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Diabetes mellitus (DM) is a well-known risk factor for atrial fibrillation (AF), but the mechanism(s) by which DM affects AF prevalence remains unclear. This study aims to evaluate the impact of diabetes mellitus severity (expressed as its known duration), antihyperglycemic treatment regimen and glycaemic control on AF prevalence. From the representative sample of 3014 participants (mean age 77.5, 49.1% female) from the cross-sectional NOMED-AF study, 881 participants (mean age 77.6 ± 0.25, 46.4% female) with concomitant DM were involved in the analysis. AF was screened using a telemonitoring vest for a mean of 21.9 ± 9.1 days. The mean DM duration was 12 ± 0.35 years, but no significant impact of DM timespan on AF prevalence was observed. No differences in the treatment pattern (oral medication vs insulin vs both oral + insulin) among the study population with and without AF were shown (p = 0.106). Metabolic control reflected by HbA1c levels showed no significant association with AF and silent AF prevalence (p = 0.635; p = 0.094). On multivariate analyses, age (Odds Ratio (OR) 1.35, 95%CI: 1.18–1.53, p < 0.001), p = 0.042), body mass index (BMI; OR 1.043, 95%CI: 1.01–1.08, p = 0.027) and LDL < 100 mg/dl (OR 0.64, 95%CI: 0.42–0.97, p = 0.037) were independent risk factors for AF prevalence, while age (OR 1.45, 95%CI: 1.20–1.75, p < 0.001), LDL < 100 mg/dl (OR 0.43, 95%CI 0.23–0.82, p = 0.011), use of statins (OR 0.51, 95%CI: 0.28–0.94, p = 0.031) and HbA1c ≤ 6.5 (OR 0.46, 95%CI: 0.25–0.85, p = 0.013) were associated with silent AF prevalence. Diabetes duration, diabetic treatment pattern or metabolic control per se did not significantly impact the prevalence of AF, including silent AF detected by prospective continuous monitoring. Independent predictors of AF were age, BMI and low LDL levels, with statins and HbA1c ≤ 6.5 being additional independent predictors for silent AF. Trial registration: NCT03243474. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a well-known risk factor for atrial fibrillation (AF), but the mechanism(s) by which DM affects AF prevalence remains unclear. This study aims to evaluate the impact of diabetes mellitus severity (expressed as its known duration), antihyperglycemic treatment regimen and glycaemic control on AF prevalence. From the representative sample of 3014 participants (mean age 77.5, 49.1% female) from the cross-sectional NOMED-AF study, 881 participants (mean age 77.6 ± 0.25, 46.4% female) with concomitant DM were involved in the analysis. AF was screened using a telemonitoring vest for a mean of 21.9 ± 9.1 days. The mean DM duration was 12 ± 0.35 years, but no significant impact of DM timespan on AF prevalence was observed. No differences in the treatment pattern (oral medication vs insulin vs both oral + insulin) among the study population with and without AF were shown (p = 0.106). Metabolic control reflected by HbA1c levels showed no significant association with AF and silent AF prevalence (p = 0.635; p = 0.094). On multivariate analyses, age (Odds Ratio (OR) 1.35, 95%CI: 1.18–1.53, p < 0.001), p = 0.042), body mass index (BMI; OR 1.043, 95%CI: 1.01–1.08, p = 0.027) and LDL < 100 mg/dl (OR 0.64, 95%CI: 0.42–0.97, p = 0.037) were independent risk factors for AF prevalence, while age (OR 1.45, 95%CI: 1.20–1.75, p < 0.001), LDL < 100 mg/dl (OR 0.43, 95%CI 0.23–0.82, p = 0.011), use of statins (OR 0.51, 95%CI: 0.28–0.94, p = 0.031) and HbA1c ≤ 6.5 (OR 0.46, 95%CI: 0.25–0.85, p = 0.013) were associated with silent AF prevalence. Diabetes duration, diabetic treatment pattern or metabolic control per se did not significantly impact the prevalence of AF, including silent AF detected by prospective continuous monitoring. Independent predictors of AF were age, BMI and low LDL levels, with statins and HbA1c ≤ 6.5 being additional independent predictors for silent AF. Trial registration: NCT03243474. [ABSTRACT FROM AUTHOR]

Background and Aim: Reports on patients with nonvalvular atrial fibrillation (NVAF), particularly in the elderly, are few from India. This paper focuses on multimorbidity pattern, antithrombotic treatment and mortality of elderly NVAF patients from the state of Kerala, India. Methods: Clinical details of NVAF patients of age = 75 years from the cohort of KERALA-AF registry were analyzed for pattern of multimorbidity, antithrombotic treatment and one-year mortality. Results: The study comprised 753 patients with a median age of 80 years (IQR = 77-84), 53.5% being male. Multimorbidity was present in 94.5% of patients. Hypertension was the most common risk factor (74.4 %, n = 560) and chronic kidney disease was the major coexisting disease (78.9%, n = 594). Based on the number of comorbidities present, patients were grouped into three groups: < 3 comorbidities (18.1%), 3-5 comorbidities (63.9%), and > 5 comorbidities (17.6%). Oral anticoagulant therapy (OAC) was received by 62.5% (n = 472) of patients, mostly Vitamin K antagonist (VKA). Direct oral anticoagulants (DOAC) were used in 11.3% of patients. Antiplatelet therapy was used in 60.6% (n = 458) and the most commonly used antiplatelet was clopidogrel (44.6%). No antithrombotic treatment was used in 12.0% of patients (n = 91). One-year all-cause mortality was 19.6% (n = 148), higher in women but not statistically significant (p = 0.06). Kaplan-Meier survival curve indicated better one-year survival for patients who received OAC treatment (log rank test p < 0.0001, HR = 0.49 (95% CI = 0.35, 0.68), concordance = 0.58). Multivariate cox proportional hazards regression model showed OAC treatment (HR, 0.5; 95% CI, 0.36-0.7, P < 0.001) and age more than 80 years (HR, 1.53; 95% CI, 1.11 -2.1, P < 0.01) as predictors of one-year mortality. Mortality was not significantly different among the groups with different clustering of multimorbidity. Conclusion: Use of oral anticoagulation was associated with a reduced risk of mortality among elderly NVAF patients in the KERALA-AF Registry. However, more than one-third of elderly NVAF patients did not receive OAC, which calls for increased sensitization and training of treating doctors regarding optimal use of OAC in the elderly NVAF patients. Funding: The study received funding from the Cardiological Society of India-Kerala Chapter (CSI-K). [ABSTRACT FROM AUTHOR]

