Ticagrelor, acting as a reversible platelet aggregation inhibitor of P2Y12 receptors (P2Y12R), is regarded as one of the first-line antiplatelet drugs for acute cardiovascular diseases. Though the probability of ticagrelor resistance is much lower than that of clopidogrel, there have been recent reports of ticagrelor resistance. In this review, we summarized the clinical application of ticagrelor and then presented the criteria and current status of ticagrelor resistance. We further discussed the potential mechanisms for ticagrelor resistance in terms of drug absorption, metabolism, and receptor action. In conclusion, the incidences of ticagrelor resistance fluctuated between 0 and 20%, and possible mechanisms mainly arose from its absorption and receptor action. Specifically, a variety of factors, such as the drug form of ticagrelor, gut microecology, and the expression and function of P-glycoprotein (P-gp) and P2Y12R, have been shown to be associated with ticagrelor resistance. The exact mechanisms of ticagrelor resistance warrant further exploration, which may contribute to the diagnosis and treatment of ticagrelor resistance.

Objectives: The relationship between hyperuricemia (HUA) and stroke remains controversial. In this systematic review, we discuss the association between HUA and stroke. Materials and methods: The PubMed, Embase, Web of Science, and Cochrane Library were searched from their earliest records to March 13th, 2024, and additional papers were identified through a manual search. Prospective studies that provided a multivariate-adjusted estimate of the association between HUA and risk of stroke incidence and mortality, represented as relative risks (RRs) with 95% confidence intervals (CIs), were eligible. Results: A total of 22 studies including 770,532 adults were eligible and included. Hyperuricemia was associated with a significantly increasing risk of both stroke incidence (pooled RR, 1.42; 95% CI, 1.31-1.53) and stroke mortality (pooled RR, 1.53; 95% CI, 1.18-1.99) in our meta-analyses. Relative risk of stroke incidence was as follows: females (pooled RR, 1.67; 95% CI, 1.44-1.92) and males (pooled RR, 1.13; 95% CI, 1.02-1.25). Relative risk of mortality was as follows: female (pooled RR, 1.41; 95% CI, 1.31-1.52) and males (pooled RR, 1.27; 95% CI, 1.20-1.34). For the risk of stroke mortality, the association between HUA and ischemic stroke (pooled RR, 1.39; 95% CI, 1.31-1.47) was more significant than that of hemorrhagic stroke (pooled RR, 1.13; 95% CI, 1.02-1.26). Conclusion: Our study confirms an association between HUA and risk of stroke, which is more pronounced in females.

N⁶-methyladenosine (m⁶A) modification is a newly discovered regulatory mechanism in eukaryotes. As one of the most common epigenetic mechanisms, m⁶A’s role in the development of atherosclerosis (AS) and atherosclerotic diseases (AD) has also received increasing attention. Herein, we elucidate the effect of m⁶A on major risk factors for AS, including lipid metabolism disorders, hypertension, and hyperglycemia. We also describe how m⁶A methylation contributes to endothelial cell injury, macrophage response, inflammation, and smooth muscle cell response in AS and AD. Subsequently, we illustrate the m⁶A-mediated aberrant biological role in the pathogenesis of AS and AD, and analyze the levels of m⁶A methylation in peripheral blood or local tissues of AS and AD, which helps to further discuss the diagnostic and therapeutic potential of m⁶A regulation for AS and AD. In summary, studies on m⁶A methylation provide new insights into the pathophysiologic mechanisms of AS and AD, and m⁶A methylation could be a novel diagnostic biomarker and therapeutic target for AS and AD.

Background: Excessive supraventricular ectopic activity (ESVEA) is correlated with the development of atrial fibrillation (AF) and is frequently observed in ischemic stroke patients. This meta-analysis aims to summarize the evidence on the association between ESVEA and the risk of AF and stroke. Methods: PubMed and Embase databases were systematically searched to identify all publications providing relevant data from inception to 23 August 2022. Hazard ratio (HR) and 95% confidence interval (CI) were pooled using fixed-effect or random-effect models. Results: We included 23,272 participants from 20 studies. Pooled results showed that ESVEA was associated with an increased risk of AF in the general population (HR: 2.57; 95% CI 2.16–3.05), increased risk of AF in ischemic stroke patients (HR: 2.91; 95% CI 1.80–4.69), new-onset ischemic stroke (HR: 1.91; 95% CI 1.30–2.79), and all-cause mortality (HR: 1.41; 95% CI 1.24–1.59). Pooled analysis indicated that ESVEA was not associated with recurrent ischemic stroke/transient ischemic attack (TIA) (HR: 1.24; 95% CI 0.91–1.67). Conclusions: ESVEA is associated with AF, new-onset ischemic stroke, and all-cause mortality.

Objectives. To evaluate the relationship between the plasma miR-223 expression level and clopidogrel resistance in acute coronary syndrome (ACS) patients. Methods. We performed a search for publications using online databases including PubMed, EMBASE, Cochrane Library, and Chinese Databases (CNKI database, Weipu database, and Wanfang database) from the inception of the databases to June 18, 2023, to identify studies reporting the relationship between the plasma miR-223 level and clopidogrel resistance in ACS patients. Two researchers independently searched and screened to ensure the consistency of the results and assess the quality of the included studies according to the Newcastle-Ottawa scale. A fixed-effects model was used for pooling data with STATA 14.0. Results. Four articles including 399 Chinese ACS patients were eligible for the meta-analysis. Low plasma miR-223 levels were independently correlated with clopidogrel resistance in Chinese ACS patients (OR 0.58, 95 CI: 0.331.04). Conclusion. Lower plasma miR-223 levels are associated with clopidogrel resistance in Chinese ACS patients, suggesting that miR-223 may be a potential diagnostic biomarker of clopidogrel resistance.

There has been limited evidence and inconsistent results on the safety and effectiveness of prior antiplatelet (PA) use for acute ischemic stroke (AIS) pat