未经证实：一些研究已经调查了全身免疫-炎症指数（SII）预测心血管疾病（CVD）的价值，但是结果不一致。因此,我们进行了荟萃分析和系统综述,以评估SII与CVD风险之间的相关性.
未经调查：两名调查人员系统地搜索了PubMed，Embase,WebofScience,科克伦图书馆,和CINAHL数据库，以确定所有检查SII水平和CVD之间关联的研究。使用基于异质性测试的固定或随机效应模型，将高SII患者与低SII患者相比的CVD风险估计值以及CVD组和对照组之间的加权平均差（WMD）汇总。我们使用纽卡斯尔-渥太华量表来评估符合条件的研究中的偏倚风险，和建议评估的分级，发展,采用评估(GRADE)系统对证据的确定性进行评级。
UNASSIGNED：共纳入13项研究，包括152,996名参与者进行分析。总体汇总结果显示，较高的SII与CVD风险增加显著相关（HR=1.39，95CI：1.20-1.61，P<0.001）。这种增加的风险可以在几乎所有的CVD亚型中观察到，包括缺血性卒中（HR=1.31，95CI：1.06-1.63，P=0.013），出血性中风（HR=1.22，95CI：1.10-1.37，P<0.001），心肌梗死(HR=1.11,95CI:1.01-1.23,P=0.027),和外周动脉疾病（HR=1.51，95CI：1.18-1.93，P=0.001）。静脉血栓形成的趋势不明显，但仍然相似（HR=4.65，95CI：0.66-32.71，P=0.122），脑小血管病（HR=1.09，95CI：0.95-1.25，P=0.233），急性冠脉综合征(HR=1.08,95CI:0.96~1.22,P=0.200)。此外，汇总结果显示，CVD发作时的SII水平明显高于普通人群（WMD=355.2，95CI：234.8-475.6，P<0.001），在不同的CVD亚型之间是一致的。等级评估表明，来自观察性研究的当前证据的质量较低或非常低。
UNASSIGNED：这项研究表明SII可能是CVD发展的潜在生物标志物，SII升高与CVD风险增加相关。然而,证据质量普遍较低。需要进行其他精心设计的研究，以确定最佳临界值并表征受益人群。
UNASSIGNED: Several studies have investigated the value of the systemic immune-inflammation index (SII) for predicting cardiovascular disease (CVD), but the results were inconsistent. Therefore, a meta-analysis and systematic
review were conducted to assess the correlation between SII and risk of CVD.
UNASSIGNED: Two investigators systematically searched PubMed, Embase, Web of Science, Cochrane library, and CINAHL databases to identify all studies that examined the association between SII levels and CVD. The risk estimates of CVD for people with high SII compared to those with low SII levels and the weighted mean difference (WMD) between the CVD and control groups were pooled using fixed- or random-effects models based on the heterogeneity test. We used the Newcastle-Ottawa Scale to assess the risk of bias in eligible studies, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system was applied to rate the certainty of evidence.
UNASSIGNED: A total of 13 studies with 152,996 participants were included for analysis. The overall pooled results showed that higher SII was significantly associated with an increased risk of CVD (HR = 1.39, 95%CI: 1.20-1.61, P < 0.001). This increased risk could be observed in almost all CVD subtypes, including ischemic stroke (HR = 1.31, 95%CI: 1.06-1.63, P = 0.013), hemorrhagic stroke (HR = 1.22, 95%CI: 1.10-1.37, P < 0.001), myocardial infarction (HR = 1.11, 95%CI: 1.01-1.23, P = 0.027), and peripheral arterial disease (HR = 1.51, 95%CI: 1.18-1.93, P = 0.001). There were no significant but still similar trends in venous thrombosis (HR = 4.65, 95%CI: 0.66-32.71, P = 0.122), cerebral small vessel disease (HR = 1.09, 95%CI: 0.95-1.25, P = 0.233), and acute coronary syndrome (HR = 1.08, 95%CI: 0.96-1.22, P = 0.200). Furthermore, the pooled results showed that SII levels at the onset of CVD were significantly higher than that in the general population (WMD = 355.2, 95%CI: 234.8-475.6, P < 0.001), which was consistent across different CVD subtypes. The GRADE assessment suggested that the quality of current evidence from observational studies was low or very low.
UNASSIGNED: This study indicated that SII may be a potential biomarker for CVD development and elevated SII is associated with an increased risk of CVD. However, the quality of evidence is generally low. Additional well-designed studies are necessary to determine the optimal cutoff value and to characterize the benefited population.
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