BackgroundAsthma and cardiovascular disease (CVD) share many risk factors. Previous meta-analyses indicated that asthma is associated with an increased risk of CVD and all-cause mortality, but these studies were limited by unstandardized search strategies and the number of articles included.ObjectiveWe sought to systematically synthesize evidence investigating the impact of asthma on all-cause mortality and CVD morbidity and mortality.MethodsWe searched in PubMed and EMBASE for observational cohort studies (inception dates to November 10, 2021) that had both asthma groups and control groups. We also manually searched the reference lists of correlative articles to include other eligible studies. Data for associations between asthma and all-cause mortality and CVD morbidity and mortality were needed.ResultsWe summarized the findings from 30 cohort studies comprising 4,157,823 participants. Asthma patients had increased CVD morbidity [relative risk (RR) = 1.28, 95% confidence interval (CI) = 1.16–1.40] and increased CVD mortality (RR = 1.25, 95% CI = 1.14–1.38). Asthma patients also had increased risk of all-cause mortality (RR = 1.38, 95% CI = 1.07–1.77). In subgroup analyses, female asthma patients had a higher risk of CVD morbidity and all-cause mortality than male asthma patients, and late-onset asthma patients had a higher risk of CVD morbidity than early-onset asthma patients.ConclusionAsthma patients have increased risk of all-cause mortality and CVD morbidity and mortality. This information reminds clinicians to be aware of the risk of CVD and all-cause mortality in asthma patients.Systematic Review Registrationhttp://www.crd.york.ac.uk/PROSPERO/, PROSPERO, identifier: CRD 42021290082.

Atherosclerosis is a risk factor for various cardiovascular diseases, and is linked to high rates of morbidity and mortality across the globe. Although numerous complex processes are involved in the development and progression of atherosclerosis, the exact mechanisms behind its pathogenesis remain unclear. Inflammation and endothelial cell damage exert a lasting effect on atherosclerosis, causing lipid and fibrous tissue accumulation in the intima of the artery to form plaques, and subsequently promoting atherosclerosis. Nod-like receptor protein 3 (NLRP3) inflammatory corpuscle is thought to be the link between lipid metabolism and inflammation. Long Potassium outflow is a vital activator of NLRP3, with a simultaneous effect as a start-up and adjustment. The majority of existing drugs for atherosclerosis targeting the NLRP3 signaling pathway target IL-1, whereas drugs targeting the critical link of potassium efflux are relatively new. This review discusses the NLRP3 inflammatory corpuscle as a critical regulator of the immunological inflammatory pathway in atherosclerosis. Moreover, current knowledge on NLRP3 inflammatory corpuscle start and activation pathways were integrated, emphasizing potassiuminvolved outflow-related proteins. We highlight potential treatment approaches for NLRP3 inflammatory corpuscle pathways, specifically targeting potassium outflow channels of targeted drugs. Collectively, these insights indicate that targeting the NLRP3 inflammatory corpuscle is a vital anti-inflammatory therapy for treating atherosclerosis.