Adipokines and stroke: A systematic review and meta-analysis of disease risk and patient outcomes.

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.

Incidence and predictors of sudden cardiac death in arrhythmogenic right ventricular cardiomyopathy: a pooled analysis.

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.

Associations between adipokines and atrial fibrillation: A systematic review and meta-analysis.

AIMS: Although overweight and obesity are associated with increased risk of atrial fibrillation (AF), the underlying mechanisms are not well characterised. Recent data suggest that this link may be partly due to abnormal adipose tissue-derived cytokines or adipokines. However, this relationship is not well clarified. To evaluate the association between adipokines and AF in a systematic review and meta-analysis. DATA SYNTHESIS: PubMed, Embase, and Web of Science Core Collection were searched from inception through 1st March 2021. Studies were included if they reported any adipokine and AF, with their quality assessed using the Newcastle-Ottawa scale. Data were independently abstracted, with unadjusted and multivariable adjusted estimates pooled in a random-effects meta-analysis. Data are presented for overall prevalent or incident AF and AF subtypes (paroxysmal, persistent, or non-paroxysmal AF). A total of 34 studies, with 31,479 patients, were included. The following adipokines were significantly associated with AF in the pooled univariate data - apelin (risk ratio for prevalent AF: 0.05 [0.00-0.50], p = 0.01; recurrent AF: 0.21 [0.11-0.42], p < 0.01) and resistin (incident AF: 2.05 [1.02-4.1], p = 0.04; prevalent AF: 2.62 [1.78-3.85], p < 0.01). Pooled analysis of multivariable adjusted effect size estimates showed adiponectin as the sole independent predictor of AF incidence (1.14 [1.02-1.27], p = 0.02). Moreover, adiponectin was associated with non-paroxysmal AF (persistent AF: 1.45 [1.08-1.94, p = 0.01; non-paroxysmal versus paroxysmal AF: 3.14 [1.87-5.27, p < 0.01). CONCLUSIONS: Adipokines, principally adiponectin, apelin, and resistin, are associated with the risk of atrial fibrillation. However, the association is not seen after multivariate adjustment, likely reflecting the lack of statistical power. Future research should investigate these relationships in larger prospective cohorts and how they can refine AF monitoring strategies. PROSPERO ID: CRD42020208879.

Atrial fibrillation incidence, prevalence, predictors, and adverse outcomes in acute coronary syndromes: A pooled analysis of data from 8 million patients.

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.

Sex differences in clinical profile, management, and outcomes of patients hospitalized for atrial fibrillation in the United States.

AIMS: This study aimed to investigate the impact of sex on the clinical profile, utilization of rhythm control therapies, cost of hospitalization, length of stay, and in-hospital mortality in patients admitted for atrial fibrillation (AF) in the United States. METHODS AND RESULTS: We used data from the Nationwide Inpatient Sample for the year 2018. Regression analysis was performed to investigate differences between men and women. A P-value ≤ 0.05 was considered significant. We included 82592 patients with a primary diagnosis of of AF 50.8% women. Women were significantly older (mean age 74 vs. 67 years, P < 0.001) and had a higher CHA2DS2-VASc score (median 4 vs. 2, P < 0.001) than men. Women had relatively higher in-hospital mortality (0.9% vs. 0.8%, P = 0.070); however, after adjustment for known risk factors female sex was no longer a predictor of mortality (P = 0.199). In sex-specific regression analyses, increased age, chronic obstructive pulmonary disease, previous stroke, heart failure, and chronic kidney disease were risk factors for in-hospital mortality in both sexes, vascular disease only in women, and race and alcohol abuse only in men. After adjusting for potential confounders, female sex was associated with lower likelihood of receiving catheter ablation [adjusted odds ratio (aOR) 0.69, 95% confidence interval (CI) 0.64-0.74] and electrical cardioversion (aOR 0.69, 95% CI 0.67-0.72), and with longer hospitalization (aOR 1.33, 95% CI 1.28-1.37), whereas sex had no influence on hospitalization costs (P = 0.339). CONCLUSION: There were differences in the risk profile, management, and outcomes between men and women hospitalized for AF. Further studies are needed to explore why women are treated differently regarding rhythm control procedures.

Accelerated Biological Aging Secondary to Cardiometabolic Risk Factors Is a Predictor of Cardiovascular Mortality: A Systematic Review and Meta-analysis.

