Context Observational studies have suggested associations between adipokines and cardiovascular disease (CVD), but the roles of certain adipokines remain controversial, and these associations have not yet been ascertained causally. Objective To investigate whether circulating adipokines causally affect the risk of CVD using two-sample Mendelian randomization (MR). Methods Independent genetic variants strongly associated with adiponectin, resistin, chemerin and retinol binding protein 4 (RBP4) were selected from public genome-wide association studies. Summary-level statistics for CVD, including coronary artery disease (CAD), myocardial infarction, atrial fibrillation (AF), heart failure (HF), stroke and its subtypes were collected. The inverse-variance weighted and Wald ratio methods were used for the MR estimates. The MR-PRESSO, weighted median, MR-Egger, leave-one-out analysis, MR Steiger and colocalization analysis were used in the sensitivity analysis. Results Genetically predicted resistin levels were positively associated with AF risk (OR 1.09; 95% CI, 1.04 to 1.13; P = 4.1×10 -5), which was attenuated to null after adjusting for blood pressure. We observed suggestive associations between higher genetically predicted chemerin levels and an increased risk of CAD (OR 1.27; 95% CI, 1.01 to 1.60; P = 0.040), higher genetically predicted RBP4 levels and an increased risk of HF (OR 1.14; 95% CI, 1.02 to 1.27; P = 0.024). There was no causal association between genetically predicted adiponectin levels and CVD risk. Conclusions Our findings reveal the causal association between resistin and AF, probably acting through blood pressure, and suggest potential causal associations between chemerin and CAD, RBP4 and HF.

Background. The role of a drug-coated balloon (DCB) in the treatment of acute myocardial infarction (AMI) is not well established. Methods. Five databases were searched for randomized controlled trials that compared DCB with stents in the treatment of AMI from their inception to 30 July 2021. The primary clinical endpoint was major adverse cardiac events (MACEs). Summary estimations were conducted using fixed-effects analysis complemented by several subgroups. The protocol was registered with PROSPERO (https://clinicaltrials.gov/ct2/show/CRD42021272886). Results. A total of 4 randomized controlled trials with 485 patients were included. On routine clinical follow-up, DCB was associated with no difference in the incidence of MACEs compared with control (risk ratio [RR] 0.59 [0.31 to 1.13]; P = 0.11 ). DCB was associated with similar MACEs compared with drug-eluting stent and lower MACEs compared with bare-metal stent. There was no difference between DCB and control in terms of all-cause mortality, cardiovascular mortality, stent thrombosis, target lesion revascularization, and minimal lumen diameter during follow-up. However, DCB was associated with a lower incidence of myocardial infarction (RR 0.16 [0.03 to 0.90]; P = 0.04 ) and lower late lumen loss (mean difference −0.20 [−0.27 to −0.13]; P < 0.00001 ). Conclusions. In treatment of patients with AMI, DCB might be a feasible interventional strategy versus control as it associated with comparable clinical outcomes. Future large-volume, well-designed randomized controlled trials to evaluating the role of the DCB in this setting are warranted.