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INTRODUCTION: Hypertensive heart failure (HHF) has a high incidence and poor prognosis. AIM: This article evaluated the efficacy and safety of Vericiguat in HHF and analyzed the relationship between C-reactive protein (CRP) levels and patient prognosis. METHODS: 110 HHF patients were divided into Placebo and Vericiguat groups. Cardiac function was assessed by echocardiography and 6-minute walk test (6MWT). Blood samples were collected to detect the levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), endothelin (ET-1), nitric oxide (NO), and CRP. RESULTS: Left ventricular end systolic diameter (LVESD) and left ventricular end diastolic dimension (LVEDD) were reduced, the left ventricular ejection fraction (LVEF) and 6MWT were increased, and the serum levels of NT-proBNP, cTnI, ET-1, NO, and CRP were decreased in Vericiguat group as against Placebo group; The total effective rate was 76.4% in Placebo group and 92.7% in Vericiguat group (P < 0.05). The adverse reaction rate was 10.9% and 9.1% (P > 0.05). The proportion of persons with poor prognosis and no improvement of cardiac function in patients with highly expressed CRP before treatment was higher as against patients with low expression of CRP (P < 0.05). Highly expressed CRP is an independent risk factor for poor prognosis. CONCLUSION: Vericiguat is safe and effective in improving cardiac function in HHF patients.
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Objective: The objective of this study was to investigate the early application of sacubitril valsartan sodium (LCZ696) following acute myocardial infarction (AMI) and its impact on ventricular remodeling and the TGF-ß1/Smad3 signaling pathway in patients. Methods: The clinical data of 73 patients with AMI admitted to the hospital from June 2021 to September 2022 were retrospectively analyzed, and the patients were grouped according to the treatment methods, including 36 cases in the control group (conventional drug treatment) and 37 cases in the observation group (conventional drug + LCZ696 treatment). The clinical efficacy, cardiac function parameters [left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), stroke volume (SV)], cardiac function biochemical indicators [N-terminal pro-B-type natriuretic peptide (NT-proBNP), galectin 3 (Gal-3), amino-terminal peptide of type III procollagen (PIIINP)], ventricular remodeling indicators [left ventricular posterior wall end-diastolic thickness (PWD), posterior wall end-systolic thickness (PWS), ventricular septal end-systolic thickness (IVSS)], ventricular hydrodynamic parameters [left ventricular flow rate in peak ejection (FRPE), flow reversal rate (FRR), flow reversal interval (FRI)], TGF-ß 1/Smad3 signaling pathway-related indicators (TGF-ß1, Smad3), quality of life score (SF-36 Quality of Life Scale) and occurrence of adverse reactions were compared between the two groups. Results: The main findings of the study are as follows: The observation group was significantly better than the control group in many aspects such as overall clinical effectiveness, cardiac function parameters, biochemical indicators, ventricular structure and function, TGF-ß1/Smad3 signaling pathway, and quality of life. Specifically, the observation group showed more significant positive effects in terms of improvement of cardiac function, adjustment of biochemical status, and adjustment of ventricular structure and fluid dynamics parameters. These results provide strong support for the application of new therapeutic approaches in the management of cardiovascular disease. After treatment, the total clinical effective rate in the observation group (89.19%) was significantly higher than that in the control group (69.44%) (P < .05). LVEF and SV in the two groups were significantly increased (P < .05), while LVEDD was significantly decreased (P < .05), and there were statistically significant differences in parameters between the two groups (P < .05). The levels of NT-proBNP, Gal-3 and PIIINP in both groups were significantly reduced (P < .05), and the levels in the observation group were significantly lower than those in the control group (P < .05). The PWD, PWS and IVSS in both groups significantly declined (P < .05), and the indicators in the observation group were significantly lower than those in the control group (P < .05). The FRPE and FRR in the two groups were significantly enhanced (P < .05), while the FRI was significantly reduced (P < .05), and the differences in the above parameters between the two groups were statistically significant (P < .05). The levels of TGF-ß1 and Smad3 in the two groups were significantly declined (P < .05), and the levels in the observation group were significantly lower than those in the control group (P < .05). During the period from before treatment to 6 months of treatment, the quality of life score in the two groups showed a significant downward trend (P < .05), and the score in the observation group after 3 months to 6 months of treatment was significantly lower than that in the control group (P < .05). During treatment, there was no statistical significance in the total incidence rate of adverse reactions between the two groups (P > .05). Conclusion: Early application of LCZ696 after AMI has a significant efficacy, and it can effectively improve the ventricular remodeling, regulate the expression levels of TGF-ß1 and Smad3, inhibit the TGF-ß1/Smad3 signaling pathway, promote the improvements of cardiac function and quality of life, and it has good safety and is worthy of clinical promotion and application. The study's key findings have important clinical implications for understanding and managing acute myocardial infarction (AMI). The observation group showed significant improvements in overall clinical efficacy, cardiac function, biochemical status, ventricular structure and function, etc., providing strong evidence for comprehensive treatment of AMI patients. This treatment method is expected to become an important part of the care and treatment strategy for AMI patients, help reduce cardiovascular risk, improve quality of life, and provide new research directions for future AMI treatment.
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Oxidized lowdensity lipoprotein (oxLDL)induced vascular endothelial damage, oxidative stress and inflammation play a vital role in the pathophysiology of atherosclerosis. Geniposide is the primary active ingredient from Gardenia jasminoides Ellis associated with antioxidative properties and cardioprotective action. However, the therapeutic mechanism of geniposide in atherosclerosis remains unclear. Hence, the present study aimed to elucidate the underlying mechanisms of geniposide in oxidative stress and inflammatory response during oxLDL injury in human umbilical vein endothelial cells (HUVECs), focusing particularly on the microRNA (miR)21/PTEN pathway. The results demonstrated that geniposide pretreatment significantly increased cell viability, decreased lactate dehydrogenase release, increased miR21 level and decreased PTEN expression under oxLDL condition. Subsequently, transfection with miR21 mimic enhanced the protection of geniposide on oxLDLinduced cytotoxicity and apoptosis (mediated by the upregulation of apoptotic rate and caspase3 activity), whereas miR21 inhibitor reversed these effects of geniposide. In addition, geniposide resulted in an antioxidant effect as evidenced by the decrease in reactive oxygen species generation, malondialdehyde content and NADPH oxidase 2 expression, and the increase in superoxide dismutase, glutathione peroxidase and catalase activities in oxLDLtreated HUVECs, which were exacerbated by miR21 mimic and reversed by miR21 inhibitor. Furthermore, geniposide mitigated the oxLDLinduced inflammatory response, demonstrated by a downregulation of proinflammatory cytokine (IL1ß, IL6, and TNFα) levels and an upregulation of antiinflammatory cytokine (IL10) level. However, miR21 mimic enhanced, whereas miR21 inhibitor attenuated, these effects of geniposide. In conclusion, the present results indicated that geniposide protects HUVECs from oxLDL injury by inhibiting oxidative stress and inflammation, and that these effects are partly due to the enhancement of the miR21/PTEN pathway.