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Background: Although dual antiplatelet therapy (DAPT) improves the outcomes of patients undergoing percutaneous coronary intervention (PCI), sex-specific differences in efficacy and safety of DAPT remain unresolved. We compared sex differences for DAPT outcomes and DAPT durations (1–3 months [short-term], 6 months [mid-term], and >12 months [extended] vs. 12 months). Methods: We searched databases through 31 December 2023 for trials reporting DAPT after PCI. The endpoints were major adverse cardiovascular and cerebrovascular events (MACCE), net adverse clinical and cerebrovascular events (NACCE), and any bleeding. Extracted data were pooled in a frequentist network and pairwise, random-effects meta-analysis. Results: Twenty-two trials (99,591 participants, 25.2% female) were included. Female sex was significantly associated with a higher 1-year MACCE risk (hazard ratio 1.14 [95% confidence interval 1.02–1.28]) and bleeding (1.13 [1.00–1.28]), but not NACCE (1.12 [0.96–1.31]). In sub-analyses, the association between female sex and MACCE was related to use of clopidogrel as the second antiplatelet agent (1.11 [1.03–1.20]), whereas higher bleeding events were related to newer P2Y12 inhibitors (P2Y12i) (1.58 [1.01–2.46]). For DAPT duration, short-term DAPT followed by P2Y12i monotherapy was non-inferior for MACCE in females and males (0.95 [95% CI 0.83–1.10; and 0.96 [0.80–1.16]) but tended to be superior in males for NACCE versus 12-month DAPT (0.96 [0.91–1.01]); mid-term DAPT tended to be associated with a lower bleeding risk in males (0.43 [0.17–1.09]). Conclusions: Female sex is associated with higher MACCE and bleeding when newer P2Y12i agents are used. Short-term DAPT followed by P2Y12i monotherapy is safe and effective in both sexes undergoing PCI. Clinical Trials Registration: PROSPERO ID: CRD42021278663. Sex differences in outcomes of clinical trials of dual antiplatelet therapy (DAPT) after percutaneous coronary interventions (PCI). [ABSTRACT FROM AUTHOR]

Summary: Obesity is reported to increase stroke risk, with adipocyte‐derived cytokines or adipokines implicated as mediators. However, the relationship between adipokines and stroke is not well clarified. Thus, we aimed to evaluate the association of adipokines with stroke using fully adjusted risk estimates that incorporated body mass index in a meta‐analysis. Data from 52 studies (62,428 patients) were pooled in a random‐effects meta‐analysis. Adiponectin was independently associated with a lower risk of pre‐existing stroke (adjusted odds ratio: 0.64 [95% confidence interval: 0.46–0.88], p < 0.01), whereas leptin (1.08 [1.00–1.17], p = 0.04), resistin (1.06 [1.04–1.08], p < 0.01) and visfatin (1.04 [1.01–1.07], p = 0.01) are associated with a higher risk of stroke, but none with incident stroke. Adipokines independently associated with an ischaemic stroke subtype were adiponectin (0.48 [0.30–0.77], p < 0.01), leptin (1.10 [1.01–1.20], p = 0.04), and resistin (1.06 [1.04–1.08], p < 0.01). Fatty acid‐binding protein‐4 (FABP‐4) independently predicted 6‐month poor functional outcomes in stroke patients (adjusted hazard ratio: 1.09 [1.06–1.12], p < 0.01); whereas both FABP‐4 (1.17 [1.03–1.34], p = 0.01) and visfatin (1.24 [1.00–1.55], p = 0.05) were predictive of 6‐month mortality. Adipokines are associated with a greater risk of pre‐existing stroke, but not with the relationship with incident stroke. Adipokines, such as FABP‐4 and visfatin, may serve as biomarkers of stroke severity and worsening of stroke outcomes. [ABSTRACT FROM AUTHOR]

