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评估心肌应变和心肌做功作为高血压性心脏病的标志物:一项荟萃分析。

Assessing Myocardial Strain and Myocardial Work as a Marker for Hypertensive Heart Disease: A Meta-Analysis.

作者信息

Rabkin Simon W

机构信息

Department of Medicine, Division of Cardiology, University of British Columbia, Vancouver, BC V5Z 1M9, Canada.

出版信息

Rev Cardiovasc Med. 2023 Jul 31;24(8):217. doi: 10.31083/j.rcm2408217. eCollection 2023 Aug.

DOI:10.31083/j.rcm2408217
PMID:39076705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11266759/
Abstract

BACKGROUND

The main objective of this study was to determine whether myocardial strain and myocardial work are altered in hypertension and whether the strain is independent of hypertension-induced left ventricular hypertrophy.

METHODS

Two systematic literature searches were conducted using Medline and EMBASE through to June 30, 2022. In the first, search terms left ventricular strain or speckle tracking AND hypertension and left ventricular hypertrophy were used in conjunction with Boolean operators to identify articles reporting left ventricular strain in patients with hypertension. In the second, the terms Global cardiac or myocardial work AND hypertension were used to identify articles. Publication bias was assessed by examination of funnel plots and calculation of the Failsafe N and Duval and Tweedie's Trim and fill. The results were presented as Forrest plots.

RESULTS

Global longitudinal strain (GLS) was significantly lower in patients with hypertension compared to those without hypertension with a mean difference of 2.0 0.1 (standard error of mean(SEM)) in the fixed effect model. Global circumferential strain (GCS) was significantly lower in hypertension. The mean difference between the hypertensive and non-hypertensive groups was 1.37 0.17. Global radial strain (GRS) was significantly ( 0.05) greater in hypertension. However, this difference was significant in only 3 and of borderline significance in 3 of 14 studies where GRS was measured. The mean difference between the hypertensive and non-hypertensive groups was 1.5 0.5 using the fixed effects model. There was a significant relationship between GLS and GCS as well as between GCS and GRS but no significant relationship between GLS and GRS. There was no significant difference in left ventricular ejection fraction (LVEF) between the hypertension and no hypertension groups. There was no significant relationship between LVEF and either GLS or GCS but a significant negative correlation was found between LVEF and GRS. GLS was further reduced in persons with hypertension and left ventricular hypertrophy (LVH) compared to hypertension without LVH. In contrast, there were no or minimal differences in GCS and GRS for individuals with hypertension and LVH compared to those without LVH. Global myocardial work index (GWI) and Global constructive work (GCW) were significantly greater in patients with hypertension compared to controls. Global wasted work (GWW) indicated significantly less wasted work in controls compared to hypertension. In contrast, Global work efficiency (GWE) was significantly lower in hypertension compared to the control.

CONCLUSIONS

There was a significant reduction in GLS and GCS in hypertension while GRS was increased. The reduction in GLS in hypertension was not dependent on the presence of LVH. GLS was further reduced in persons with hypertension when LVH was present. In contrast, there were no or minimal differences in GCS and GRS for individuals with LVH compared to those without LVH. GLS was independent of left ventricle (LV) ejection fraction. GWI, GCW and GWW were greater in hypertension while GWE was lower in hypertension compared to controls. These data support the contention that GLS and indices of global work are early markers of hypertensive heart disease.

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/0ebc85db96bd/2153-8174-24-8-217-g13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/1ba7d4ef8d10/2153-8174-24-8-217-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/7eedf8bc2fd8/2153-8174-24-8-217-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/5ebe46713a86/2153-8174-24-8-217-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/fe05e0cd5c25/2153-8174-24-8-217-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/accedeafaa85/2153-8174-24-8-217-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/fa838f7ccf20/2153-8174-24-8-217-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/489cb58bda48/2153-8174-24-8-217-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/63b4c37fdfec/2153-8174-24-8-217-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/a218237e7fdf/2153-8174-24-8-217-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/805672111667/2153-8174-24-8-217-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/e775b2c805a9/2153-8174-24-8-217-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/94e12e3597c0/2153-8174-24-8-217-g12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/0ebc85db96bd/2153-8174-24-8-217-g13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/1ba7d4ef8d10/2153-8174-24-8-217-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/7eedf8bc2fd8/2153-8174-24-8-217-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/5ebe46713a86/2153-8174-24-8-217-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/fe05e0cd5c25/2153-8174-24-8-217-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/accedeafaa85/2153-8174-24-8-217-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/fa838f7ccf20/2153-8174-24-8-217-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/489cb58bda48/2153-8174-24-8-217-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/63b4c37fdfec/2153-8174-24-8-217-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/a218237e7fdf/2153-8174-24-8-217-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/805672111667/2153-8174-24-8-217-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/e775b2c805a9/2153-8174-24-8-217-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/94e12e3597c0/2153-8174-24-8-217-g12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71e9/11266759/0ebc85db96bd/2153-8174-24-8-217-g13.jpg
摘要

背景

本研究的主要目的是确定高血压患者的心肌应变和心肌做功是否发生改变,以及应变是否独立于高血压引起的左心室肥厚。

方法

通过检索Medline和EMBASE直至2022年6月30日进行了两项系统文献检索。第一项检索中,使用左心室应变或斑点追踪、高血压和左心室肥厚等检索词,并结合布尔运算符来识别报告高血压患者左心室应变的文章。第二项检索中,使用整体心脏或心肌做功、高血压等检索词来识别文章。通过检查漏斗图、计算失效安全数以及Duval和Tweedie的修剪和填充法评估发表偏倚。结果以森林图呈现。

结果

在固定效应模型中,高血压患者的整体纵向应变(GLS)显著低于无高血压患者,平均差异为2.0±0.1(平均标准误差(SEM))。高血压患者的整体圆周应变(GCS)显著降低。高血压组与非高血压组之间的平均差异为1.37±0.17。高血压患者的整体径向应变(GRS)显著(P<0.05)更高。然而,在14项测量GRS的研究中,只有3项差异具有显著性,3项差异具有临界显著性。使用固定效应模型,高血压组与非高血压组之间的平均差异为1.5±0.5。GLS与GCS之间以及GCS与GRS之间存在显著关系,但GLS与GRS之间无显著关系。高血压组与无高血压组的左心室射血分数(LVEF)无显著差异。LVEF与GLS或GCS之间均无显著关系,但LVEF与GRS之间存在显著负相关。与无左心室肥厚的高血压患者相比,有高血压和左心室肥厚(LVH)的患者GLS进一步降低。相比之下,有高血压和LVH的个体与无LVH的个体在GCS和GRS方面无差异或差异极小。与对照组相比,高血压患者的整体心肌做功指数(GWI)和整体建设性做功(GCW)显著更高。与高血压患者相比,对照组的整体无用功(GWW)表明无用功显著更少。相比之下,高血压患者的整体做功效率(GWE)显著低于对照组。

结论

高血压患者的GLS和GCS显著降低,而GRS升高。高血压患者GLS的降低不依赖于LVH的存在。存在LVH时,高血压患者的GLS进一步降低。相比之下,有LVH的个体与无LVH的个体在GCS和GRS方面无差异或差异极小。GLS独立于左心室(LV)射血分数。与对照组相比,高血压患者的GWI、GCW和GWW更高,而GWE更低。这些数据支持了GLS和整体做功指标是高血压性心脏病早期标志物的观点。

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