This is the first meta-analysis investigating the relationship between NAFLD and CVD independent of the impact of DM. Our findings suggested that NAFLD increases the risk of CVD in populations with comparable DM profiles. Diabetic patients diagnosed with NAFLD might benefit from a more early cardiovascular risk assessment, thereby reducing CVD morbidity and mortality.

Background: The genetic determinants of response to clopidogrel and aspirin are incompletely characterized. Recently, PEAR1 (platelet endothelial aggregation receptor-1) rs12041331 polymorphism has been shown to influence the platelet reactivity, but its impact on cardiovascular outcomes remains unclear in patients treated with antiplatelet agents. Methods and Results: In this prospective cohort study, 2439 Chinese patients with acute coronary syndrome or stable coronary artery disease undergoing coronary stent implantation and receiving clopidogrel and aspirin were consecutively recruited. Their platelet reactivity was determined by light transmission aggregometry at 5 and 30 days after coronary intervention. Genotyping was performed using an improved multiplex ligation detection reaction technique. All patients completed a 30-day follow-up for clinical outcomes. Genotyping for PEAR1 showed 768 (38.3%) GG homozygotes, 941 (46.9%) GA heterozygotes, and 298 (14.8%) AA homozygotes. The 30-day incidence of major adverse cardiovascular events, the composite of cardiovascular death, nonfatal myocardial infarction, and ischemic stroke were significantly higher in AA homozygotes than in non-AA homozygotes (adjusted hazard ratio, 2.78; 95% CI, 1.13–6.82; P =0.026), irrespective of CYP2C19*2 loss-of-function polymorphism and known outcome predictors including age, sex, smoking, and diabetes mellitus. The ADP-induced platelet aggregation was significantly lower in AA homozygotes than that in GG homozygotes at both time points, although no significant difference was found for the arachidonic acid–induced platelet aggregation among the 3 groups. Conclusions: About 15% of Chinese patients undergoing coronary stent implantation were AA homozygotes for PEAR1 rs12041331. These patients had ≈3-fold increase in short-term major adverse cardiovascular events risk compared with non-AA homozygotes, and the adverse clinical outcome is unlikely to be mediated by suboptimal pharmacological response to aspirin or clopidogrel. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT01968499.

Abstract:Objective: To evaluate the clinical effect of postconditioning on patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Methods: Randomized controlled trials were identified by searching relevant databases published up to April 2nd, 2014. A meta-analysis of eligible studies was performed by Stata 12.0 and Review Manager 5.2 with a fixed-effect model. Results: Ten studies providing adverse cardiac events in a total of 1346 STEMI patients treated with primary PCI were identified. The occurrence of heart failure was significantly reduced in patients treated with postconditioning compared with usual care (risk ratio (RR) 0.533; 95% confidence intervals (CI) 0.368-0.770), whereas non-fatal reinfarction slightly increased in the postconditioning group (RR 2.746; 95% CI 1.007-7.488). No significant difference in total major adverse cardiac events (MACEs) was observed between the two groups (RR 0.876; 95% CI 0.671-1.144). Conclusions: Postconditioning in STEMI patients undergoing primary PCI significantly reduces the risk of heart failure, but fails to decrease the incidence of total MACEs and the risk of non-fatal reinfarction.

Background: Lipoprotein concentrations have been associated with the major risk of bleeding events. However, whether plasma levels of LDL-C are associated with the risk of biopsy-related endobronchial hemorrhage remain elusive. Therefore, the present study was initiated to investigate the explicit association of low-density lipoprotein cholesterol (LDL-C) with endobronchial biopsy (EBB)-induced refractory hemorrhage in patients with lung cancer. Methods: This retrospective study included a total of 659 consecutive patients with lung cancer who had undergone EBB at a tertiary hospital between January 2014 and April 2018. Using multiple regression analysis, the association between LDL-C and the risk of EBB-induced refractory hemorrhage was assessed after adjusting for potential confounding factors. Results: A significant proportion (13.8%, 91/659) of the patients experienced refractory hemorrhage following EBB. In multivariate regression analysis, higher plasma LDL-C concentrations were associated with increased risk of EBBinduced refractory hemorrhage in patients with lung cancer after adjusting for potential confounders (P < 0.05). Using the lowest quartile of plasma LDL-C as the reference group, the odds ratio (95% confidence interval) of Q2, Q3, and Q4 were 2.32 (1.07, 5.03), 2.37 (0.94, 5.95), and 3.65 (1.16, 11.51), respectively (P for trend < 0.05). Moreover, this association was noticeably more pronounced in male patients with lung cancer in the subgroup analysis (P < 0.05). Conclusions: Plasma LDL-C was positively correlated with the increased risk of EBB-induced refractory hemorrhage in patients with lung cancer; predominantly, the associated risk was more pronounced in male patients with lung cancer.