diameter, significant interactions were evident for systolic BP, diastolic BP, mean arterial pressure (MAP) and LDL-cholesterol. For example, a 10 mmHg rise in systolic BP was associated with a −0.92 μm difference (95% CI −0.96 to −0.88 μm) in arteriolar diameter for those without diabetes, and a −0.58 μm difference (95% CI −0.76 to −0.41 μm) among those with diabetes. No interactions were observed for arteriolar tortuosity or venular diameters. We provide clear evidence of the modifying effect of diabetes on cardiometabolic risk factor associations with retinal microvascular architecture. These observations suggest the occurrence of preclinical disease processes, and may be a sign of impaired autoregulation due to hyperglycaemia, which has been suggested to play a pivotal role in the development of diabetes-related microvascular complications. The data supporting the results reported here are available through the UK Biobank (https://www.ukbiobank.ac.uk/enable-your-research/apply-for-access). The online version contains peer-reviewed but unedited supplementary material available at 10.1007/s00125-022-05745-y.
登录
查看更多内容
DOI：
10.1136/bmj.k2234
发表时间：
2018-06-13
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Forouhi NG;Misra A;Mohan V;Taylor R;Yancy W
通讯作者：
Yancy W
影响因子：
5.4
作者：
Said MA;Eppinga RN;Lipsic E;Verweij N;van der Harst P
通讯作者：
van der Harst P
影响因子：
16.2
作者：
Nguyen, Thanh Tan;Wang, Jie Jin;Wong, Tien Yin
通讯作者：
Wong, Tien Yin
影响因子：
3.1
作者：
Popovic, Natasa;Radunovic, Miroslav;Popovic, Tomo
通讯作者：
Popovic, Tomo
DOI：
10.1111/j.1549-8719.2011.00134.x
发表时间：
2011-11
期刊：
Microcirculation (New York, N.Y. : 1994)
影响因子：
--
作者：
Shankar A;Sabanayagam C;Klein BE;Klein R
通讯作者：
Klein R