Aims: Using advanced longitudinal analyses, this real‐world investigation examined medication adherence levels and patterns for incident atrial fibrillation (AF) patients with significant cardiovascular and noncardiovascular multimorbid conditions for each of 5 medication classes (β‐blockers, calcium channel blockers/digoxin, antiarrhythmics, anticoagulants, antiplatelets). The population was derived from a large cohort covering a wide age spectrum/diversified US geographical areas/wide range of socioeconomic–disability status. Methods: The patients were drawn from 3 different health plans. Adherence was defined in terms of the proportion of day covered (PDC), and its patterns were modelled in terms of group‐based trajectory, with each pattern profiled in terms of comorbid history, demographic variables and health plan factors using multinomial regression modelling. Results: The total population consisted of 1 978 168 patients, with the AF cohort being older (average age of 64.6 years relative to 44.7 years for the non‐AF cohort) and having fewer females (47.8% relative to 55.4 for the non‐AF cohort). The AF cohort had significant cardiovascular/noncardiovascular multimorbidities and was much sicker than the non‐AF cohort. A 6‐group based trajectory solution appears to be the most logical outcome for each medication class according to assessed criteria. For each medication class, it consisted of one consistent adherent group (PDC ≥ 0.84), one fast declining group (PDC ≤ 0.11) and 4 intermediate nonadherence groups (slow decline [0.30–0.74 PDC range], occasional users [0.24–0.55 PDC range] and early gap/increased adherence [0.62–0.75]). The most consistent adherent groups were much lower than 50% of the total population and equal to 12.5–27.0% of the population, with the fast declining nonadherent pattern in the 5.6–35.0% of the population and the intermediate nonadherence equal to ~61% of the population. Conclusion: Our findings confirm that medication adherence is of major concern among multimorbid patients, with adherence levels lower much than those reported in the literature. There are 3 patterns of intermediate nonadherence (slow decline, occasional users, early gap/increased adherence), which were found to be eligible for interventions aimed at improving their adherence levels for each medication class. This may help improve cardiovascular medication adherence using large medication nonadherence improvement programmes. [ABSTRACT FROM AUTHOR]

Background: Consistent adherence levels to multiple long‐term medications for patients with cardiovascular conditions are typically advocated in the range of 50% or higher, although very likely to be much lower in some populations. We investigated this issue in a large cohort covering a broad age and geographical spectrum, with a wide range of socio‐economic disability status. Methods: The patients were drawn from three different health plans with a varied mix of socio‐economic/disability levels. Adherence patterns were examined on a monthly basis for up to 12 months past the index date for myocardial infarction (MI) using longitudinal analyses of group‐based trajectory modelling. Each of the non‐adherent patterns was profiled from comorbid history, demographic and health plan factors using main effect logistic regression modelling. Four medication classes were examined for MI: betablockers, statin, ACE inhibitors and anti‐platelets. Results: The participant population for the MI/non‐MI cohorts was 1,987,605 (MI cohort: mean age 62 years, 45.9% female; non‐MI cohort: mean age 45 years, 55.3% females). Cohorts characterized by medication non‐adherence dominated the majority of MI population with values ranging from 74% to 82%. There were four types of consistent non‐adherence patterns as a function of time for each medication class: fast decline, slow decline, occasional users and early gap followed by increased adherence. The characteristics of non‐adherence profiles eligible for improvement included patients with a prior history of hypertension, diabetes mellitus and stroke as co‐morbidities, and Medicare plan. Conclusions: We found consistent patterns of intermediate non‐adherence for each of four drug classes for MI cohorts in the order of 56% who are eligible for interventions aimed at improving cardiovascular medication adherence levels. These insights may help improve cardiovascular medication adherence using large medication non‐adherence improvement programs. [ABSTRACT FROM AUTHOR]

We explored how dynamic changes in monocyte subset counts (as opposed to static values to specific time points), and their phagocytic and NFκB activity relate to major adverse cardiovascular events (MACE) and left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI). Changes in counts, phagocytic activity and intracellular levels of inhibitory κB kinase β (IKKβ) (a marker of NFκB activity) of monocyte subsets (CD14++CD16−CCR2+ [Mon1], CD14++CD16+CCR2+ [Mon2] and CD14+CD16++CCR2− [Mon3]) were measured by flow cytometry in patients with STEMI at baseline, and again after one week, two weeks, and one month. LVEF was measured by echocardiography at baseline and six months after STEMI. Baseline data included 245 patients (mean ± SD age 60 ± 12 years; 22% female), who were followed for a median of 46 (19–61) months. Multivariate Cox regression demonstrated that more prominent dynamic reduction in Mon2 by week 1 (n = 37) was independently associated with fewer MACE (HR 0.06, 95% CI 0.01–0.55, p = 0.01). Also, less prominent reduction in Mon2 at month 1 (n = 24) was independently predictive of 6-month LVEF. None of the other dynamic changes in monocyte subsets were associated with changes in survival from MACE. Neither phagocytic activity nor IKKβ were associated with survival for each monocyte subset. We showed how distinct pattern of dynamic changes in Mon2 are related to both MACE risk and recovery of cardiac contractility. Further research is needed to understand the mechanism of the monocyte effect and possibilities of their pharmacological manipulation. [ABSTRACT FROM AUTHOR]

Background: To date, incident and recurrent MI remains a major health issue worldwide, and efforts to improve risk prediction in population health studies are needed. This may help the scalability of prevention strategies and management in terms of healthcare cost savings and improved quality of care. Methods: We studied a large‐scale population of 4.3 million US patients from different socio‐economic and geographical areas from three health plans (Commercial, Medicare, Medicaid). Individuals had medical/pharmacy benefits for at least 30 months (2 years for comorbid history and followed up for 6 months or more for clinical outcomes). Machine‐learning (ML) algorithms included supervised (logistic regression, neural network) and unsupervised (decision tree, gradient boosting) methodologies. Model discriminant validity, calibration and clinical utility were performed separately on allocated test sample (1/3 of original data). Results: In the absence of MI in comorbid history, the overall incidence rates were 0.442 cases/100 person‐years and in the presence of MI history, 0.652. ML algorithms showed that supervised formulations had incrementally higher discriminant validity than unsupervised techniques (e.g., for incident MI outcome in the absence of MI in comorbid history: logistic regression "LR" – c index 0.921, 95%CI 0.920–0.922; neural network "NN" – c index 0.914, 95%CI 0.913–0.915; gradient boosting "GB" – c index 0.902, 95%CI 0.900–0.904; decision tree "DT" – c index 0.500, 95%CI 0.495–0.505). Calibration and clinical utility showed good to excellent results. Conclusion: ML algorithms can substantially improve the prediction of incident and recurrent MI particularly in terms of the non‐linear formulation. This approach may help with improved risk prediction, allowing implementation of cardiovascular prevention strategies across diversified sub‐populations with different clusters of complexity. [ABSTRACT FROM AUTHOR]