BACKGROUND: Chronological aging is one of the major risk factors of cardiovascular (CV) disease (CVD); however, the effect of biological aging on CVD and outcomes remain poorly understood. Herein, we evaluated the association between leukocyte telomere length (LTL), a marker of biological age, and CV outcomes. METHODS: We searched PubMed, Embase, Ovid Medline, and Web of Science Core Collection for the studies on the association between LTL and myocardial infarction (MI), CV death, and/or CVD risk factors from inception to July 2020. Extracted data were pooled in a random-effects meta-analysis and summarized as risk ratio (RR) and corresponding 95% confidence interval (CI) per LTL tertile. RESULTS: A total of 32 studies (n = 144,610 participants) were included. In a pooled analysis of MI and LTL in a multivariate-adjusted model, the shortest LTL was associated with a 39% higher risk of MI (RR, 1.39; 95% CI, 1.16-1.67; P < 0.001). After adjusting for chronological age and traditional covariance, we showed a 28% increased risk of CV death in the shortest tertile of LTL (RR, 1.28; 95% CI, 1.05-1.56; P = 0.01). Analysis of the studies that investigated the association between CV risk factors and LTL (n = 7) showed that diabetes mellitus is associated with a 46% increased risk of LTL attrition (RR, 1.46; 95% CI, 1.46-2.09; P = 0.039). CONCLUSIONS: This study shows a strong association between LTL, a marker of biological aging, and the risk of MI and CV death. Cardiometabolic risk factors contribute to telomere attrition and therefore accelerates biological aging.

Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications.

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.

Polygenic risk score and coronary artery disease: A meta-analysis of 979,286 participant data.

BACKGROUND AND AIMS: Coronary artery disease (CAD) is a complex disease with a strong genetic basis. While previous studies have combined common single-nucleotide polymorphisms (SNPs) into a polygenic risk score (PRS) to predict CAD risk, this association is poorly characterised. We performed a meta-analysis to estimate the effect of PRS on the risk of CAD. METHODS: Online databases were searched for studies reporting PRS and CAD. PRS computation was based on log-odds (PRSLN), pruning or clumping and thresholding (PRSP/C + T), Lassosum regression (PRSLassosum), LDpred (PRSLDpred), or metaGRS (PRSmetaGRS). The reported odds ratio (OR), hazard ratio (HR), C-indexes and their corresponding 95% confidence interval (95% CI) were pooled in a random-effects meta-analysis. RESULTS: Forty-nine studies were included (979,286 individuals). There was a significant association between 1-standard deviation [SD] increment in PRS and adjusted risks of both incident and prevalent CAD (OR [95% CI]: 1.67 [1.57-1.77] for PRSmetaGRS, 1.46 [1.26-1.68] for PRSLDpred). The risk of incident CAD was highest for PRSP/C + T (HR [95% CI]: 1.49 [1.26-1.78]), PRSmetaGRS (1.37 [1.27-1.47]), and PRSLDpred (1.36 [1.31-1.42]). Analysis of model performance demonstrated that PRS predicted incident CAD with C-index of up to 0.71. Importantly, addition of PRS to clinical risk scores resulted in modest but statistically significant improvements in CAD risk prediction, with 1.5% observed for PRSP/C + T (p < 0.001) and 1.6% for PRSLDpred (p < 0.001). CONCLUSIONS: Polygenic risk score is strongly associated with increased risks of CAD. Future prospective studies should explore the usefulness of polygenic risk scores for identifying individuals at a high risk of developing CAD.

Rhythm monitoring strategies for atrial fibrillation detection in patients with cryptogenic stroke: A systematic review and meta-analysis.

OBJECTIVE: To summarize data on atrial fibrillation (AF) detection rates and predictors across different rhythm monitoring strategies in patients with cryptogenic stroke (CS) or embolic stroke of undetermined source (ESUS). METHODS: MEDLINE, Embase, and Web of Science were searched to identify all published studies providing relevant data through July 6, 2020. Random-effects meta-analysis method was used to pool estimates. RESULTS: We included 47 studies reporting on a pooled population of 8,215 patients with CS or ESUS. Using implantable cardiac monitor (ICM), the pooled rate of AF was 12.2% (95% CI 9.4-15.0) at 3 months, 16.0% (95% CI 13.2-18.8) at 6 months, 18.7% (95% CI 15.7-21.7) at 12 months, 22.8% (95% CI 19.1-26.5) at 24 months, and 28.5% (95% CI 17.6-39.3) at 36 months. AF rates were significantly higher in patients with ESUS vs CS (22.0% vs 14.2%; p < 0.001) at 6 months, and in studies using Reveal LINQ vs Reveal XT ICM (19.1% vs 13.0%; p = 0.001) at 12 months. Using mobile cardiac outpatient telemetry (MCOT), the pooled rate of AF was 13.7% (95% CI 10.2-17.2) at 1 month. Predictors of AF detection with ICM included older age, CHA2DS2-VASc score, left atrial enlargement, P wave maximal duration and prolonged PR interval. CONCLUSION: The yield of ICM increases with the duration of monitoring. More than a quarter of patients with CS or ESUS will be diagnosed with AF during follow-up. About one in seven patients had AF detected within a month of MCOT, suggesting that a non-invasive rhythm monitoring strategy should be considered before invasive monitoring.

