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葡萄糖耐量状态的变化与心血管疾病事件风险的关系:德黑兰血脂和血糖研究。

Change in glucose intolerance status and risk of incident cardiovascular disease: Tehran Lipid and Glucose Study.

机构信息

Metabolic Disorders Research Center, Golestan university of Medical Sciences, Gorgan, Iran.

Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, No. 24, Yamen Street, Velenjak, P.O. Box: 19395-4763, Tehran, Iran.

出版信息

Cardiovasc Diabetol. 2020 Mar 30;19(1):41. doi: 10.1186/s12933-020-01017-4.

DOI:10.1186/s12933-020-01017-4
PMID:32228577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7106714/
Abstract

BACKGROUND

To assess the impact of changes in different glucose tolerance states on risk of incident cardiovascular disease (CVD)/coronary heart disease (CHD).

METHODS

A total of 4094 Iranians (43.9% men) aged ≥ 30 years, without diabetes and CVD at enrolment were included. The following categories were defined both at baseline visit and 3 years later (second visit): normal fasting glucose (NFG), normal glucose tolerance (NGT), NFG and NGT (NFG/NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and IFG and/or IGT (IFG/IGT). Changes in the categories, i.e. regression to normoglycemia, remaining in previous status and progression to diabetes were assessed. We used Cox's proportional hazard models adjusted for traditional risk factors and their changes, to estimate the hazard ratio (HR) with 95% confidence interval (CI) of different changing categories for incident CVD/CHD.

RESULTS

During a median follow-up of 12.42 years, 428 subjects (men = 265) experienced CVD. Considering persistent NFG/NGT as reference, participants who shifted from NFG/NGT to IFG/IGT showed a lower hazard of CVD in the fully adjusted model, HR 0.72 [95% CI 0.52-0.996, P = 0.048]. Moreover, subjects who shifted from IFG, IGT and IFG/IGT to diabetes had an increased risk of CVD/CHD. The risk however, was only statistically significant for those with IFG/IGT, 1.61 [(1.03-2.51), P = 0.04] for CVD and 1.75 [(1.10-2.78), P = 0.02] for CHD; considering IFG/IGT at both visits as reference. Furthermore, those who regressed from IFG/IGT to normoglycemia were at the same risk as those remained in IFG/IGT state, 1.12 [(0.79-1.60), P = 0.52] for CVD and 1.04 [(0.70-1.53), P = 0.85] for CHD. Among a subgroup of population with insulin data (n = 803) those with insulin resistance (IR) that converted to diabetes showed a higher risk for CVD, 3.68 [(1.49-9.06), P = 0.01] and CHD, 2.76 [(1.00-7.60), P = 0.05] events in the fully adjusted model.

CONCLUSIONS

Among participants with IFG, IGT or IFG/IGT at baseline, only those who developed diabetes had a higher risk of developing CVD/CHD. Persistent IFG/IGT was not associated with higher risk, compared with those reverted to normoglycemia. Moreover, subjects who converted from NFG/NGT to incident IFG/IGT showed a signal for lower risk of CVD/CHD.

摘要

背景

评估不同葡萄糖耐量状态变化对心血管疾病(CVD)/冠心病(CHD)发病风险的影响。

方法

共纳入 4094 名伊朗人(43.9%为男性),年龄均≥30 岁,入组时无糖尿病和 CVD。在基线访视和 3 年后(第二次访视),将以下类别定义为:正常空腹血糖(NFG)、正常葡萄糖耐量(NGT)、NFG 和 NGT(NFG/NGT)、空腹血糖受损(IFG)、葡萄糖耐量受损(IGT)和 IFG 和/或 IGT(IFG/IGT)。评估了类别变化,即回归正常血糖、保持以前状态和进展为糖尿病的情况。我们使用 Cox 比例风险模型,根据传统风险因素及其变化进行调整,以估计不同变化类别的发病 CVD/CHD 的风险比(HR)及其 95%置信区间(CI)。

结果

在中位随访 12.42 年期间,428 名受试者(男性 265 名)发生 CVD。考虑到持续的 NFG/NGT 为参考,与 IFG/IGT 相比,从 NFG/NGT 转变为 IFG/IGT 的参与者在完全调整后的模型中 CVD 的风险较低,HR 为 0.72 [95%CI 0.52-0.996,P=0.048]。此外,从 IFG、IGT 和 IFG/IGT 转变为糖尿病的受试者 CVD/CHD 的风险增加。然而,仅对于 IFG/IGT ,风险具有统计学意义,CVD 为 1.61 [1.03-2.51,P=0.04],CHD 为 1.75 [1.10-2.78,P=0.02];考虑到两次访视均为 IFG/IGT 为参考。此外,那些从 IFG/IGT 恢复到正常血糖的患者与仍处于 IFG/IGT 状态的患者风险相同,CVD 为 1.12 [0.79-1.60,P=0.52],CHD 为 1.04 [0.70-1.53,P=0.85]。在有胰岛素数据的人群亚组(n=803)中,那些从胰岛素抵抗(IR)转化为糖尿病的患者 CVD 风险更高,HR 为 3.68 [1.49-9.06,P=0.01],CHD 为 2.76 [1.00-7.60,P=0.05],在完全调整后的模型中。

结论

在基线时 IFG、IGT 或 IFG/IGT 的参与者中,只有发展为糖尿病的患者 CVD/CHD 的风险更高。与恢复正常血糖的患者相比,持续的 IFG/IGT 与更高的风险无关。此外,从 NFG/NGT 转变为新发 IFG/IGT 的患者 CVD/CHD 的风险信号较低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/82e2e530c90b/12933_2020_1017_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/3de8dca6f91b/12933_2020_1017_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/832308ac1843/12933_2020_1017_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/82e2e530c90b/12933_2020_1017_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/3de8dca6f91b/12933_2020_1017_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/832308ac1843/12933_2020_1017_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18b8/7106714/82e2e530c90b/12933_2020_1017_Fig3_HTML.jpg

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