Background: Evidence for the relationship between glycated hemoglobin (HbA1c) levels and risk of cardiovascular diseases (CVD) in patients with gout remained sparse and limited. This study aims to explore the associations between HbA1c levels and risks of incident CVD in patients with gout. Methods: We included patients with gout who had an HbA1c measurement at baseline from the UK Biobank. CVD events were identified from through medical and death records. We used multivariable Cox proportional hazards model with a restricted cubic spline to assess the potential non-linear effect of HbA1c on CVD risk. Results: We included a total of 6,685 patients (mean age 59.7; 8.1% females) with gout for analyses. During a mean follow-up of 7.3 years, there were 1,095 CVD events documented with an incidence of 2.26 events per 100 person-years (95% confidence interval [CI]: 2.13–2.40). A quasi J-shaped association between HbA1c and risk of CVD was observed, with the potentially lowest risk found at the HbA1c of approximately 5.0% (hazard ratio [HR] = 0.65, 95% CI: 0.53–0.81). When compared with the HbAlc level of 7%, a significantly decreased risk of CVD was found from 5.0 to 6.5%, while an increased risk was observed at 7.5% (HR = 1.05) and 8.0% (HR = 1.09). Subgroup analyses yielded similar results to the main findings in general. Conclusions: Based on data from a nationwide, prospective, population-based cohort, we found a quasi J-shaped relationship between HbA1c and risk of CVD in patients with gout. More high-quality evidence is needed to further clarify the relationship between HbA1c and CVD risk in patients with gout. [ABSTRACT FROM AUTHOR]

The article focuses on recommending anticoagulant therapy for a patient with secondary atrial fibrillation triggered by community-acquired pneumonia, emphasizing the high risk of future cardiovascular events without treatment. Topics discussed include the patient's risk factors for stroke, the importance of oral anticoagulation in preventing stroke recurrence, and adherence to guideline-recommended management strategies for atrial fibrillation, highlighting the need for comprehensive care.

Monocytes derive from bone marrow and circulate in the blood. They phagocytose, produce cytokines and present antigens. Individual monocyte subsets play distinct roles in the pathogenesis of cardiovascular disease, but their implications in gestational hypertensive disease are unclear. Our objective was to examine the difference in monocyte subsets between pregnant women with or without previous hypertension in pregnancy. Women were enrolled in a prospective observational study in which monoclonal antibodies against cell surface receptors were used to detect monocytes in the peripheral blood by flow cytometry. We compared 17 pregnant women with previous hypertension in pregnancy (Group 1) and 42 pregnant women without previous gestational hypertensive disease (Group 2) with 27 healthy, non-pregnant controls (Group 3). The pregnant women were studied at 13 ± 1 weeks gestation. Monocyte subsets were quantified by flow cytometry: Mon1 (CD14++CD16-CCR2+), Mon2 (CD14++CD16+CCR2+), Mon3 (CD14+CD16+CCR2-), their aggregates with platelets and expression of the surface markers. The groups were well-matched for age, body mass index and ethnicity (P > 0.05 for all). Mon1 counts were higher in women with a history of gestational hypertension or preeclampsia compared to other groups (Group 1 = 441 per µl (376–512); Group 2 = 357 (309–457); Group 3 = 323 (277–397); P < 0.001). Mon3 was higher in both groups of pregnant women compared to non-pregnant controls (Group 1 = 51 (38–62); Group 2 = 38 (29–58); Group 3 = 26 (20–40), P = 0.002). Increased monocytes in women with a previous hypertensive pregnancy generates a hypothesis that these cells may link hypertension in pregnancy, chronic inflammation and future cardiovascular risk. [ABSTRACT FROM AUTHOR]

Background: With the spread of COVID‐19 pandemic, there have been reports on its impact on incident myocardial infarction (MI) emanating from studies with small to modest sample sizes. We therefore examined the incidence of MI in a very large population health cohort with COVID‐19 using a methodology which integrates the dynamicity of prior comorbid history. We used two approaches, i.e. main effect modelling and a machine learning (ML) methodology, accounting for the complex dynamic relationships among comorbidity and other variables. Methods: We studied a very large prospective 18–90‐year US population, including 4,289,481 patients from medical databases in a 12‐month investigation of those with/without newly incident COVID‐19 cases together with a 2‐year comorbid profile in the baseline period. Incident MI outcomes were examined in relationship to diverse multimorbid conditions, COVID‐19 status and demographic variables—with ML accounting for the dynamic nature of changing multimorbidity risk factors. Results: Multimorbidity, defined as a composite of cardiometabolic/noncardiometabolic comorbid profile, significantly contributed to the onset of confirmed COVID‐19 cases. Furthermore, a main effect model (C‐index value 0.932; 95%CI 0.930–0.934) had medium to large effect sizes with incident MI outcomes in a COVID‐19 cohort for the classic multimorbid conditions in medical history profile which includes prior coronary artery disease (OR 4.61 95%CI 4.49–4.73); hypertension (OR 3.55 95%CI 3.55–3.83); congestive heart failure (2.31 95%CI 2.24–2.37); valvular disease (1.43 95%CI 1.39–1.47); stroke (1.30 95%CI 1.26–1.34); and diabetes (1.26 95%CI 1.23–1.34). COVID‐19 status (1.86 95%CI 1.79–1.93) contributed an independent large size risk effect for incident MI. The ML algorithm demonstrated better discriminatory validity than the main effect model (training: C‐index 0.949, 95%CI 0.948–0.95; validation: C‐index 0.949, 95%CI 0.948–0.95). Calibration of the ML‐based formulation was satisfactory and better than the main effect model. Decision curve analysis demonstrated that the ML clinical utility was better than the 'treat all' strategy and the main effect model. The ML logistic regression model was better than the neural network algorithm. Conclusion: The very large investigation conducted herein confirmed the importance of cardiometabolic and noncardiometabolic multimorbidity in increasing vulnerabilities to a higher risk of COVID‐19 infections. Furthermore, the presence of COVID‐19 infections increased incident MI complications both in terms of independent effects and interactions with the multimorbid profile and age. [ABSTRACT FROM AUTHOR]

The article offers information about the anticoagulation in atrial fibrillation and rheumatic heart disease. It mentions that stroke prevention in atrial fibrillation has been changed by the availability of the direct oral anticoagulants. It discusses the clinical trials of stroke prevention in patients with atrial fibrillation.

Background: Cardiac arrhythmias are associated with poorer outcomes in patients with heart failure (HF), diabetes mellitus (DM), and chronic kidney disease (CKD). Previous studies have shown inconsistent conclusions regarding the association between sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the risk of developing arrhythmias. This study aims to investigate the association of SGLT2i treatment with arrhythmia outcomes in clinical trials of patients with HF, DM, or CKD. Methods: MEDLINE, EMBASE, and ClinicalTrials.gov were searched from inception up to 27 August 2020. Randomized controlled trials that randomized patients with DM, CKD, or HF to SGLT2i or placebo were included. The outcomes of interest include atrial fibrillation (AF), embolic stroke, atrial flutter (AFL), AF/AFL, ventricular tachycardia (VT), and cardiac arrest. Relative risks (RRs) and 95% confidence intervals (CI) were pooled using a random-effects model. Results: Out of 4,532 citations, 22 trials with altogether 52,115 patients were included (mean age 63.2 years; 33,747 [64.8%] of participants were men). SGLT2i were associated with a lower risk of AF (RR 0.82, 95% CI 0.70–0.96), embolic stroke (RR 0.32, 95% CI 0.12–0.85), AF/AFL (RR 0.82, 95% CI 0.71–0.95), and VT (RR 0.73, 95% CI 0.53–0.99), while the risk reductions in AFL (RR 0.83, 95% CI 0.58–1.17) and cardiac arrest (RR 0.83, 95% CI 0.61–1.14) did not reach statistical significance. The associations appeared to be consistent across different baseline conditions (DM vs CKD vs HF; atherosclerotic cardiovascular disease [ASCVD] vs no ASCVD) and the SGLT2i used. Conclusions: SGLT2i reduced the risk of cardiac arrhythmias. Our study provides further evidence for recommending the use of SGLT2i in patients with DM, CKD, and HF. Further research is needed to fully elucidate the mechanism by which SGLT2i protect against arrhythmias. [ABSTRACT FROM AUTHOR]

