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. 2024 Jul 12;14(1):16078.
doi: 10.1038/s41598-024-67143-1.

Effect of early endothelial function improvement on subclinical target organ damage in hypertensives

Xiaodong Huang  1   2 , Xianwei Huang  1   2 , Mandong Pan  1   2 , Jiyan Lin  1   2 , Liangdi Xie  3
Affiliations

Effect of early endothelial function improvement on subclinical target organ damage in hypertensives

Xiaodong Huang et al. Sci Rep. .

Abstract

Endothelial dysfunction is acknowledged as a marker for subclinical target organ damage (STOD) in hypertension, though its therapeutic potential has not yet been clarified. This study assessed whether early endothelial function improvement (EEFI) reduced STOD in patients with essential hypertension (EH). We conducted a retrospective cohort analysis of 456 EH patients initially free from STOD. Endothelial function was assessed using brachial artery flow-mediated dilation (FMD), with values ≤ 7.1% indicating dysfunction. Patients were initially categorized by endothelial status (dysfunction: n = 180, normal: n = 276), and further divided into improved or unimproved groups based on changes within three months post-enrollment. During a median follow-up of 25 months, 177 patients developed STOD. The incidence of STOD was significantly higher in patients with initial dysfunction compared to those with normal function. Kaplan-Meier analysis indicated that the improved group had a lower cumulative incidence of STOD compared to the unimproved group (p < 0.05). Multivariable Cox regression confirmed EEFI as an independent protective factor against STOD in EH patients (p < 0.05), regardless of their baseline endothelial status, especially in those under 65 years old, non-smokers, and with low-density lipoprotein cholesterol levels ≤ 3.4 mmol/L. In conclusion, EEFI significantly reduces STOD incidence in EH patients, particularly in specific subgroups, emphasizing the need for early intervention in endothelial function to prevent STOD.

Keywords: Endothelial function; Essential hypertension; Flow-mediated dilation; Subclinical target organ damage.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Flowchart for identifying study cohorts from the Hypertension Target Organ Damage and Its Risk Factors—Fuzhou Study database. EH essential hypertension, FMD flow-mediated dilation, CVD cardiovascular disease.
Figure 2
Figure 2
Cumulative hazard curves for STOD in the improved (dotted line) and unimproved (solid line) groups of EH patients with initial impaired (a) and unimpaired (b) endothelial function. EH essential hypertension, STOD subclinical target organ damage.
Figure 3
Figure 3
Cox regression analysis of STOD in patients with essential hypertension who had initial impaired endothelial function (a) and its subgroups (b). STOD subclinical target organ damage, BMI body mass index, LDL-C low-density lipoprotein-cholesterol, EEFI early endothelial function improvement.
Figure 4
Figure 4
Cox regression analysis of STOD in patients with essential hypertension who had initial normal endothelial function (a) and its subgroups (b). STOD subclinical target organ damage, BMI body mass index, LDL-C low-density lipoprotein-cholesterol, eGFR estimated glomerular filtration rate, EEFI early endothelial function improvement.
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