Objective
To investigate the clinical application value of longitudinal peak strain(LPS) and peak strain dispersion(PSD) in evaluating left ventricular systolic function and synchrony in patients with essential hypertension.
Methods
Fifty-five patients with essential hypertension were enrolled, including 30 patients with non-left ventricular hypertrophy (NLVH), 25 patients with left ventricular hypertrophy (LVH), at the same time, 30 healthy volunteers were selected as the control group. Echocardiography was performed in all three groups, and two-dimensional dynamic images of the left ventricular apical four-chamber, three-chamber, and two-chamber′s long-axis views were collected for three consecutive cardiac cycles. The myocardial layer-specific strain was used to measure the LPS of the left ventricular myocardium of subendocardium, the middle layer, the subepicardium, and the myocardial strain and the PSD of the whole myocardial layers. Correlation analysis and ROC curve analysis were performed.
Results
The LPS in the control group, NLVH group and LVH group were decreased in turn from inner to out myocardial layers.Compared with the control group, the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer of NLVH group were decreased (P 0.05). The LPS in the subendocardial, middle, subepicardial, and whole myocardial layer of LVH group were all reduced (P 0.05). Compared with the control group, the PSD of the NLVH group and the LVH group increased (P<0.05). Compared with the NLVH group, the PSD of the LVH group increased (P<0.05). Inter-ventricular septum thickness (IVSd) and the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer were negatively correlated (r=-0.537, -0.518, -0.266, -0.471; all P<0.05), left ventricle posterior wall thickness (LVPWd) and the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer were negatively correlated (r=-0.539, -0.524, -0.283, -0.478; all P<0.05). The area under the ROC curve (AUC) of the LPS in the subendocardial, middle, subepicardial, and whole myocardial layer and PSD for the diagnosis of hypertension were 0.685, 0.652, 0.510, 0.623, 0.995, respectively. The cut-off values were -21.70%, -18.90%, -16.95%, -19.45%, 46.50 ms, and the sensitivities were 94.4%, 83.3%, 77.8%, 94.4%, 100%, respectively, and the specificities were 47.8%, 52.2%, 39.1%, 39.1%, 95.7%, respectively.
Conclusions
The layer-specific strain can quantitatively evaluate myocardial longitudinal strain in patients with essential hypertension, provide a non-invasive test for early diagnosis of hypertensive heart disease, and the evaluation of left ventricular myocardial stratification. PSD for evaluating primary synchronous changes in left ventricular myocardial contraction in patients with hypertension has certain advantages.
Key words:
Echocardiography; Hypertension; Ventricular function; Layer-specific strain; Peak strain dispersion
Abstract Background and aims: Obesity often coexists with diabetes has been recognized as a risk factor for diabetic complications. Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, and the metabolic syndrome (MetS) is one of the most common symptoms of diabetes. The purpose of this study was to explore the relationship between DR and some induces, including NC, CVAI, PWNC and so on; as well as the relationship between DR and MetS. Methods: From 2018 to 2019, a total of 562 diabetics from the Hulan District of Harbin, Heilongjiang, were selected and completed a questionnaire survey. The questionnaire included basic patient information, anthropometric parameters, blood pressure, biochemical parameters and fundus photography results. Results: In both men and women, a one standard deviation (SD) increase in NC、CVAI and PWNC was not associated with the prevalence of DR (P>0.05). However, in both men and women, a one SD increase in NC、CVAI and PWNC was significantly associated with the prevalence of MetS (P<0.05). These association were all adjusted for potential confounding factors. Moreover, DR was not associated with MetS(P>0.05). Conclusions: NC, CVAI and PWNC are associated with the prevalence of MetS. NC in men and CVAI in women had the largest area under the ROC curve compared to the other induces, which may be convenient and valuable anthropometric measurements for early prevention of MetS. However, these induces had no association with DR and there is no relationship between DR and MetS.
Abstract Background In the present study, we measured the serum vascular endothelial cadherin (VEC) and vinculin (Vcn) concentrations in patients with acute aortic dissection (AAD) to evaluate their diagnostic value for this condition. Methods One hundred patients with AAD and 60 matched controls were included in the study. The serum concentrations of VEC and Vcn were measured using enzyme-linked immunosorbent assays. Results The serum VEC and Vcn concentrations were significantly higher in participants with AAD than in healthy controls. Receiver operating characteristic analysis generated areas under the curves for VEC and Vcn that were diagnostic for AAD (0.604 and 0.665, respectively). The optimal cut-off values were 3.986 ng/µL and 128.1 pg/mL, the sensitivities were 43.0% and 35.0%, and the specificities were 73.3% and 90.0%, respectively. In addition, the use of a combination of serum VEC and Vcn increased the AUC to 0.739, with a sensitivity of 56.0% and a specificity of 76.7%. A high serum Vcn concentration was associated with a higher risk of poor visceral malperfusion in participants with AAD (odds ratio [OR] = 1.007, 95% confidence interval [CI]: 1.001–1.013, p = 0.014). In participants with refractory pain, the adjusted OR for the serum VEC concentration increased to 1.172 (95% CI: 1.010–1.361; p = 0.036), compared with participants without refractory pain. Conclusion This study is the first to show the diagnostic value of serum VEC and Vcn for AAD and their relationships with the clinical characteristics of patients with AAD. Thus, VEC and Vcn are potential serum markers of AD.