The authors also estimated brain-derived age (BDA) by applying a ML algorithm which they had previously developed for 1693 participants in the Tromsø Study, who also had magnetic resonance imaging (MRI) brain scans [[6]]. Alzheimer's disease and related dementias (ADRDs) have debilitating effects on affected individuals including reduced quality of life, cognitive and verbal decline, reduced mobility and eventual death. ECG-derived HDA could also help to improve understanding of the pathophysiology of ADRD, which is crucial to help support the development of more targeted therapies to improve outcomes for people with ADRD. [Extracted from the article]

Background: The global burden of atrial fibrillation (AF) and diabetes mellitus (DM) is constantly rising, leading to an increasing healthcare burden of stroke. AF often remains undiagnosed due to the occurrence in an asymptomatic, silent form, i.e., silent AF (SAF). The study aims to evaluate the relationships between DM and AF prevalence using a mobile long-term continuous ECG telemonitoring vest in a representative Polish and European population ≥ 65 years for detection of AF, symptomatic or silent. Methods: A representative sample of 3014 participants from the cross-sectional NOMED-AF study was enrolled in the analyses (mean age 77.5, 49.1% female): 881 (29.2%) were diagnosed with DM. AF was screened using a telemonitoring vest for a mean of 21.9 ± 9.1days. Results: Overall, AF was reported in 680 (22.6%) of the whole study population. AF prevalence was higher among subjects with concomitant DM (DM+) versus those without DM (DM−) [25%, 95% CI 22.5-27.8% vs 17%; 95% CI 15.4–18.5% respectively, p < 0.001]. DM patients were commonly associated with SAF [9%; 95% CI 7.9–11.4 vs 7%; 95% CI 5.6–7.5 respectively, p < 0.001], and persistent/permanent AF [12.2%; 95% CI 10.3–14.3 vs 6.9%; 95% CI 5.9–8.1 respectively, p < 0.001] compared to subjects without DM. The prolonged screening was associated with a higher percentage of newly established AF diagnosis in DM+ vs DM− patients (5% vs 4.5% respectively, p < 0.001). In addition to shared risk factors, DM+ subjects were associated with different AF and SAF independent risk factors compared to DM− individuals, including thyroid disease, peripheral/systemic thromboembolism, hypertension, physical activity and prior percutaneous coronary intervention/coronary artery bypass graft surgery. Conclusions: AF affects 1 out of 4 subjects with concomitant DM. The higher prevalence of AF and SAF among DM subjects than those without DM highlights the necessity of active AF screening specific AF risk factors assessment amongst the diabetic population. Trial registration: NCT03243474 [ABSTRACT FROM AUTHOR]

Background: Cardiac arrhythmias are associated with poorer outcomes in patients with heart failure (HF), diabetes mellitus (DM), and chronic kidney disease (CKD). Previous studies have shown inconsistent conclusions regarding the association between sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the risk of developing arrhythmias. This study aims to investigate the association of SGLT2i treatment with arrhythmia outcomes in clinical trials of patients with HF, DM, or CKD. Methods: MEDLINE, EMBASE, and ClinicalTrials.gov were searched from inception up to 27 August 2020. Randomized controlled trials that randomized patients with DM, CKD, or HF to SGLT2i or placebo were included. The outcomes of interest include atrial fibrillation (AF), embolic stroke, atrial flutter (AFL), AF/AFL, ventricular tachycardia (VT), and cardiac arrest. Relative risks (RRs) and 95% confidence intervals (CI) were pooled using a random-effects model. Results: Out of 4,532 citations, 22 trials with altogether 52,115 patients were included (mean age 63.2 years; 33,747 [64.8%] of participants were men). SGLT2i were associated with a lower risk of AF (RR 0.82, 95% CI 0.70–0.96), embolic stroke (RR 0.32, 95% CI 0.12–0.85), AF/AFL (RR 0.82, 95% CI 0.71–0.95), and VT (RR 0.73, 95% CI 0.53–0.99), while the risk reductions in AFL (RR 0.83, 95% CI 0.58–1.17) and cardiac arrest (RR 0.83, 95% CI 0.61–1.14) did not reach statistical significance. The associations appeared to be consistent across different baseline conditions (DM vs CKD vs HF; atherosclerotic cardiovascular disease [ASCVD] vs no ASCVD) and the SGLT2i used. Conclusions: SGLT2i reduced the risk of cardiac arrhythmias. Our study provides further evidence for recommending the use of SGLT2i in patients with DM, CKD, and HF. Further research is needed to fully elucidate the mechanism by which SGLT2i protect against arrhythmias. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to evaluate whether device measured amplitudes of atrial electrogram (AEGM) would change when measured in sinus rhythm (SR) transitioning to paroxysmal atrial fibrillation (AF) from previous steady SR, and significance of such change. Methods: From the IMPACT trial's database we selected two groups; (A) those who developed AF (n = 164), and (B) propensity‐matched control (n = 459) who stayed in SR during continuous Home Monitoring (HM) to compare AEGMs amplitudes at baseline SR and transition phase. Results: During 420.0 ± 349.2 days (mean ± SD) from first postenrollment HM transmission to AF event transmission in Group A, and corresponding 515.3 ± 407.0 days in Group B, baseline and transition AEGM amplitude were 2.88 ± 1.146 and 2.74 ± 1.186 mV, respectively, for Group A (p =.1), and 2.88 ± 1.155 and 2.79 ± 1.145, respectively, for Group B (p <.005). Comparison of differences of AEGM amplitude, 0.14 ± 1.072 mV in Group A and 0.09 ± 0.893 mV in Group B were insignificant (p =.3). Age, sex, and hypertension identified as confounders had no association to AEGM changes (p = NS). Conclusions: Independent of age, sex, and hypertension, AEGMs amplitudes decline over a long period of time in patients with defibrillators and substrate for AF. The significance of such change remains unclear as it occurs whether patients develop AF or not, but raises a possibility of progressive atrial myopathy that patients with substrate for AF may be predisposed to. [ABSTRACT FROM AUTHOR]

