BackgroundThe clinical benefits of omega-3 fatty acids (FAs) supplementation in preventing and treating coronary heart disease (CHD) remain controversial. Therefore, this study aimed to investigate the clinical benefits of omega-3 FA supplementation, with special attention given to specific subgroups.MethodsRandomized controlled trials (RCTs) that compared the effects of omega-3 FA supplementation for CHD vs. a control group and including at least 1,000 patients were eligible for the inclusion in this meta-analysis. The relative risk (RR) of all-cause death, major adverse cardiovascular events (MACEs), cardiovascular death, myocardial infarction (MI), stroke, and revascularization were estimated. We analyzed the association between cardiovascular risk and omega-3 FA supplementation in the total subjects. We focused on the cardiovascular risk compared to omega-3 FA in subgroups with different development stages of CHD, omega-3 FA supplementation application dose, diabetes, and sex. PROSPERO Registration Number: CRD42021282459.ResultsThis meta-analysis included 14 clinical RCTs, including 1,35,291 subjects. Omega-3 FA supplementation reduced the risk of MACE (RR; 0.95; CI: 0.91–0.99; p for heterogeneity 0.27; I2 = 20%; p = 0.03), cardiovascular death (RR; 0.94; CI: 0.89–0.99; p for heterogeneity 0.21; I2 = 25%; p = 0.02), and MI (RR; 0.86; CI: 0.79–0.93; p for heterogeneity 0.28; I2 = 19%; p < 0.01), but had no significant effect on all-cause death, stroke, and revascularization. In the subgroup analysis, omega-3 FA supplementation decreased the incidence of MACE and cardiovascular death in acute patients with MI, the risk of MI and stroke in patients with CHD, and the risk of MI in patients with high-risk CHD. 0.8–1.2 g omega-3 FA supplementation reduced the risk of MACE, cardiovascular death, and MI. It was revealed that gender and diabetes have no significant association between omega-3 FA supplementation and MACE risk.ConclusionsOmega-3 FA supplementation had a positive effect in reducing the incidence of MACE, cardiovascular death, MI. Regardless of the stage of CHD, omega-3 FA supplementation can prevent the occurrence of MI. The 0.8–1.2 g omega-3 FA supplementation alleviated CHD risk more effectively than lower or higher doses.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42021282459.
BackgroundSeveral trials have considered the safety and clinical benefits of colchicine as a treatment option for secondary prevention in patients with coronary atherosclerotic heart disease (CAD), but its safety and clinical benefits remain controversial. The purpose of this study was to explore the clinical benefits of colchicine, focusing on certain subgroups of patients.MethodsRandomized controlled trials (RCTs) of colchicine in subjects with acute or chronic CAD compared with controls were included to assess all-cause mortality, non-cardiovascular mortality, gastrointestinal adverse effects, diarrhea, MACE, cardiovascular mortality, MI, stroke, and revascularization. We analyzed the association of cardiovascular, mortality, and gastrointestinal risk with colchicine in all subjects. We also focused on the cardiovascular risk of colchicine in subgroups with different drug doses, different treatment durations, age, gender, and associated comorbidities.ResultsThis meta-analysis included 15 clinical RCTs, including 13,539 subjects. Colchicine reduced the risk of MACE (RR: 0.65; 95% CI: 0.38–0.77, p for heterogeneity < 0.01; I2 = 70%; p < 0.01), stroke (RR: 0.48; 95% CI: 0.30–0.76; p heterogeneity = 0.52; I2 = 0%; p < 0.01), MI by 40% (RR: 0.60; 95% CI: 0.43–0.83; p for heterogeneity = 0.01; I2 = 59%; p < 0.01) and risk of revascularization (RR: 0.68; 95% CI: 0.56–0.83; p for heterogeneity = 0.17; I2 = 40%; p < 0.01), but had no significant effect on risk of cardiovascular death and risk of all-cause mortality. In addition, colchicine increased the risk of gastrointestinal side effects and diarrhea. In a subgroup analysis, low-dose colchicine and treatment duration > 1 month reduced the risk of MACE, MI, stroke, and revascularization. Also, the cardiovascular benefits of colchicine were observed in subjects up to 65 years of age. The results showed that hypertension and diabetes did not have a specific effect on colchicine and MACE risk.ConclusionColchicine has a positive effect in reducing the incidence of MACE, MI, stroke, and revascularization, but can increase the risk of gastrointestinal and diarrhea events. Low-dose colchicine significantly reduces the risk of MACE more than high-dose colchicine, and the benefits of long-term treatment are higher than those of short-term treatment. Long-term low-dose colchicine treatment may significantly reduce the risk of cardiovascular events. Furthermore, colchicine significantly reduced the risk of cardiovascular events in patients up to 65 years of age, but it did not appear to reduce cardiovascular risk in patients over 65 years of age or in preoperative PCI patients.Systematic review registration[https://www.crd.york.ac.uk/prospero/], identifier [CDR42022332170].
Type 2 diabetes mellitus (T2DM) is a chronic progressive metabolic disease that has become a growing health problem worldwide, and the dangers of hyperglycemia and its chronic complications have long been considered a goal of diabetes treatment. In recent years, tirzepatide has become the first dual GIP/GLP-1R agonist approved for the treatment of diabetes mellitus in the United States as a new hypoglycemic medicine. Its hypoglycaemic and weight loss effects have been demonstrated in several large clinical trials, and there is also evidence that it has great potential for cardiovascular protection. In addition, the very concept of synthetic peptides opens up many unknown possibilities for tirzepatide. Ongoing trials (NCT04166773) and evidence suggest that it appears to be a promising drug in the areas of NAFLD, renal, and neuroprotection. Based on preclinical studies and clinical trials, the aim of this article is to discuss the latest clinical developments in tirzepatide, to focus on its differences with other incretin therapies, and to suggest future possibilities and mechanisms of tirzepatide therapy.
Objective: To observe the cerebral protective effect of dagliflozin, a sodium-glucose co-transport protein 2 (SGLT2) inhibitor, in aging mice and to explore its molecular mechanism. Methods: 1. 66 male C57BL/6 mice were divided into control group (13) and model group ( 53), and the model group was moulded by subcutaneous injection of D-galactose into the back of the neck, while the control group was treated with equal amount of saline for 8 weeks. The weight of each group of mice was observed and recorded every 7 days, and two groups of mice were randomly selected for frozen sections of brain tissue at the end of the modelling period to verify the aging model. 2. After the aging model was successfully established, the aging groups were divided into 5 groups: model group, dagliflozin-treated group (high and low dose), and dagliflozin + ex527-inhibited group (high and low dose). Fasting blood glucose was measured in each group every 2 weeks for 8 weeks. At the end of treatment, Morris water maze was performed at the end of the treatment. After execution of the mice, the organ indices of heart, brain, liver, kidney and spleen were measured; the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum were determined. Results: After the successful establishment of the aging model, it was found that during the treatment phase of dagliflozin. 1) The organ indices of mice in the aging group were significantly lower than those of other groups, and no significant hypoglycemia was observed throughout the treatment process. 2) In the water maze test, mice in the aging group had a significantly longer latency in the plateau phase compared to the control and treatment groups, while the number of times the mice crossed the original plateau and the percentage of time spent exploring the original plateau quadrant were reduced after the plateau was removed. 3
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