A number of studies have shown that aldosterone serves an important role in promoting renal interstitial fibrosis, although the specific mechanism remains to be elucidated. A previous study revealed that the fibrotic effect of aldosterone was associated with the expression of allograft inflammatory factor 1 (AIF‑1) in RAW264.7 macrophage cells, in a time‑ and concentration‑dependent manner. However, the exact mechanism through which aldosterone promotes renal interstitial fibrosis remains unknown. In the present study, the effects of aldosterone on renal inflammatory cell infiltration, collagen deposition and the expression levels of AIF‑1, phosphatidylinositol 3‑kinase (PI3K), AKT serine/threonine kinase (AKT), mammalian target of rapamycin (mTOR), the oxidative stress factor NADPH oxidase 2 (NOX2) and nuclear transcription factor erythroid‑related factor 2 (Nrf2) were assessed in normal rats, rats treated with aldosterone, rats treated with aldosterone and spironolactone and those treated with spironolactone only (used as the control). The effect of aldosterone on these factors was also investigated in the renal interstitium of unilateral ureteral obstruction (UUO) rats. Additionally, the AIF‑1 gene was overexpressed and knocked down in macrophage RAW264.7 cells, and the effects of aldosterone on PI3K, AKT, mTOR, NOX2 and Nrf2 were subsequently investigated. The results showed that aldosterone promoted inflammatory cell infiltration, collagen deposition and the expression of AIF‑1, PI3K, AKT, mTOR and NOX2, but inhibited the expression of Nrf2. In the UUO rats, aldosterone also promoted renal interstitial inflammatory cell infiltration, collagen deposition and the expression of AIF‑1, NOX2, PI3K, AKT and mTOR, whereas the expression of Nrf2 was downregulated by aldosterone compared with that in the UUO‑only group; the influence of aldosterone was counteracted by spironolactone in the normal and UUO rats. In vitro, aldosterone upregulated the expression levels of AKT, mTOR, NOX2 and Nrf2 in RAW264.7 cells compared with those in untreated cells. Suppressing the expression of AIF‑1 inhibited the effects of aldosterone, whereas the overexpression of AIF‑1 enhanced these effects in RAW264.7 cells. These findings indicated that aldosterone promoted renal interstitial fibrosis by upregulating the expression of AIF‑1 and that the specific mechanism may involve AKT/mTOR and oxidative stress signaling.
Angiotensin II (Ang II) is an important profibrotic factor, and the tumor-promoting microRNA miR-21 was recently linked to fibrotic disorders. We aimed to investigate whether and how miR-21 mediates Ang II-induced renal fibrosis. In renal tubular epithelial cells, Ang II upregulated miR-21 and fibrosis-related indicators but decreased PPARα expression. miR-21 overexpression promoted PPARα downregulation, activated the TGF-β1/Smad3 pathway and induced fibrogenesis, while miR-21 suppression exerted opposite effects. In Ang II-treated cells, reduced PPARα expression, TGF-β1/Smad3 pathway activation and fibrogenesis were all exacerbated by miR-21 upregulation but alleviated by miR-21 inhibition. The dual-luciferase assay confirmed PPARα as the target of miR-21. PPARα silencing alone could overactivate the TGF-β1/Smad3 pathway in the presence or absence of Ang II. Importantly, the regulatory effects of miR-21 knockdown and the angiotensin type 1 receptor blocker losartan alone or in combination on the PPARα/TGF-β1/Smad3 pathway in Ang II-treated cells were almost the same. More crucially, PPARα restoration abolished the profibrotic effect of miR-21 overexpression. In addition, inhibiting miR-21 in Ang II-treated mice effectively ameliorated the abnormally activated PPARα/TGF-β1/Smad3 pathway, albuminuria, and renal fibrosis without lowering blood pressure. These results demonstrated that miR-21 extensively mediates Ang II-induced kidney fibrosis via amplifying the TGF-β1/Smad3 pathway by targeting PPARα.
Acute lung injury (ALI) induced by lipopolysaccharide (LPS) is a significant medical condition characterized by severe pulmonary inflammation and tissue damage. NLRP3 inflammasome-driven inflammation is essential in ALI pathogenesis, inspiring novel therapeutic strategies that focus on NLRP3 and inflammation. In this study, we investigated the therapeutic potential of 5-deoxy-rutaecarpine (5-DR), a rutaecarpine derivative, in attenuating LPS-induced ALI. In this study, we evaluated the effects of 5-DR treatment in mice exposed to LPS, lung tissues, bronchoalveolar lavage fluid, and serum were collected for analysis. LPS-stimulated J774A.1 mouse macrophages were used to further investigate the anti-inflammatory effects of 5-DR in vitro. Various techniques including histopathology, Western blotting, and luciferase reporter assay were employed. 5-DR treatment significantly reduced lung edema, inflammatory cell infiltration in mice with LPS burden, and reduced the levels of inflammatory mediators like interleukin-1β in the mice and in LPS-stimulated J774A.1 mouse macrophages. Further western blotting analysis showed 5-DR decreased the levels of NLRP3, cleaved caspase-1, and mature IL-1β in mice and J774A.1 cells exposed to LPS. Additionally, NF-κB pathway activation significantly diminished the inhibition of the NLRP3 inflammasome by 5-DR. Our findings highlight the therapeutic potential of 5-DR as a promising candidate for treating LPS-induced ALI, offering insights into its underlying mechanism that targets NLRP3 inflammasome-mediated inflammation.
Diabetic retinopathy (DR) is a complication of diabetes with a complex pathophysiology and multiple factors involved. Recently, it has been found that the upregulation of the renin-angiotensin-aldosterone system (RAAS) leads to overexpression of angiotensin II (Ang II), which induces oxidative stress, inflammation, and angiogenesis in the retina. Therefore, RAAS may be a promising therapeutic target in DR. Notably, RAAS inhibitors are often used in the treatment of hypertension. Still, the potential role and mechanism of DR must be further [...]
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