Background With the establishment of the heart-gut axis concept, accumulating studies suggest that the gut microbiome plays an important role in the pathogenesis of cardiovascular diseases. Yet, little evidence has been reported in characterizing the gut microbiota shift in atrial fibrillation. Methods We include the result of the global alterations that occur in the intestinal microbiota in a cohort of 50 patients with atrial fibrillation and 50 matched controls based on a strategy of metagenomic and metabolomic analyses. Results The alterations include a dramatic elevation in microbial diversity and a specific perturbation of gut microbiota composition. Overgrowth of Ruminococcus , Streptococcus , and Enterococcus , as well as reduction of Faecalibacterium , Alistipes , Oscillibacter , and Bilophila were detected in patients with atrial fibrillation. A gut microbial function imbalance and correlated metabolic pattern changes were observed with atrial fibrillation in both fecal and serum samples. The differential gut microbiome signatures could be used to identify patients with atrial fibrillation. Conclusions Our findings characterize the disordered gut microbiota and microbial metabolite profiles in atrial fibrillation. Further research could determine whether intervention strategies targeting intestinal microbiome composition might be useful to counteract the progression of atrial fibrillation.

Background and AimsThe American Heart Association has recently established seven ideal cardiovascular health metrics for cardiovascular health promotion and disease reduction (i.e., non-smoking, normal body mass index, physically active, healthy diet, and normal levels of cholesterol, blood pressure and fasting blood glucose). The present study seeks to evaluate how well these metrics predict mortality from all causes and cardiovascular diseases in adult Chinese living in a northern industrial city.Methods and ResultsData of 95,429 adults who participated in the Kailuan cohort study from June 2006 to October 2007 was analyzed. All participants underwent questionnaire assessment, clinical examination, laboratory assessments and were followed up biannually. During a median follow-up of 4.02 years, 1,843 deaths occurred, with 597 deaths resulting from cardiovascular diseases. Lower mortality rates from all causes and cardiovascular diseases were observed among the subjects who met a higher number of the ideal health metrics. Compared to the participants who met none or one ideal health metric, those meeting ≥5 ideal health metrics had a lower risk of all-cause mortality by 30% (adjusted hazard ratio, 0.70; 95% confidence interval, 0.56–0.88) and a lower risk of mortality from cardiovascular diseases by 39% (adjusted hazard ratio, 0.61; 95% confidence interval, 0.41–0.89) . Four metrics (smoking status, physical activity, blood pressure and fasting blood glucose) were significantly associated with all-cause mortality. Three metrics (physical activity, blood pressure and fasting blood glucose) were significantly associated with mortality from cardiovascular diseases.ConclusionThe number of ideal health metrics is negatively associated with mortality rates from all causes and cardiovascular diseases among adults in a Northern Chinese industrial city. The data supports the AHA recommendation of ideal health metrics for adults from Northern China.

Abnormal aortic adventitial fibroblasts (AFs) play essential roles in the development of vascular remodeling and disorders. Previous studies revealed that microRNA-122 (miR-122) levels were elevated in the aortic adventitia of hypertensive rats with vascular injury. Here, we aim to evaluate the biological effects and underlying mechanisms of miR-122 in rat AFs. Exposure to angiotensin II (ATII) in rat AFs resulted in decreased levels of sirtuin 6 (SIRT6), elabela (ELA), and angiotensin-converting enzyme 2 (ACE2). Additionally, stimulation with ATII contributed to a decline in autophagic flux and obvious increases in cellular migration, oxidative stress, and apoptosis, which were exacerbated by the transfection of miR-122-5p mimic but were rescued by miR-122-5p inhibitor, exogenous replenishment of ELA, and recombinant adeno-associated virus expressing SIRT6 (rAAV-SIRT6), respectively. Moreover, stimulation with miR-122-5p mimic led to a marked reduction in the levels of SIRT6 and ELA in rat AFs, which were elevated by stimulation with rAAV-SIRT6. Furthermore, miR-122-5p inhibitor-mediated pro-autophagic, anti-oxidant and anti-apoptotic effects in rat AFs were partially suppressed by 3-methyladenine, SIRT6 small interfering RNA (siRNA) and ELA siRNA, which were linked with the downregulation in the protein levels of LC3-II, beclin-1, and ACE2 and the upregulation of p62 expression and bax/bcl-2 ratio. Our findings indicated that miR-122-5p inhibition prevented ATII-mediated loss of autophagy, and the promotion of apoptosis and oxidative stress via activating the SIRT6-ELA-ACE2 signaling. MiR-122-5p may be a novel predictive biomarker of adventitial injury, and targeting the SIRT6-ELA-ACE2 signaling may have the potential therapeutic importance of controlling vascular remodeling and disorders.