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BackgroundAn increase in the incidence of atrial fibrillation (AF) during the acute phase of myocardial infarction (AMI) has been observed. But it is still unclear whether the implications of new-onset AF on in-hospital and long-term prognosis are of similar magnitude.MethodsUsing data from the CBD Bank study, 3,824 consecutive AMI patients, without prior AF, were analyzed. During the index hospitalization, all patients were monitored by continuous cardiac monitoring, twice daily performed 12- or 18-lead ECGs and timely ECG checks when cardiac symptoms occurred. Follow-up visits were routinely scheduled after discharge. Primary outcomes were all-cause death and cardiovascular death occurring during hospitalization and long-term follow-up. Secondary outcome was MACEs during hospitalization.ResultsDuring the median hospital stay of 9.0 (7.0, 11.0) days, new-onset AF was documented in 133 (3.48%) patients; 95 (71.43%) patients had AF attacks within 3 days following AMI. Independent risk factors associated with new-onset AF were older age, larger left atrial diameter, higher level of NT-proBNP, and primary PCI. New-onset AF was found to be significantly associated with in-hospital all-cause death (OR 4.33, 95%CI: 2.37-7.89, P < 0.001), cardiovascular death (OR 4.10, 95%CI: 2.18-7.73, P < 0.001), and MACEs (OR 2.51, 95%CI: 1.46-4.33, P = 0.001). A total of 112 new-onset AF and 3,338 non-AF patients were followed up for 1,090 (365, 1,694) days after discharge. There was no significant association between new-onset AF and long-term all-cause death (HR 1.21, 95%CI: 0.77-1.92, P = 0.406) or cardiovascular death (HR 1.09, 95%CI: 0.61-1.97, P = 0.764).ConclusionNew-onset AF following AMI is strongly associated with an increased risk of adverse in-hospital prognosis, but it does not affect prognosis in those who survive until hospital discharge.

Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory demyelinating disorders of the central nervous system (CNS). Various genetic and environmental factors have been identified to contribute to etiology of MS and NMO. Aquaporin 4 (AQP4), is the most abundant water channel in CNS. AQP4 is expressed in astrocytes of the brain, spinal cord, optic nerve and supportive cells in sensory organs. In contrast to MS, immunoreactivity of AQP4 is abolished in NMO lesions. However, conflicting results have been reported regarding the association between AQP4 polymorphisms and demyelinating disorders. Considering the ethnic differences of genetic variations, replications in other cohorts are required. In this study, single nucleotide polymorphisms (SNPs) of AQP4 gene in patients with NMO/neuromyelitis optica spectrum disorders (NMOSD), and MS in the Northern Han Chinese population were examined. Six selected AQP4 SNPs were genotyped by high-resolution melting (HRM) method. Compared with healthy control (HC), there was no significant difference of AQP4 allele and genotype frequency in MS or NMO/NMOSD group. This study showed no significant association of common AQP4 SNPs with MS or NMO/NMOSD, strongly suggesting that polymorphisms of AQP4 gene are unlikely to confer MS or NMO/NMOSD susceptibility, at least in Northern Han Chinese population.