Aims: Glimepiride has good cardiovascular safety. However, whether glimepiride benefits clinical cardiovascular outcomes is unclear.Methods and results: A total of 21 451 inpatients with type 2 diabetes (T2D) and chronic heart failure (CHF) were analysed, including 638 who received glimepiride treatment and 20 813 who did not. Propensity score matching yielded 509 pairs (glimepiride and non-glimepiride groups), and both groups were followed up. Kaplan–Meier and Cox regression analyses were used to compare all-cause mortality, cardiovascular mortality, hospitalizations and emergency visits for heart failure, and hospitalizations for acute myocardial infarction or stroke. During follow-up, the all-cause mortality [adjusted hazard ratio (HR), 0.47; 95% confidence interval (CI), 0.35–0.63; P < 0.001], cardiovascular mortality (adjusted HR, 0.34; 95% CI, 0.24–0.48; P < 0.001), and number of hospitalizations and emergency visits for heart failure (adjusted HR, 0.42; 95% CI, 0.36–0.50; P < 0.001) and hospitalizations for acute myocardial infarction or stroke (adjusted HR, 0.53; 95% CI, 0.38–0.73; P < 0.001) were significantly lower in the glimepiride group; the conclusion remained similar in all subgroups. Furthermore, high-dose glimepiride use (2–4 mg/day) was associated with lower cardiovascular mortality than low-dose (1 mg/day) (adjusted HR, 0.55; 95% CI, 0.31–0.99; P = 0.047). Glimepiride exhibited good molecular docking with soluble epoxide hydrolase (sEH) and increased the level epoxyeicosatrienoic acid (EET).Conclusion: Long-term continuous glimepiride use is associated with better survival, fewer hospitalizations and emergency visits for heart failure, and fewer hospitalizations for acute myocardial infarction or stroke in patients with T2D and CHF. High-dose glimepiride has greater cardiovascular protective advantages than low-dose glimepiride. The cardiovascular protective effect of glimepiride may be related to the EET level increase through sEH inhibition.Trial registration: ClinicalTrials.gov NCT05538819. https://www.clinicaltrials.gov/ct2/show/NCT05538819

The coronavirus disease (COVID-19) pandemic has continued for 5 years. Sporadic cases continue to occur in different locations. Type 2 diabetes mellitus (T2DM) is associated with a high risk of a poor prognosis in patients with COVID-19. Successful control of blood glucose levels can effectively decrease the risks of severe infections and mortality. However, the effects of different treatments were reported differently and even adversely. This retrospective study included 4,922 patients who have been diagnosed as COVID-19 and T2DM from 138 Hubei hospitals. The clinical characteristics and outcomes were compared and calculated their risk for death using multivariate Cox regression and Kaplan–Meier curves. After adjustment of age, sex, comorbidities, and in-hospital medications, metformin and alpha-glucosidase inhibitor (AGI) use performed lower all-cause mortality (adjusted hazard ratio [HR], 0.41; 95% confidence interval [CI]: 0.24–0.71; p = 0.001 for metformin; 0.53, 0.35–0.80, p = 0.002 for AGIs), while insulin use was associated with increased all-cause mortality (adjusted HR, 2.07, 95% CI, 1.61–2.67, p < 0.001). After propensity score-matched (PSM) analysis, adjusted HRs for insulin, metformin, and AGIs associated with all-cause mortality were 1.32 (95% CI, 1.03–1.81; p = 0.012), 0.48 (95% CI, 0.23–0.83, p = 0.014), and 0.59 (95% CI, 0.35–0.98, p = 0.05). Therefore, metformin and AGIs might be more suitable for patients with COVID-19 and T2DM while insulin might be used with caution.