Introduction Methods Results Conclusion Access site complications remain common following atrial fibrillation (AF) catheter ablation. Femoral vascular closure devices (VCDs) reduce time to hemostasis compared with manual compression, although large‐scale data comparing clinical outcomes between the two approaches are lacking.Two cohorts of patients undergoing AF ablation were identified from 36 healthcare organizations using a global federated research network (TriNetX): those receiving a VCD for femoral hemostasis, and those not receiving a VCD. A 1:1 propensity score matching (PSM) model based on baseline characteristics was used to create two comparable cohorts. The primary outcome was a composite of all‐cause mortality, vascular complications, bleeding events, and need for blood transfusion. Outcomes were assessed during early (within 7 days of ablation) and extended follow‐up (within 8–30 days of ablation).After PSM, 28 872 patients were included (14 436 in each cohort). The primary composite outcome occurred less frequently in the VCD cohort during early (1.97% vs. 2.60%, odds ratio (OR) 0.76, 95% confidence interval (CI) 0.65–0.88; p < .001) and extended follow‐up (1.15% vs. 1.43%, OR 0.80, 95% CI 0.65–0.98; p = .032). This was driven by a lower rate of vascular complications during early follow‐up in the VCD cohort (0.83% vs. 1.26%, OR 0.66, 95% CI 0.52–0.83; p < .001), and fewer bleeding events during early (0.90% vs. 1.23%, OR 0.73, 95% CI 0.58–0.92; p = .007) and extended follow‐up (0.36% vs. 0.59%, OR 0.61, 95% CI 0.43–0.86; p = .005).Following AF ablation, femoral venous hemostasis with a VCD was associated with reduced complications compared with hemostasis without a VCD. [ABSTRACT FROM AUTHOR]

The author reflects on the possible link between vitamin K antagonists (VKA) like warfarin and reduced bone mineral density (BMD) and its effects like higher risks of fracture and osteoporosis. Other topics include the effects of VKA to the osteocalcin protein, and a systematic review and meta-analysis on the fracture risks in patients with atrial fibrillation who were treated with oral anticoagulation (OAC) drug.

Atrial fibrillation (AF) is the most common cardiac arrhythmia, characterized by irregular atrial activity. AF is related to increased risk of thromboembolic events, heart failure, and premature mortality. Recent advances in our understanding of its pathophysiology include a potentially central role for inflammation and presence of cardiovascular risk factors. The role of physical activity and exercise in the development and progression of AF, however, are not yet fully understood. Physical activity is protective for modifiable cardiovascular risk factors, including those associated with AF. Indeed, emerging research has demonstrated beneficial effects of exercise on AF-specific outcomes, including AF recurrence postablation. Counterintuitively, the prevalence of AF in veteran endurance athletes seems higher compared with the general population. In this review, we discuss the novel evidence and underlying mechanisms underpinning the role of exercise as medicine in the development and management of AF but also the counterintuitive detrimental role of excessive endurance exercise. Finally, we advocate regular (but not long-term high-intensity endurance) exercise training as a safe and effective strategy to reduce the risk of incident AF and to minimize the associated risk of secondary cardiovascular events. [ABSTRACT FROM AUTHOR]

The authors discuss a study published within the issue which investigated whether atrial fibrillation (AF) is associated with increased risk of cognitive decline in community-dwelling patients. Topics include pathophysiological mechanism of cognitive impairment, importance of multimodal approach in AF patients, and indication of a potential mechanistic correlation of AF and cognitive impairment.

Summary: Quality of warfarin therapy in patients with a mechanical prosthetic heart valve (MPHV) has been barely investigated. We analysed determinants of low time in the therapeutic range (TiTR <60%) in 2111 patients with MPHVs from the nationwide PLECTRUM study by the Italian Federation of Anticoagulation Clinics. Overall, 48·5% of patients had a TiTR of < 60%. At logistic regression analysis, arterial hypertension (odds ratio [OR] 1·502, P < 0·001), diabetes (OR 1·732, P < 0·001), heart failure (OR 1·484, P = 0·004), mitral site (vs. aortic) (OR 1·399, P = 0·006), international normalised ratio (INR) ranges of 2·5–3·5 (OR 2·575, P < 0·001) and 3·0–4·0 (OR 8·215, P < 0·001) associated with TiTR < 60%. TiTR is substantially suboptimal in MPHV patients, particularly in higher INR ranges. [ABSTRACT FROM AUTHOR]

Endogenous fibrinolysis is a powerful natural defense mechanism against lasting arterial thrombotic occlusion. Recent prospective studies have shown that impaired endogenous fibrinolysis (or hypofibrinolysis) can be detected in a significant number of patients with acute coronary syndrome (ACS) using global assays and is a strong marker of future cardiovascular risk. This novel risk biomarker is independent of traditional cardiovascular risk factors and unaffected by antiplatelet therapy. Most prospective prognostic data have been obtained using a global assay using native whole blood at high shear or plasma turbidimetric assays, which are described herein. Tests of endogenous fibrinolysis could be used to identify patients with ACS who, despite antiplatelet therapy, remain at high cardiovascular risk. This review discusses the impact of currently available medications and those in development that favorably modulate fibrinolytic status and may offer a potential new avenue to improve outcomes in ACS. [ABSTRACT FROM AUTHOR]

Ying Gue and Gregory Lip discuss the accompanying study by Ana-Catarina Pinho-Gomes and co-workers on blood pressure lowering treatment in patients with atrial fibrillation. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is the commonest sustained cardiac arrhythmia and is associated with significant morbidity and mortality. There is plenty of evidence available to support the presence of a prothrombotic or hypercoagulable state in AF, but the contributory factors are multifactorial and cannot simply be explained by blood stasis. Abnormal changes in atrial wall (anatomical and structural, as 'vessel wall abnormalities'), the presence of spontaneous echo contrast to signify abnormal changes in flow and stasis ('flow abnormalities'), and abnormal changes in coagulation, platelet, and other pathophysiologic pathways ('abnormalities of blood constituents') are well documented in AF. The presence of these components therefore fulfils Virchow's triad for thrombogenesis. In this review, we present an overview of the established and professed pathophysiological mechanisms for thrombogenesis in AF and its management implications. [ABSTRACT FROM AUTHOR]

This article discusses the disparities in the use of oral anticoagulants (OAC) for stroke prevention in patients with atrial fibrillation (AF), particularly focusing on sex disparities. The article highlights that although female patients with AF have higher thromboembolic risks than men, they are often under-treated with OAC compared to men. However, the introduction of non-vitamin K antagonist oral anticoagulants (NOACs) has helped mitigate the disparities in OAC use between men and women. The study suggests that the sex disparity in OAC prescribing for stroke prevention in AF is improving over time, especially in the NOAC era, although under-prescription to female patients still persists. The article acknowledges the limitations of the study and emphasizes the need for further research to assess long-term outcomes and address disparities in other therapeutic strategies. [Extracted from the article]

