Asymptomatic atrial fibrillation burden and thromboembolic events: piecing evidence together

<p><b>Background</b>: Contributory evidence on a direct association between asymptomatic atrial fibrillation (AF) burden and thromboembolic events is conflicting and contradictory. The aim of the article is to gather evidence available for a direct correlation between burden and stroke.</p> <p><b>Methods</b>: A literature search was performed to capture studies reporting data on the impact of asymptomatic AF burden on the risk of stroke. Data was then extracted from each included study including burden of AF, hazard ratio (HR) for stroke, and CHADS₂ score. A random effects meta-analysis was carried out on the log-transformed HRs for different subgroups of AF burden. A meta-regression was performed on the two variables: burden of asymptomatic AF and CHADS₂ score.</p> <p><b>Results</b>: The random-effect pooled analysis performed on a single subgroup of the six studies reporting data on HR, showed a HR of 2.150 (95% CI 1.523–3.003) for stroke during asymptomatic AF compared to sinus rhythm. At univariate meta-regression, no correlation was detected between burden of asymptomatic AF and HR for stroke (p-value 0,874). When CHADS₂ score was included in the regression model as a covariate, no significant association was detected (p-value 0,939).</p> <p><b>Conclusion</b>: A direct correlation between burden of asymptomatic AF and HR for stroke cannot be detected in our pooled analysis. However, due to the limitations acknowledged in the analysis, our findings need to be confirmed in large cohort studies.</p

Meta-Analysis of Genome-Wide Association Studies for Abdominal Aortic Aneurysm Identifies Four New Disease-Specific Risk Loci

Rationale: Abdominal aortic aneurysm (AAA) is a complex disease with both genetic and environmental risk factors. Together, 6 previously identified risk loci only explain a small proportion of the heritability of AAA. Objective: To identify additional AAA risk loci using data from all available genome-wide association studies (GWAS). Methods and Results: Through a meta-analysis of 6 GWAS datasets and a validation study totalling 10,204 cases and 107,766 controls we identified 4 new AAA risk loci: 1q32.3 (SMYD2), 13q12.11 (LINC00540), 20q13.12 (near PCIF1/MMP9/ZNF335), and 21q22.2 (ERG). In various database searches we observed no new associations between the lead AAA SNPs and coronary artery disease, blood pressure, lipids or diabetes. Network analyses identified ERG, IL6R and LDLR as modifiers of MMP9, with a direct interaction between ERG and MMP9. Conclusions: The 4 new risk loci for AAA appear to be specific for AAA compared with other cardiovascular diseases and related traits suggesting that traditional cardiovascular risk factor management may only have limited value in preventing the progression of aneurysmal disease