Understanding the global burden of atrial fibrillation and regional variations: We need improvement

This editorial refers to 'Global variations in the prevalence, treatment, and impact of atrial fibrillation in a multinational cohort of 153,152middle-aged individuals' by P.G. Joseph et al., pp. 1523-1531

Stroke and bleeding risk in atrial fibrillation: navigating the alphabet soup of risk-score acronyms (CHADS2, CHA2DS2-VASc, R2CHADS2, HAS-BLED, ATRIA, and more)

: atrial fibrillation, stroke, bleeding, risk assessment.Stroke prevention is central to the management of patients with atrial fibrillation (AF). As effective stroke prophylaxis essentially requires oral anticoagulants (OAC) an understanding of the risks and benefits of OAC therapy is needed. While AF increases stroke risk 5-fold, this risk is not homogeneous. Many stroke risk factors also confer an increased risk of bleeding. Various stroke and bleeding risk stratification schemes have been developed to help inform clinical decision making. These scores were derived and validated in different study cohorts, ranging from highly selected clinical trial cohorts to 'real world' populations. Thus, their performance and classification accuracy varies depending on their derivation cohort(s). In the present review, we provide an overview of currently available stroke and bleeding risk stratification schemes. We particularly focus on the CHA2DS2-VASc and HAS-BLED schemes, as these are recommended by the latest European guidelines on AF management. Other risk stratification schemes (CHADS2, R2CHADS2, ATRIA, HEMORRHAGES, QStroke, etc.) and their place in the decision-making are also considered

Relationship between Renal Function, Fibrin Clot Properties and Lipoproteins in Anticoagulated Patients with Atrial Fibrillation

Background: Mechanisms by which chronic kidney disease (CKD) influences fibrin clot properties in atrial fibrillation (AF) remain ill-defined. We aimed to investigate the effects of AF and CKD on fibrin clot properties and lipoproteins, and determine the relationship between these factors. Methods: Prospective cross-sectional study of patients recruited from cardiology services in Liverpool between September 2019 and October 2021. Primary groups consisted of anticoagulated AF patients with and without CKD in a 1:1 ratio. Control group comprised anticoagulated patients without AF or CKD. Fibrin clot properties were analysed using turbidity and permeation assays. Detailed lipoprotein characteristics, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), small dense LDL and oxidised LDL, were measured. Results: Fifty-six anticoagulated patients were enrolled (median age 72.5; 34% female); 46 with AF (23 with CKD and 23 without CKD) and 10 controls. AF was associated with changes in three indices of fibrin clot properties using PTT (T(lag) 314 vs. 358 s, p = 0.047; Abs(peak) 0.153 vs. 0.111 units, p = 0.031; T(lysis50%) 884 vs. 280 s, p = 0.047) and thrombin reagents (T(lag) 170 vs. 132 s, p = 0.031; T(max) 590 vs. 462 s, p = 0.047; T(peak50%) 406 vs. 220 s, p = 0.005) while the concomitant presence of CKD led to changes in fibrin clot properties using kaolin (T(lag) 1072 vs. 1640 s, p = 0.003; T(max) 1458 vs. 1962 s, p = 0.005; T(peak50%) 1294 vs. 2046, p = 0.008) and PPP reagents (T(lag) 566 vs. 748 s, p = 0.044). Neither of these conditions were associated with changes in fibrin clot permeability. Deteriorating eGFR was significantly correlated to the speed of clot formation, and CKD was independently associated with unfavourable clot properties (T(lag) −778, p = 0.002; T(max) −867, p = 0.004; T(peak50%) −853, p = 0.004 with kaolin reagent). AF alone was not associated with changes in lipoprotein distribution while AF patients with CKD had lower total cholesterol, LDL-C and small dense LDL due to the presence of other risk factors. No significant relationship was observed between fibrin clot properties and lipoprotein distribution. Conclusions: There are important changes that occur in fibrin clot properties with AF and CKD that may account for the increased risk of thromboembolic complications. However, these changes in fibrin clot properties were not attributable to alterations in lipoprotein distribution

Cardiac fibrosis in patients with atrial fibrillation: Mechanisms and clinical implications

atrial fibrillation, heart failure, cardiac fibrosisAtrial fibrillation (AF) is associated with structural, electrical and contractile remodeling of the atria. Development and progression of atrial fibrosis is the hallmark of structural remodeling in AF and is considered to be substrate for AF perpetuation. In contrast, experimental and clinical data on impact of ventricular fibrotic processes in pathogenesis of AF and its complications are controversial. Ventricular fibrosis appears to contribute to abnormalities in cardiac relaxation and contractility, and development of heart failure, a common finding in AF. Given the frequent coexistence of AF and heart failure and the fact that both conditions affect patient prognosis better understanding of mutual impact of fibrosis in AF and heart failure is of particular interest. In this review article, we provide an overview on the general mechanisms of cardiac fibrosis in AF, differences between fibrotic processes in atria and ventricles, and the clinical and prognostic significance of cardiac fibrosis in AF

The association of appendicular lean mass and grip strength with low-density lipoprotein, very low-density lipoprotein, and high-density lipoprotein particle diameter: a Mendelian randomization study of the UK Biobank cohort

Reduced muscle mass and reduced strength are frequently associated with both alterations in blood lipids and poorer cardiometabolic outcomes in epidemiological studies; however, a causal association cannot be determined from such observations. Two-sample Mendelian randomization (MR) was applied to assess the association of genetically determined appendicular lean mass (ALM) and handgrip strength (HGS) with serum lipid particle diameter.Methods and resultsMendelian randomization was implemented using summary-level data from the largest genome-wide association studies on ALM (n = 450 243), HGS (n = 223 315), and lipoprotein [low-density lipoprotein (LDL), very LDL (VLDL), and high-density lipoprotein (HDL)] particle diameters (n = 115 078). Inverse variance-weighted (IVW) method was used to calculate the causal estimates. Weighted median-based method, MR-Egger, and leave-one-out method were applied as sensitivity analysis. Greater ALM had a statistically significant positive effect on HDL particle diameter (MR-Egger: β = 0.055, SE = 0.031, P = 0.081; IVW: β = 0.068, SE = 0.014, P < 0.001) and a statistically significant negative effect on VLDL particle diameter (MR-Egger: β = −0.114, SE = 0.039, P = 0.003; IVW: β = −0.081, SE = 0.017, P < 0.001). Similarly, greater HGS had a statistically significant positive effect on HDL particle diameter (MR-Egger: β = 0.433, SE = 0.184, P = 0.019; IVW: β = 0.121, SE = 0.052, P = 0.021) and a statistically significant negative effect on VLDL particle diameter (MR-Egger: β = −0.416, SE = 0.163, P = 0.011; IVW: β = −0.122, SE = 0.046, P = 0.009). There was no statistically significant effect of either ALM or HGS on LDL particle diameter.ConclusionThere were potentially causal associations between both increasing ALM and HGS and increasing HDL particle size and decreasing VLDL particle size. These causal associations may offer possibilities for interventions aimed at improving cardiovascular disease risk profile

Performance of stroke risk scores in older people with atrial fibrillation not taking warfarin: comparative cohort study from BAFTA trial

Objective To compare the predictive power of the main existing and recently proposed schemes for stratification of risk of stroke in older patients with atrial fibrillation