Abstract: Background: Monocyte‐platelet aggregates (MPAs) form when Mon1, Mon2 or Mon3 monocyte subsets adhere to platelets. They are pathophysiologically linked to coronary artery disease (CAD). However, their individual roles in the occurrence of diffuse CAD remain unknown. Materials and methods: Peripheral blood from 50 patients with diffuse CAD, 40 patients with focal CAD and 50 age‐matched patients with normal coronary arteries was analysed by flow cytometry to quantify MPAs associated with individual monocyte subsets. Cutaneous forearm microcirculation was assessed using laser Doppler flowmetry at rest and after iontophoresis of acetylcholine (endothelium‐dependent vasodilation) and sodium nitroprusside (endothelium‐independent vasodilation) at 100 μA for 60 seconds. Patients with CAD had repeat assessment at 6 and 12 months. Results: Baseline counts of MPAs with Mon2 subset (CD14++CD16+CC2+ monocytes) were significantly higher in patients with diffuse CAD compared to focal CAD (P = .001) and patients without CAD (P = .006). On multivariate regression, MPAs with Mon2 independently predicted diffuse CAD (odds ratio 1.10, 95% confidence interval 1.02‐1.19, P = .01) and correlated negatively with endothelium‐dependent microvascular vasodilation (r = −.37, P = .008), an association which persisted after adjustment for covariates. Longitudinal observation confirmed the persistence of an inverse relationship between MPAs with Mon2 and endothelium‐dependent microvascular function. Conclusion: Monocyte‐platelet aggregates with Mon2 are increased in patients with diffuse CAD and therefore could represent an important contributor to accelerated coronary atherosclerotic progression by a mechanism involving microvascular endothelial dysfunction. [ABSTRACT FROM AUTHOR]

Discontinuation of oral anticoagulants may expose non-valvular atrial fibrillation (NVAF) patients to an increased risk of stroke. This study describes the real-world discontinuation rates and compared the risk of drug discontinuation among NVAF patients initiating apixaban, warfarin, dabigatran, or rivaroxaban. This retrospective cohort study evaluated newly-anticoagulated NVAF patients in the MarketScan® data population from 01/01/2012 through 12/31/2014. Discontinuation was defined as a lack of subsequent prescription of the index drug within 30 days after the last supply day of the last prescription. A Cox model was used to estimate the hazard ratio (HR) of discontinuation, adjusted for age, sex, and comorbidities. Among 45,361 eligible NVAF patients, 15,461 (34.1%) initiated warfarin; 7,438 (16.4%) apixaban; 4,661 (10.3%) dabigatran; and 17,801 (39.2%) initiated rivaroxaban treatment. Compared to warfarin, patients who initiated dabigatran (adjusted HR [aHR]: 0.84, 95% confidence interval [CI]: 0.80–0.87, P<0.001), rivaroxaban (aHR: 0.70, 95% CI: 0.68–0.73, P<0.001), or apixaban (aHR: 0.57, 95% CI: 0.55–0.60, P<0.001) were 16%, 30%, and 43% less likely to discontinue treatment, respectively. When compared to apixaban, patients who initiated dabigatran (aHR: 1.46, 95% CI: 1.38–1.54, P<0.001) or rivaroxaban (aHR: 1.23, 95% CI: 1.17–1.28, P<0.001) were more likely to discontinue treatment. Among newly-anticoagulated NVAF patients in the real-world setting, initiation on rivaroxaban, dabigatran, or apixaban was associated with a significantly lower risk of discontinuation compared to warfarin. When compared to apixaban, patients who initiated treatment with warfarin, dabigatran, or rivaroxaban were more likely to discontinue treatment. [ABSTRACT FROM AUTHOR]

Background: When assessing ischemic stroke risk in patients with atrial fibrillation (AF), the CHA2DS2-VASc score is calculated based on the baseline risk factors, and the outcomes are determined after a follow-up period. However, the stroke risk in patients with AF does not remain static, and with time, patients get older and accumulate more comorbidities.Objectives: This study hypothesized that the "Delta CHA2DS2-VASc score," which reflects the change in score between baseline and follow-up, would be more predictive of ischemic stroke compared with the baseline CHA2DS2-VASc score.Methods: A total of 31,039 patients with AF who did not receive antiplatelet agents or oral anticoagulants, and who did not have comorbidities of the CHA2DS2-VASc score except for age and sex, were studied. The Delta CHA2DS2-VASc scores were defined as the differences between the baseline and follow-up CHA2DS2-VASc scores. During 171,956 person-years, 4,103 patients experienced ischemic stroke. The accuracies of baseline, follow-up, and Delta CHA2DS2-VASc scores in predicting ischemic stroke were analyzed and compared.Results: The mean baseline CHA2DS2-VASc score was 1.29, which increased to 2.31 during the follow-up, with a mean Delta CHA2DS2-VASc score of 1.02. The CHA2DS2-VASc score remained unchanged in only 40.8% of patients. Among 4,103 patients who experienced ischemic stroke, 89.4% had a Delta CHA2DS2-VASc score ≥1 compared with only 54.6% in patients without ischemic stroke, and 2,643 (64.4%) patients had ≥1 new-onset comorbidity, the most common being hypertension. The Delta CHA2DS2-VASc score was a significant predictor of ischemic stroke that performed better than baseline or follow-up CHA2DS2-VASc scores, as assessed by the C-index and the net reclassification index.Conclusions: In this AF cohort, the authors demonstrated that the CHA2DS2-VASc score was not static, and that most patients with AF developed ≥1 new stroke risk factor before presentation with ischemic stroke. The Delta CHA2DS2-VASc score, reflecting the change in score between baseline and follow-up, was strongly predictive of ischemic stroke, reflecting how stroke risk in AF is a dynamic process due to increasing age and incident comorbidities. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is associated with an increased risk of stroke compared with the general population. AF-related stroke confers a higher mortality andmorbidity risk, and thus, early detection and assessment for the initiation of effective stroke prevention with oral anticoagulation are crucial. Simple and practical risk assessment tools are essential to facilitate stroke and bleeding risk assessment in busy clinics and wards to aid decision making. At present, the CHA2DS2VASc score is recommended by guidelines as the most simple and practical method of assessing stroke risk in AF patients. Alongside this, the use of the HAS-BLED score aims to identify patients at high risk of bleeding for more regular review and follow-up, and draws attention to potentially reversible bleeding risk factors. The aim of this review article is to summarize the current risk scores available for both stroke and bleeding in AF patients, and the recommendations for their use. [ABSTRACT FROM AUTHOR]

Aims: Comparative data between the HAS‐BLED, GARFIELD‐AF and ORBIT score are limited in anticoagulated Asian patients with atrial fibrillation (AF). We compared the performance of the 3 scores in a nationwide registry. Methods: AF patients treated with oral anticoagulants in the COOL‐AF registry were studied. We fitted the variables of the HAS‐BLED, GARFIELD‐AF and ORBIT score to major bleeding in Cox model. We explored a modified HAS‐BLED by addition of sex and body weight. Discrimination, calibration, net reclassification index (NRI) and decision curve analysis were used to compare the performance of the 3 models. Results: Of 3402 patients in the registry, 2568 patients who received oral anticoagulant at baseline were studied. Majority of patients (91.1%) received warfarin. The rate of major bleeding was 2.11 per 100 person‐years. The C‐statistics of the GARFIELD‐AF, HAS‐BLED, modified HAS‐BLED and ORBIT score were 0.65 (95% confidence interval [CI] 0.63–0.67), 0.66 (95%CI 0.64–0.68), 0.69 (95%CI 0.67–0.71) and 0.64 (95%CI 0.62–0.66) respectively. There was good agreement between predicted and observed bleeding in the deciles of HAS‐BLED and GARFIELD‐AF scores, while the modified HAS‐BLED score and ORBIT score overestimated the risk in the last decile. The modified HAS‐BLED score had superior NRI than the HAS‐BLED score (26.9%, 95%CI 9.7%–42.2%) and the ORBIT score (31.9%, 95%CI 9.0–53.6%). The NRI between the modified HAS‐BLED and GARFIELD‐AF score was similar. The net benefit curve of the 4 models were overlapping among different thresholds. Conclusions: The clinical utility for bleeding prediction of GARFIELD‐AF, HAS‐BLED, modified HAS‐BLED and ORBIT scores were similar in anticoagulated Asian patients with AF participating in the COOL‐AF registry. We found no advantage of the ORBIT over HAS‐BLED score for bleeding risk prediction, even in direct oral anticoagulant users. [ABSTRACT FROM AUTHOR]