Aims: Arrhythmogenic right ventricular cardiomyopathy (ARVC), an inherited heart muscle abnormality, is a major cause of sudden cardiac death (SCD). However, the burden of SCD and risk factors in ARVC are not clearly described. Thus, we estimated the rates and predictors of SCD in ARVC in a meta-analysis.Methods and Results: PubMed, Embase, and Web of Science were searched through 7 April 2021. Prospective studies reporting SCD from ARVC cohorts were included. Data were independently extracted by two reviewers and pooled in a random-effects meta-analysis. Fifty-two studies (n = 5485 patients) with moderate-to-low risk of bias were included. The pooled annualized rates of SCD were 0.65 per 1000 [95% confidence interval 0.00-6.43, I2 0.00%] in those with an implantable cardioverter-defibrillator (ICD) and 7.21 (2.38-13.79, I2 0.0%) in non-ICD cohorts: 7.14 in probands and 8.44 for 2010 Task Force Criteria (TFC). Multivariable predictors of life-threatening arrhythmic events including SCD were: age at presentation [adjusted hazard ratio 0.98 (0.97-0.99)], male sex [2.08 (1.29-3.36)], right ventricular (RV) dysfunction [6.99 (2.17-22.49)], QRS fragmentation [6.55 (3.33-12.90)], T-wave inversion [1.12 (1.02-1.24)], syncope at presentation [2.83 (2.40-4.08)], previous non-sustained ventricular tachyarrhythmia [2.53 (1.44-4.45)], and the TFC score [1.96 (1.02-3.76)], (P < 0.05). Predictors of appropriate ICD therapy were RV dysfunction, syncope, and inducible ventricular arrhythmia (P < 0.01).Conclusion: This meta-analysis demonstrates a high burden of SCD in ARVC patients, especially among probands and ARVC defined by the modified TFC. Better strategies are required to improve patient management and prevent SCD in ARVC. PROSPERO ID: CRD42020211761. [ABSTRACT FROM AUTHOR]

Recent preclinical and observational cohort studies have implicated imbalances in gut microbiota composition as a contributor to atrial fibrillation (AF). The gut microbiota is a complex and dynamic ecosystem containing trillions of microorganisms, which produces bioactive metabolites influencing host health and disease development. In addition to host-specific determinants, lifestyle-related factors such as diet and drugs are important determinants of the gut microbiota composition. In this review, we discuss the evidence suggesting a potential bidirectional association between AF and gut microbiota, identifying gut microbiota-derived metabolites as possible regulators of the AF substrate. We summarize the effect of gut microbiota on the development and progression of AF risk factors, including heart failure, hypertension, obesity, and coronary artery disease. We also discuss the potential anti-arrhythmic effects of pharmacological and diet-induced modifications of gut microbiota composition, which may modulate and prevent the progression to AF. Finally, we highlight important gaps in knowledge and areas requiring future investigation. Although data supporting a direct relationship between gut microbiota and AF are very limited at the present time, emerging preclinical and clinical research dealing with mechanistic interactions between gut microbiota and AF is important as it may lead to new insights into AF pathophysiology and the discovery of novel therapeutic targets for AF. [ABSTRACT FROM AUTHOR]

Objective: To summarize data on the prevalence/incidence, risk factors and prognosis of atrial fibrillation (AF) in patients with acute coronary syndromes (ACS). Methods: MEDLINE, Embase, and Web of Science were searched to identify all published studies providing relevant data through August 23, 2020. Random‐effects meta‐analysis method was used to pool estimates. Results: We included 109 studies reporting data from a pooled population of 8 239 364 patients. The prevalence rates were 5.8% for pre‐existing AF, 7.3% for newly diagnosed AF, and 11.3% for prevalent (total) AF, in patients with ACS. Predictors of newly diagnosed AF included age (per year increase) (adjusted odds ratio [aOR]: 1.05), C‐reactive protein (aOR: 1.49), left atrial (LA) diameter (aOR: 1.08), LA dilatation (aOR: 2.32), left ventricular ejection fraction <40% (aOR: 1.82), hypertension (aOR: 1.87), and Killip ˃ 1 (aOR: 1.85), p <.01 in all analyzes. Newly diagnosed AF was associated with an increased risk of acute heart failure (adjusted hazard ratio [aHR]: 3.20), acute kidney injury (aHR: 3.09), re‐infarction (aHR: 1.96), stroke (aHR: 2.15), major bleeding (aHR: 2.93), and mortality (aHR: 1.80) in the short term; and with an increased risk of heart failure (aHR: 2.21), stroke (aHR: 1.75), mortality (aHR: 1.67), CV mortality (aHR: 2.09), sudden cardiac death (aHR: 1.53), and a composite of major adverse cardiovascular events (aHR: 1.54) in the long term (beyond 1 month), p <.05 in all analyzes. Conclusion: One in nine patients with ACS has AF, with a high proportion of newly diagnosed AF. AF, in particular newly diagnosed AF, is associated with poor short‐term and long‐term outcomes in patients with ACS. [ABSTRACT FROM AUTHOR]

