Inflammatory cytokines and their correlations with different left ventricular geometries and functions in PHT patients.

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To investigate relationships between hypersensitive C-reactive protein (hs-CRP), tumor necrosis factor -α (TNF-α), interleukin-17A (IL-17A), and interferon -γ (IFN-γ), with left ventricular geometry (LVG) and function in patients with primary hypertension (PHT). A total of 396 PHT patients were assigned into four groups: Normal Geometry (NG), Concentric Remodeling (CR), Eccentric Hypertrophy (EH), and Concentric Hypertrophy (CH). The correlation between hs-CRP, TNF-α, IL-17A, IFN-γ, and clinical, biochemical parameters were analyzed by Pearson correlation analysis and Logistic regression. Receiver Operating Characteristic (ROC) curve was used to analyze the clinical values of hs-CRP, TNF-α, IL-17A, and IFN-γ for abnormal LVG prediction. NG, CR, EH, and CH group all presented increasingly higher levels of Hs-CRP, TNF-α, IL-17A, and IFN-γ, and the increase was the most prominent in the CH group. Pearson correlation analysis showed that hs-CRP, IL-17A, and IFN-γ were all positively correlated with LASct. Hs-CRP, TNF-α, and IL-17A were all negatively correlated with GLS, LASr, and LAScd. However, IFN-γ was only negatively correlated with GLS and LAScd. Logistic regression analysis showed that hs-CRP and IL-17A were independently correlated with CR; hs-CRP, TNF-α, IFN-γ, and IL-17A were independently correlated with EH and CH. ROC curve analysis showed that the area under the curve (AUC) of hs-CRP was 0.816. When the optimal diagnostic threshold of hs-CRP was 3.04mg/L, the sensitivity and specificity of the abnormal LVG were 72.1% and 81.5%, respectively. In PHT patients, hs-CRP, TNF-α, IL-17A, and IFN-γ were correlated with abnormal LVG and left ventricular function, suggesting that inflammatory cytokines may be involved in the process of PHT-induced abnormal left ventricular structure and function. In addition, hs-CRP can be used as a health screening index for patients at high risk of abnormal LVG.