In the present meta-analysis, several ocular neovascular diseases, such as age-related macular degeneration, diabetic retinopathy, and retinal vein occlusion, were included. Sensitivity analysis was undertaken to evaluate the variation of the risk of arterial thromboembolic events with anti-VEGF among different diseases. Intravitreal anti-VEGF significantly TH-302 decreased the risk of arterial thromboembolic events by 32% in patients with diabetic macular edema, with the 95% confidence intervals of 6% to 64%; no difference in this risk was detected in patients with neovascular age-related macular degeneration and retinal vein occlusion. In patients with diabetes mellitus, increased VEGF-mediated angiogenesis has been implicated in retinopathy and nephropathy, whereas a defective angiogenic response to ischemia, which might be attributable to a VEGF signaling defect in which there is reduced receptor signaling despite higher ligand expression, could lead to poor clinical outcomes. Therefore, the targets within the system that lead to altered VEGF signaling, such as low dose systemic anti-VEGF, may be beneficial in diabetic patients. The sensitivity analysis according to the type of diseases showed that intravitreal anti-VEGF increased the risks of cerebrovascular accidents by 52% in neovascular age-related macular degeneration, with the 95% confidence intervals of -32% to 83%. However, the point estimates of all three trials were distributed across the 1.0 risk ratio. Two estimates have shown a possible risk of cerebrovascular accidents of intravitreal anti-VEGF. However, a larger epidemiological study found that no statistically significant relationship between intravitreal anti-VEGF use and stroke. Therefore, the small differences of cerebrovascular accidents between intravitreal anti-VEGF and placebo in the two trials might be due to chance finding, but not drug-related. Although we tried to conduct a thorough review of the existing literature, this present analysis has limitations inherent to any systematic review. First, the incidences of arterial thromboembolic events showed significant heterogeneity among the included studies. This may reflect differences in sample sizes, disease types, interventions, concomitant treatment, study durations, and many other factors among these studies. Despite these differences, the risk ratios reported by all of these studies showed remarkable homogeneity. In addition, combination data by using a randomeffects model may be able to achieve more conservative estimates. Second, the included trials were done at various clinical centers, and the ability to detect arterial thromboembolic events and the classification of events might vary among these institutions, which could result in a bias of reported incidence rates. Third, only published studies were included in the present meta-analysis. To avoid the publication bias, we searched in multiple databases. In addition, to find potential publication biases, we explored asymmetry in funnel plots and detect heterogeneity using Egger’s linear regression, and no publication bias was found. Finally, the findings of this meta-analysis are based on the study level, not on patient-level source data, and some confounding factors cannot be properly assessed and incorporated into the results. Despite these limitations, the strength evidence from the present meta-analysis data suggests that the intravitreal use of anti-VEGF agents is not associated with an increased risk of arterial thromboembolic events.