BackgroundIn recent decades, tranexamic acid (TXA) antifibrinolytic therapy before aneurysm clipping or embolization has been widely reported, but its safety and efficacy remain controversial. This meta-analysis evaluated the efficacy and safety of TXA therapy in aneurysmal subarachnoid hemorrhage (aSAH) patients, aiming to improve the evidence-based medical knowledge of treatment options for such patients.MethodsPubmed, Web of Science, and Cochrane Library databases were searched up to 1 March 2021 for randomized controlled trials (RCTs). We extracted safety and efficacy outcomes and performed a meta-analysis using the Review Manager software. We performed two group analyses of TXA duration and daily dose.ResultsTen RCT studies, enrolling a total of 2,810 participants (1,410 with and 1,400 without TXA therapy), matched the selection criteria. In the TXA duration group: TXA did not reduce overall mortality during the follow-up period [RR 1.00 (95% CI 0.81–1.22)]. The overall rebleeding rate in the TXA group was 0.53 times that of the control group, which was statistically significant [RR 0.53 (95% CI 0.39–0.71)]. However, an RR of 0.43 was not statistically significant in the subgroup analysis of short-term therapy [RR 0.43 (95% CI 0.13–1.39)]. The overall incidence of hydrocephalus was significantly higher in the TXA group than in the control group [RR 1.13 (95% CI 1.02–1.24)]. However, the trend was not statistically significant in the subgroup analysis [short-term: RR 1.10 (95% CI 0.99–1.23); long-term: RR 1.22 (95% CI 0.99–1.50)]. Treatment with TXA did not cause significant delayed cerebral ischemia [RR 1.18 (95% CI 0.89–1.56)], and its subgroup analysis showed an opposite and insignificant effect [short-term: RR 0.99 (95% CI 0.79–1.25); long-term: RR 1.38 (95% CI 0.86–2.21)]. Results in the daily dose group were consistent with those in the TXA duration group.ConclusionsTranexamic acid does not reduce overall mortality in patients with aSAH, nor does it increase the incidence of delayed cerebral ischemia. Tranexamic acid in treating aSAH can reduce the incidence of rebleeding. However, there is no statisticalsignificance in the ultra-early short-term and low daily dose TXA therapy, which may be due to the lack of relevant studies, and more RCT experiments are needed for further study.Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/display_record.asp? PROSPERO, identifier: 244079.

Myocardial ischemia/reperfusion injury (I/RI) may potentiate cardiac remodeling and heart failure, while effective therapies for I/RI remain lacking. Circulating human plasma‐derived extracellular vesicles (hEV) have great potential to protect against I/RI. However, the effective delivery of hEV in vivo remains a limiting factor for clinical application. The present study constructs a biomimetic delivery system of platelet membrane‐fused hEV (P‐hEV), utilizing the natural affinity of platelets for hEV delivery to the injured vascular and myocardial sites. The results show that platelet membrane and hEV membrane fusion can be achieved through repeated extrusion. Compared to non‐modified hEV, P‐hEV uptake is greatly enhanced in human umbilical vein endothelial cells (HUVECs) stressed by oxygen‐glucose deprivation/reperfusion (OGD/R). Functionally, P‐hEV inhibits HUVEC and neonatal rat cardiomyocyte (NRCM) apoptosis and promotes HUVECs migration and tube formation under OGD/R stress in vitro. Intravenous delivery of P‐hEV more effectively targets and accumulates at injury sites in the heart. Furthermore, P‐hEV significantly enhances protection against acute I/RI and attenuates cardiac remodeling at three weeks post‐I/RI. In conclusion, the platelet membrane‐fused hEV delivery system enhances the target delivery of EV to protect against myocardial I/RI, presenting a novel drug delivery system for ischemic heart diseases.

It is well known that exercise is beneficial for cardiovascular health. Oxidative stress is the common pathological basis of many cardiovascular diseases. The overproduction of free radicals, both reactive oxygen species and reactive nitrogen species, can lead to redox imbalance and exacerbate oxidative damage to the cardiovascular system. Maintaining redox homeostasis and enhancing anti‐oxidative capacity are critical mechanisms by which exercise protects against cardiovascular diseases. Moderate‐intensity exercise is an effective means to maintain cardiovascular redox homeostasis. Moderate‐intensity exercise reduces the risk of cardiovascular disease by improving mitochondrial function and anti‐oxidative capacity. It also attenuates adverse cardiac remodeling and enhances cardiac function. This paper reviews the primary mechanisms of moderate‐intensity exercise‐mediated redox homeostasis in the cardiovascular system. Exploring the role of exercise‐mediated redox homeostasis in the cardiovascular system is of great significance to the prevention and treatment of cardiovascular diseases.

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