Purpose Qualitative research on atrial fibrillation (AF) patient's experiences and perceptions of taking the non-vitamin K antagonist oral anticoagulants (NOACs) for stroke prevention is limited. This study explores patients' experiences of dabigatran and their recommendations for development of educational materials. Patients and methods Semi-structured individual interviews with 8 warfarin-naive and 8 warfarin-experienced AF patients, using qualitative deductive thematic analysis. Results The four main overarching themes included: understanding the diagnosis; reaching a treatment decision; challenges of living with OAC; and patient perceptions of treatment. Patients discussed their shock of diagnosis, and seeking information and support at that time. Narratives suggest patients preferred to be led by the doctor when making treatment decisions, and would often compare dabigatran to warfarin. Patients reported side-effects and challenges with both treatment options, and discussed their beliefs surrounding medications, including misconceptions. In addition to the original framework, two further themes were added: challenges of living with AF, and patient recommendations. Generally patients found AF symptoms distressing, which impacted their quality of life. Patient recommendations included the content and delivery of educational materials and development of tools to help with their understanding of AF and anticoagulation, as well as treatment adherence and anxiety surrounding symptoms and side effects. Conclusion Patient recommendations emphasised the need for interventions to relieve anxiety surrounding the diagnosis and possible treatment side effects. Tailored ‘disease-specific’ support is essential to ensure efficacious treatment. This qualitative study highlights the need for patient involvement in the development of educational materials and resources for patients commencing treatment with NOACs. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Wide variation in reported rates of stroke across cohorts of patients with atrial fibrillation" by G. R. Quinn and colleagues that was published in the previous issue.

The article discusses the risk factor of stroke in patient with atrial fibrillation (AF). It examines the efficacy of oral anticoagulation (AOC) treatment in reducing stroke and mortality. It mentions that the risk of stroke in AF is not homogenous and varies with age and concomitant comorbidities. It notes the comparison of stroke risk stratification schemes.

The article discusses how to manage occult atrial fibrillation (AF)diagnosed on long-term monitoring. Topics include understanding the relationship between occult AF and thromboembolism, the use of observational studies and clinical trials to guide the management of occult AF, and stroke prevention in the presence of risk factors which is oral anticoagulants (OAC) with a vitamin K antagonist.

AIMS AZD0837 is a novel oral anticoagulant investigated in clinical studies for stroke prevention in patients with atrial fibrillation (AF). It is bioconverted to its active form, AR-H067637, a potent, specific and reversible thrombin inhibitor. The effects on coagulation biomarkers were correlated with the pharmacokinetic (PK) exposure of AR-H067637 to guide selection of the effective dose regimen for a confirmatory efficacy study in AF patients. METHODS Blood samples were obtained from 601 AF patients randomized to one of four doses of AZD0837 (blinded treatment) or dose-adjusted vitamin K antagonists (VKA, open treatment) for 3-9 months. A pharmacodynamic model was developed to describe the time course of the AR-H067637 exposure dependent effects and the effect of VKA on fibrin D-dimer. The thrombin generation measured ex vivo in venous plasma was also investigated. RESULTS The PK exposure of AR-H067637 was stablewith an interindividual variability of 33% and no orminor influence of patient demographics or comedications. For AZD0837, D-dimer levels decreased with more rapid onset than for VKA. The decrease in D-dimer levels correlated with steady-state plasma concentrations (Css) of ARH067637, with a maximum decrease of baseline D-dimer levels estimated to approximately 60% for both AZD0837 and VKA therapy. The effect on thrombin generation correlated closely with the plasma concentration of AR-H067637. CONCLUSIONS The effects on thrombin generation and fibrin D-dimer levels correlated with the plasma concentration of its active form and provided comparable effects to well-controlled VKA therapy at an exposure at least corresponding to the 300 mg once daily dose of AZD0837. [ABSTRACT FROM AUTHOR]

STUDY QUESTION What are the risks of all cause mortality, thromboembolism, major bleeding, and recurrent gastrointestinal bleeding associated with restarting antithrombotic treatment after gastrointestinal bleeding in patients with atrial fibrillation? METHODS This Danish cohort study (1996-2012) included all patients with atrial fibrillation discharged from hospital after gastrointestinal bleeding while receiving antithrombotic treatment. Restarted treatment regimens were single or combined antithrombotic drugs with oral anticoagulation and antiplatelets. Follow-up started 90 days after discharge to avoid confounding from use of previously prescribed drugs on discharge. Risks of all cause mortality, thromboembolism, major bleeding, and recurrent gastrointestinal bleeding were estimated with competing risks models and time dependent multiple Cox regression models. STUDY ANSWER AND LIMITATIONS 4602 patients (mean age 78 years) were included. Within two years, 39.9% (95% confidence interval 38.4% to 41.3%, n=1745) of the patients had died, 12.0% (11.0% to 13.0%, n=526) had experienced thromboembolism, 17.7% (16.5% to 18.8%, n=788) major bleeding, and 12.1% (11.1% to 13.1%, n=546) recurrent gastrointestinal bleeding. 27.1% (n=924) of patients did not resume antithrombotic treatment. Compared with non-resumption of treatment, a reduced risk of all cause mortality was found in association with restart of oral anticoagulation (hazard ratio 0.39, 95% confidence interval 0.34 to 0.46), an antiplatelet agent (0.76, 0.68 to 0.86), and oral anticoagulation plus an antiplatelet agent (0.41, 0.32 to 0.52), and a reduced risk of thromboembolism was found in association with restart of oral anticoagulation (0.41, 0.31 to 0.54), an antiplatelet agent (0.76, 0.61 to 0.95), and oral anticoagulation plus an antiplatelet agent (0.54, 0.36 to 0.82). Restarting oral anticoagulation alone was the only regimen with an increased risk of major bleeding (1.37, 1.06 to 1.77) compared with nonresumption of treatment; however, the difference in risk of recurrent gastrointestinal bleeding was not significant between patients who restarted an antithrombotic treatment regimen and those who did not resume treatment. WHAT THIS STUDY ADDS Among patients with atrial fibrillation who experience gastrointestinal bleeding while receiving antithrombotic treatment; subsequent restart of oral anticoagulation alone was associated with better outcomes for all cause mortality and thromboembolism compared with patients who did not resume treatment. This was despite an increased longitudinal associated risk of bleeding. FUNDING, COMPETING INTERESTS, DATA SHARING This study was supported by a grant from Boehringer-Ingelheim. Competing interests are available in the full paper on bmj.com. The authors have no additional data to share. [ABSTRACT FROM AUTHOR]