Objective: To summarize data on the rates and predictors of left atrial thrombus/left atrial appendage thrombus (LAT/LAAT) detection by transoesophageal echocardiography (TEE) before electrical cardioversion (ECV) or catheter ablation (CA) for atrial fibrillation (AF). Methods: EMBASE, MEDLINE, and Web of Science Core Collection were searched to identify all studies providing relevant data and published by October 7, 2020. A random‐effects meta‐analysis method was used to pool effect size estimates. Results: A total of 85 studies were included, reporting data from 56 660 patients with AF. In patients undergoing CA and ECV, the pooled prevalence of LAT/LAAT was 1.8% and 7.5% in those not on oral anticoagulation (OAC), 1.8% and 5.5% in those taking OAC, and 1.3% and 4.9% in case of adequate OAC, respectively. According to the type of OAC, the prevalence was 2.0% and 7.6% for vitamin K antagonist, 1.3% and 3.5% for direct oral anticoagulant. Predictors of LAT/LAAT detection were nonparoxysmal AF (odds ratio [OR]: 3.6, 95% confidence interval: 2.4–5.2), hypertension (OR: 2.9, 1.2–7.0), previous stroke (OR: 3.0, 1.6–5.63), heart failure (OR: 4.3, 2.7–6.8), and CHADS2 score ≥2 (OR: 3.3, 1.9–5.8) for patients undergoing CA; and heart failure (OR: 2.8, 1.3–6.2) and the CHA2DS2‐VASc score (OR: 2.55, 1.5–4.5) for those undergoing ECV. Conclusion: The prevalence of LAT/LAAT in AF patients undergoing ECV or CA varies widely, mainly due to differences in patient risk profiles and OAC types. Further research should determine whether the predictors of LAT/LAAT detection identified by this study could be used to select patients who require preprocedural TEE. [ABSTRACT FROM AUTHOR]

Although electrocardiography (ECG) is a cost-effective and convenient tool for routine screening of left ventricular hypertrophy (LVH), its performance has been shown to be poor. The Peguero-Lo Presti, a novel voltage criterion, was found to be potentially better than the most commonly used criteria. We conducted a systematic review and meta-analysis of its diagnostic accuracy compared to Cornell and Sokolow-Lyon voltage criteria. Bibliographic databases were searched to identify relevant articles. Pooled sensitivity, specificity, diagnostic odds ratio (DOR), and summary receiver operating characteristic (ROC) curves were performed for comparison. Ten studies reporting data from 5984 individuals were included in the meta-analysis. Peguero-Lo Presti had the highest pooled sensitivity (43.0%, 95% confidence interval [CI]: 30.2-56.9) followed by Cornell (26.1%; 95% CI: 16.9-37.9) and Sokolow Lyon (22.0%; 95% CI: 14.1-32.7). However, Peguero-Lo Presti had the lesser pooled specificity (90.5%; 95% CI: 86.3-93.5) and Cornell the highest (94.9%; 95% CI: 90.3-97.3). The pooled DOR was 6.63 (95% CI: 3.95-11.13), 5.50 (95% CI: 3.64-8.30), and 2.94 (95% CI: 2.20-3.92) for Peguero-Lo Presti, Cornell, and Sokolow-Lyon, respectively. Peguero-Lo Presti had the best accuracy according to summary ROC curves, with an area under the curve of 0.827 compared to 0.715 for Cornell, and 0.623 for Sokolow-Lyon. In conclusion, according to this meta-analysis, Peguero-Lo Presti has a better diagnostic performance than Cornell and Sokolow-Lyon and might be more useful in routine clinical practice as a screening tool for LVH. [ABSTRACT FROM AUTHOR]

Introduction: Recent research has unravelled an increasing list of cardiac conditions and risk factors that may be responsible for the abnormal underlying atrial substrate that predisposes to atrial fibrillation (AF). Atrial fibrosis has been demonstrated as the pivotal structural abnormality underpinning conduction disturbances that promote AF in different disease models. Despite the advancement in our discoveries of the molecular mechanisms involved in the profibrotic milieu, targeted therapeutics against atrial fibrosis remain lacking. Areas covered: This review is focused on detailing the key molecular signalling pathways that contribute to atrial fibrosis including: angiotensin II, transforming growth factor (TGF- ß1), connective tissue growth factor (CTGF) and endothelin-1. We also discussed the potential therapeutic options that may be useful in modulating the abnormal atrial substrate. In addition, we examined the new paradigm of AF care in lifestyle and risk factor management that has been shown to arrest and reverse the atrial remodelling process leading to improved AF outcomes. Expert commentary: The future of AF care is likely to require an integrated approach consisting of aggressive risk factor management in addition to the established paradigm of rate and rhythm management and anticoagulation. Translational studies on molecular therapeutics to combat atrial fibrosis is urgently needed. [ABSTRACT FROM AUTHOR]

The article offers information on relationship between atrial fibrillation (AF) and thromboembolism. It mentions factors associated with embolic stroke after catheter ablation of AF over a long‐term follow‐up period; and also mentions peri‐atrial epicardial adipose tissue (EAT) which is associated with postablation embolic stroke.