Background-The efficacy of additional complex fractionated atrial electrogram (CFAE) ablation after pulmonary vein antrum isolation (PVAI) in patients with atrial fibrillation (AF) remains controversial. This meta-analysis was performed to assess the additional efficacy of CFAEs ablation after a single procedure without antiarrhythmic drugs. Methods and Results-Trials were identified in MEDLINE, Cochrane Library, Embase, Google Scholar, reviews, and reference lists of relevant papers. Controlled cohort studies comparing the long-term efficacy of combined CFAEs plus PVAI ablation with PVAI alone were included. The primary end point was the maintenance of sinus rhythm without antiarrhythmic drugs. Seven controlled trials (9 comparisons) with a total of 622 participants (332 patients underwent PVAI plus CFAE ablation and 330 patients underwent PVAI alone) were included in the meta-analysis. In an overall pooled estimate, compared with PVI alone, long-term rates of sinus rhythm maintenance (relative risk, 1.17, 95% confidence interval, 1.03 to 1.33, Pϭ0.019) were increased by additional CFAE ablation. Subgroup analysis demonstrated that additional CFAEs ablation increased rates of sinus rhythm maintenance in nonparoxysmal AF (relative risk, 1.35; 95% confidence interval, 1.04 to 1.75; Pϭ0.022), whereas had no effect on patients with paroxysmal AF (relative risk, 1.04; 95% confidence interval, 0.92 to 1.18; Pϭ0.528). Conclusions-Adjuvant CFAE ablation in addition to standard PVAI increases the rate of long-term sinus rhythm maintenance in nonparoxysmal AF patients after a single procedure without antiarrhythmic drugs but does not provide additional benefit to sinus rhythm maintenance in paroxysmal AF patients. (Circ Arrhythm Electrophysiol. 2011;4:143-148.)

Air pollution is known to be a major risk factor for cardiopulmonary disease, but this is unclear for cardiometabolic disease (e.g. diabetes). This is of considerable public health importance, given the nationwide epidemic of diabetes, accompanied by severe air pollution, in China. The evidence so far remained inadequate to answer questions of whether individuals with cardiometabolic dysfunctions are susceptible to air pollution and whether air pollution exacerbates diabetes development via certain biological pathways. In this manuscript, we summarize the results and limitations of studies exploring these two topics and elaborate our design of a prospective panel study (SCOPE) as a solution. We assessed and compared the health effect of air pollution among pre-diabetic individuals and matched healthy controls through four repeated clinical visits over 1 year. Comprehensive evaluation was made to both health endpoints and exposure. The primary biomarkers were assessed to reveal the impact on multiple biological pathways, including glycolipid metabolism and insulin resistance, endothelial function, and inflammation. Detailed chemical and size fractional components of particulate matter were measured in this study, along with the application of personal monitors. The work should increase our understanding of how air pollution affects individuals with cardiometabolic dysfunction and the underlying mechanisms.

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It has been reported that the variants of the PDE4D (phosphodiesterase 4D) gene are associated with stroke, especially with the combination of cardio-embolic and carotid stroke in the Icelandic population, but it is still very controversial as to whether PDE4D is a susceptible gene for stroke in other populations. In the present study, we tested whether the PDE4D gene variation also confers stroke risk in a Chinese population. Our hypothesis was tested in a case-control study of a Chinese population comprising 639 stroke patients (including 253 with cerebral thrombosis, 171 with lacunar infarction and 215 with intracerebral haemorrhage) and 887 healthy controls. Three SNPs (single nucleotide polymorphisms) (rs966221, rs456009 and rs2910829) in PDE4D were chosen based on the significant association with stroke reported previously in a Western population, and these were genotyped using PCR/RFLP (restriction-fragment-length polymorphism) and confirmed by sequencing. We found that only SNP83 (rs966221) was associated with stroke. Allele C of rs966221 is a risk allele, conferring an increased risk for atherothrombotic strokes [OR (odds ratio), 1.51; 95% CI (confidence interval), 1.09-2.10] independent of conventional risk factors. Haplotype analysis confirmed that haplotype G-C-C was associated with increased risk for atherothrombotic stroke (OR, 1.80; 95% CI, 1.300-2.491). Our findings support that SNP83 of PDE4D is a genetic risk factor for atherothrombotic strokes in a Chinese population.