Background COVID-19 pandemic has become a serious global public health problem. Although the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor type 1 blockers (ARBs) has been recommended in patients with COVID-19 and cardiovascular diseases (CVDs), according to the results of some small-sample retrospective analyses; however, there is still a lack of sufficient evidence to validate their efficacy. This multicenter retrospective study investigated whether ACEI/ARB administration was beneficial in patients with COVID-19 and CVDs. Methods A total of 11,231 patients with confirmed COVID-19 and CVDs, from 138 hospitals in Hubei Province, were included in this multicenter retrospective study. We compared the clinical characteristics and outcomes between the ARB and non-ARB groups and analyzed the risk factors for in-hospital death using univariate and multivariate Cox regression analyses and Kaplan–Meier curves. Results In the multivariate Cox regression model, after adjusting for age, gender, comorbidities, and in-hospital medications, ARB use was associated with lower all-cause mortality (adjusted HR, 0.53; 95% CI, 0.38–0.73; P < 0.001). After propensity score-matched analysis, the adjusted HR for the use of ARB associated with all-cause mortality was 0.62 (95% CI, 0.40–0.88; P = 0.02). Further subgroup analyses found that the adjusted HRs for the use of ARB associated with all-cause mortality were 0.52 (95% CI, 0.30–0.89; P = 0.016), 0.37 (95% CI, 0.21–0.64; P < 0.001), 0.42 (95% CI, 0.28–0.64; P < 0.001), and 0.55 (95% CI, 0.37–0.84; P = 0.005) in patients with heart failure, diabetes, and hypercholesterolemia, and severe COVID-19, respectively. Conclusions ARB administration was significantly associated with a lower risk of all-cause mortality in patients with COVID-19 and CVDs. Trial registration ClinicalTrials.gov NCT05615792.

Cardiorenal syndrome (CRS) is characterized by a complex, bidirectional interaction between cardiac and renal dysfunction, posing a significant challenge in clinical practice. Although these two organ dysfunctions share common pathophysiological pathways, there remains a major unmet need for therapies that specifically target these shared mechanisms. Oxidative stress, chronic low-grade inflammation, and progressive tissue fibrosis are pivotal, interconnected drivers involved in the progression of both chronic heart failure and chronic kidney disease, constituting a critical pathological triad in CRS. This review aims to systematically elucidate the interplay among reactive oxygen species (ROS), immune cell infiltration, proinflammatory cytokine signaling, and fibrotic pathway activation in the pathogenesis of CRS. We also provide a comprehensive overview of the current landscape of novel pharmacological candidates that target key nodes in the oxidative stress–inflammation–fibrosis axis, including small molecules, biologics, and repurposed drugs. By integrating preclinical evidence with clinical trial data, this review highlights the therapeutic potential of concurrently attenuating oxidative stress, inflammation, and fibrosis to disrupt the vicious cycle of CRS and ultimately improve patient outcomes.

Myocardial injury is both a common complication among hospitalized coronavirus disease 2019 (COVID‐19) patients and a major predictor of adverse clinical outcomes. However, its long‐term effects remain poorly defined. In this prospective cohort study of 2185 COVID‐19 survivors (531 with myocardial injury), we assessed 1‐year post‐discharge outcomes using Kaplan–Meier analysis and multivariable Cox regression before and after propensity score matching. Myocardial injury was associated with higher all‐cause mortality (adjusted hazard ratio [aHR] 3.14) and major adverse cardiovascular events (MACE) (aHR 5.22). Long‐term use of angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers (ACEI/ARB) was associated with reduced mortality (aHR 0.44) and MACE (aHR 0.58) in the myocardial injury group. At 1 year, 71.5% of survivors reported persistent symptoms—most commonly fatigue and sleep difficulties—and those with myocardial injury had poorer quality of life. This study provides the prospective evidence from China's Omicron era on the prognostic value of myocardial injury, combining hard clinical endpoints with patient‐reported outcomes and the first analysis of the ACEI/ARB association in this population. These findings highlight the prognostic importance of myocardial injury and the potential role of ACEI/ARB therapy in post‐discharge management, supporting targeted follow‐up strategies for this high‐risk population.