Source Citation: Davidson KW, Barry MJ, Mangione CM, et al. Screening for atrial fibrillation: US Preventive Services Task Force recommendation statement. JAMA. 2022;327:360-7. 35076659. [ABSTRACT FROM AUTHOR]

IMPORTANCE Atrial fibrillation (AF) is associated with an increase in mortality and morbidity, with a substantial increase in stroke and systemic thromboembolism. Strokes related to AF are associated with higher mortality, greater disability, longer hospital stays, and lower chance of being discharged home than strokes unrelated to AF. OBJECTIVE To provide an overview of current concepts and recent developments in stroke prevention in AF, with suggestions for practical management. EVIDENCE REVIEW A comprehensive structured literature search was performed using MEDLINE for studies published through March 11,2015, that reported on AF and stroke, bleeding risk factors, and stroke prevention. FINDINGS The risk of stroke in AF is reduced by anticoagulant therapy. Thromboprophylaxis can be obtained with vitamin K antagonists (VKA, eg, warfarin) or a non-VKA oral anticoagulant (NOAC). Major guidelines emphasize the important role of oral anticoagulation (OAC) for effective stroke prevention in AF. Initially, clinicians should identify low-risk AF patients who do not require antithrombotic therapy (ie, CHA2DS2-VASc score, 0 for men; 1 for women). Subsequently, patients with at least 1 stroke risk factor (except when the only risk is being a woman) should be offered OAC. A patient's individual risk of bleeding from antithrombotic therapy should be assessed, and modifiable risk factors for bleeding should be addressed (blood pressure control, discontinuing unnecessary medications such as aspirin or nonsteroidal anti-inflammatory drugs). The international normalized ratio should be tightly controlled for patients receiving VKAs. CONCLUSIONS AND RELEVANCE Stroke prevention is central to the management of AF, irrespective of a rate or rhythm control strategy. Following the initial focus on identifying low-risk patients, all others with 1 or more stroke risk factors should be offered OAC. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) confers increased risk of stroke and other thromboembolic events, and oral anticoagulation therefore is the essential part of AF management to reduce the risk of these complications. Until recently, the vitamin K antagonists (VKAs, e.g., warfarin) were the only oral anticoagulants available, acting by decreased synthesis of vitamin K-dependent coagulation factors (II, VI, IX, and X). The VKAs had many limitations: delayed onset and prolonged offset of action, variability of anticoagulant effect among patients, multiple food and drug interactions affecting pharmacological properties of warfarin, narrow therapeutic window, and obligatory regular laboratory control, which all made warfarin "inconvenient" both for patients and clinicians. The limitations of VKAs led to development of a new class of drugs collectively defined as non-VKA oral anticoagulants (NOACs), which included direct thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban, and edoxaban). The NOACs avoid many of the VKA drawbacks. In this review, we will focus on the current evidence justifying the use of NOACs in non-valvular AF. [ABSTRACT FROM AUTHOR]

Background: Data on the use of oral anticoagulation (OAC) and antiplatelet therapy and the risk of bleeding and stroke amongst Asian patients with atrial fibrillation (AF) are limited. We investigated the risks of bleeding and stroke with use of oral anticoagulation (OAC) and antiplatelet therapy as mono- or combination therapy, in patients with AF from a Chinese nationwide cohort study. Methods: We studied a cohort of 10384 patients (57.2% men, age 67.8 ± 13.2 yrs) between 1999 and 2010 from the National Health Insurance Research Database in Taiwan. Records of prescriptions were obtained during follow-up. The main outcome was a recurrent stroke during the follow-up period. Time-dependent Cox proportional hazards models were used for this analysis. Results: We documented 1009 events for bleeding, as well as 224 hemorrhagic stroke and 1642 ischemic stroke events during a median 3.2 (interquartile range, 1.05-6.54) years’ follow-up. Compared with warfarin users, patients with antiplatelet therapy had a lower risk of bleeding (adjusted relative risk [RR], 0.59, 95% confidence interval [CI], 0.49-0.71, p<0.001) whilst combination therapy had a non-statistically significant higher bleeding risk (RR, 1.33, 95%, 0.91-1.94, p = 0.20). Patients on antiplatelet monotherapy had a similar risk for ischemic stroke compared with OAC (RR 1.05, 95% CI, 0.89-1.25, p = 0.50), whilst those on combination therapy had a significantly higher risk (RR 1.90, 95% CI, 1.34-2.70, p<0.001). Conclusion: In a national representative cohort, antiplatelet therapy had no significant difference in ischemic stroke risk to warfarin. For bleeding, aspirin had a lower risk compared to warfarin. This may reflect poor anticoagulation control, highlighting important missed opportunities for improved stroke prevention, especially in countries where anticoagulation management is suboptimal. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus is recognized as a stroke risk factor in atrial fibrillation (AF). Patients with diabetes with retinopathy have an increased risk for systemic cardiovascular complications, and severe diabetic retinopathy predisposes to ocular bleeding. We hypothesized that patients with diabetes, retinopathy, and AF have increased stroke/thromboembolism (TE) and severe bleeding risks when compared with patients with diabetes and AF who do not have retinopathy or to patients with AF and without diabetes.Methods: We tested our hypothesis in a large "real-world" cohort of individuals with AF from the Loire Valley Atrial Fibrillation project.Results: Of 8,962 patients with AF in our dataset, 1,409 (16%) had documented diabetes mellitus. Of these, 163 (1.8% of the whole cohort) were patients with diabetic retinopathy. After a follow-up of 31 ± 36 months, when compared with patients without diabetes, the risk of stroke/TE in patients with diabetes with no retinopathy increased 1.3-fold (relative risk [RR], 1.30; 95% CI, 1.07-1.59; P = .01); in patients with diabetes with retinopathy, the risk of stroke/TE was increased 1.58-fold (RR, 1.58; 95% CI, 1.07-2.32; P = .02). There was no significant difference when patients with diabetes with no retinopathy were compared with patients with diabetes with retinopathy (RR, 1.21; 95% CI, 0.80-1.84; P = .37). A similar pattern was seen for mortality and severe bleeding. On multivariate analysis, the presence of diabetic retinopathy did not emerge as an independent predictor for stroke/TE or severe bleeding.Conclusions: Crude rates of stroke/TE increased in a stepwise fashion when patients without diabetes and with AF were compared with patients with diabetes with no retinopathy and patients with diabetes with retinopathy. However, we have shown for the first time, to our knowledge, that the presence of diabetic retinopathy did not emerge as an independent predictor for stroke/TE or severe bleeding on multivariate analysis. [ABSTRACT FROM AUTHOR]