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评估 T2DM 合并糖尿病周围神经病变患者亚临床左心室心肌功能障碍:一项心血管磁共振研究。

Assessment of subclinical LV myocardial dysfunction in T2DM patients with diabetic peripheral neuropathy: a cardiovascular magnetic resonance study.

机构信息

Department of Radiology, West China Hospital, Sichuan University, 37# Guo Xue Xiang, Chengdu, Sichuan, China.

Laboratory of Cardiovascular Diseases, Regenerative Medicine Research Center, West China Hospital, Sichuan University, 37# Guo Xue Xiang, Chengdu, Sichuan, China.

出版信息

Cardiovasc Diabetol. 2024 Jun 24;23(1):217. doi: 10.1186/s12933-024-02307-x.

Abstract

BACKGROUND

Diabetic peripheral neuropathy (DPN) is the most prevalent complication of diabetes, and has been demonstrated to be independently associated with cardiovascular events and mortality. This aim of this study was to investigate the subclinical left ventricular (LV) myocardial dysfunction in type 2 diabetes mellitus (T2DM) patients with and without DPN.

METHODS

One hundred and thirty T2DM patients without DPN, 61 patients with DPN and 65 age and sex-matched controls who underwent cardiovascular magnetic resonance (CMR) imaging were included, all subjects had no symptoms of heart failure and LV ejection fraction ≥ 50%. LV myocardial non-infarct late gadolinium enhancement (LGE) was determined. LV global strains, including radial, circumferential and longitudinal peak strain (PS) and peak systolic and diastolic strain rates (PSSR and PDSR, respectively), were evaluated using CMR feature tracking and compared among the three groups. Multivariable linear regression analyses were performed to determine the independent factors of reduced LV global myocardial strains in T2DM patients.

RESULTS

The prevalence of non-infarct LGE was higher in patients with DPN than those without DPN (37.7% vs. 19.2%, p = 0.008). The LV radial and longitudinal PS (radial: 36.60 ± 7.24% vs. 33.57 ± 7.30% vs. 30.72 ± 8.68%; longitudinal: - 15.03 ± 2.52% vs. - 13.39 ± 2.48% vs. - 11.89 ± 3.02%), as well as longitudinal PDSR [0.89 (0.76, 1.05) 1/s vs. 0.80 (0.71, 0.93) 1/s vs. 0.77 (0.63, 0.87) 1/s] were decreased significantly from controls through T2DM patients without DPN to patients with DPN (all p < 0.001). LV radial and circumferential PDSR, as well as circumferential PS were reduced in both patient groups (all p < 0.05), but were not different between the two groups (all p > 0.05). Radial and longitudinal PSSR were decreased in patients with DPN (p = 0.006 and 0.003, respectively) but preserved in those without DPN (all p > 0.05). Multivariable linear regression analyses adjusting for confounders demonstrated that DPN was independently associated with LV radial and longitudinal PS (β = - 3.025 and 1.187, p = 0.014 and 0.003, respectively) and PDSR (β = 0.283 and - 0.086, p = 0.016 and 0.001, respectively), as well as radial PSSR (β = - 0.266, p = 0.007).

CONCLUSIONS

There was more severe subclinical LV dysfunction in T2DM patients complicated with DPN than those without DPN, suggesting further prospective study with more active intervention in this cohort of patients.

摘要

背景

糖尿病周围神经病变(DPN)是糖尿病最常见的并发症,已被证明与心血管事件和死亡率独立相关。本研究旨在探讨伴有和不伴有 DPN 的 2 型糖尿病(T2DM)患者的亚临床左心室(LV)心肌功能障碍。

方法

纳入了 130 例无 DPN 的 T2DM 患者、61 例 DPN 患者和 65 例年龄和性别匹配的对照者,所有患者均无心力衰竭症状和 LV 射血分数≥50%。采用心血管磁共振(CMR)成像测定 LV 心肌非梗死性晚期钆增强(LGE)。采用 CMR 特征追踪技术评估 LV 整体应变,包括径向、环向和纵向峰值应变(PS)以及峰值收缩期和舒张期应变率(PSSR 和 PDSR),并比较三组之间的差异。采用多变量线性回归分析确定 T2DM 患者 LV 整体心肌应变降低的独立因素。

结果

与无 DPN 患者相比,DPN 患者的非梗死性 LGE 发生率更高(37.7% vs. 19.2%,p=0.008)。LV 径向和纵向 PS(径向:36.60±7.24% vs. 33.57±7.30% vs. 30.72±8.68%;纵向:-15.03±2.52% vs. -13.39±2.48% vs. -11.89±3.02%)以及纵向 PDSR[0.89(0.76,1.05)1/s vs. 0.80(0.71,0.93)1/s vs. 0.77(0.63,0.87)1/s]均显著降低,从对照组依次至无 DPN 的 T2DM 患者再至有 DPN 的患者(均 p<0.001)。两组患者的 LV 径向和环向 PDSR 以及环向 PS 均降低(均 p<0.05),但两组之间无差异(均 p>0.05)。有 DPN 的患者的径向和纵向 PSSR 降低(p=0.006 和 0.003),而无 DPN 的患者则无变化(均 p>0.05)。多变量线性回归分析校正混杂因素后显示,DPN 与 LV 径向和纵向 PS(β=-3.025 和 1.187,p=0.014 和 0.003)和 PDSR(β=0.283 和-0.086,p=0.016 和 0.001)以及径向 PSSR(β=-0.266,p=0.007)独立相关。

结论

伴有 DPN 的 T2DM 患者的亚临床 LV 功能障碍比无 DPN 的患者更严重,提示在这组患者中需要进一步进行前瞻性研究并采取更积极的干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a96/11197260/6f0230893dda/12933_2024_2307_Fig1_HTML.jpg

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