Atrial thrombus detection on transoesophageal echocardiography in patients with atrial fibrillation undergoing cardioversion or catheter ablation: A pooled analysis of rates and predictors.

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 CHA2 DS2 -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.

Meta-Analysis Comparing the Frequency of Carotid Artery Stenosis in Patients With Atrial Fibrillation and Vice Versa.

Atrial fibrillation (AF) and carotid stenosis (CS) can coexist and this association has been reported to result in a higher risk of stroke than attributed to either condition alone. Here we aimed to summarize the data on the association of CS and AF. MEDLINE and Embase were searched to identify all published studies providing relevant data through February 27, 2020. Random-effects meta-analysis method was used to pool estimates of prevalence. Heterogeneity was assessed by mean I-squared statistic. Forty-eight studies were included, 20 reporting on the prevalence of carotid disease in a pooled population of 49,070 AF patients, and 28 on the prevalence of AF in a total of 2,288,265 patients with carotid disease. The pooled prevalence of CS in AF patients was 12.4% (95% confidence interval [CI] 8.7 to 16.0, I2 93%; n = 3,919), ranging from 4.4% to 24.3%. The pooled prevalence of carotid plaque was 48.4% (95% CI 35.2 to 61.7, I2 = 99%; n = 4292). The prevalence of AF in patients with CS was 9.3% (95% CI 8.7 to 10.0, I2 99%; n = 2,286,518), ranging from 3.6% to 10.0%. This prevalence was much higher (p <0.001) in patients undergoing carotid artery stenting (12.7%, 95% CI 11.3 to 14.02, I2 38.3%) compared with those undergoing carotid endarterectomy (6.9%, 95% CI 8.3 to 10.4, I2 94.1%). There was no difference in AF prevalence between patients with CS, with and without previous cerebrovascular event (p >0.05). In conclusion, AF and CS frequently coexist, with about one in ten patients with AF having CS, and vice versa. In addition, nonstenotic carotid disease is present in about half of AF patients. These findings have important implications for AF screening in patients with CS, stroke prevention, and the opportunities to intervene on common risk factors.

Self-reported physical activity and atrial fibrillation risk: A systematic review and meta-analysis.

BACKGROUND: Although physical activity (PA) is an important component of cardiovascular disease prevention and treatment, its role in atrial fibrillation (AF) risk is less well established. OBJECTIVE: The purpose of this study was to systematically summarize the evidence pertaining to the relationship of PA and risk of AF. METHODS: We searched the PubMed and Embase databases for prospective cohort studies reporting the risk of AF associated with a specific PA volume through March 2020. From each study, we extracted the risk associated with a given PA level, in comparison with insufficiently active ("inactive") individuals. The reported risk was normalized to metabolic equivalent of task (MET)-minutes per week. A random-effects meta-analysis was used to compare AF risk between those who met and those who did not meet PA recommendations (450 MET-minutes per week), and a dose-response analysis between the level of PA and the risk of AF was performed. RESULTS: Fifteen studies reporting data from 1,464,539 individuals (median age 55.3 years; 51.7% female) were included. Individuals achieving guideline-recommended level of PA had a significantly lower risk of AF (hazard ratio 0.94; 95% confidence interval 0.90-0.97; P = .001). Dose-response analysis showed that PA levels up to 1900 MET-minutes per week were associated with a lower risk of AF, with less certainty beyond that level. CONCLUSION: PA at guideline-recommended levels and above are associated with a significantly lower AF risk. However, at 2000 MET-minutes per week and beyond, the benefit is less clear.

The Role of MSC Therapy in Attenuating the Damaging Effects of the Cytokine Storm Induced by COVID-19 on the Heart and Cardiovascular System.

The global pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has led to 47 m infected cases and 1. 2 m (2.6%) deaths. A hallmark of more severe cases of SARS-CoV-2 in patients with acute respiratory distress syndrome (ARDS) appears to be a virally-induced over-activation or unregulated response of the immune system, termed a "cytokine storm," featuring elevated levels of pro-inflammatory cytokines such as IL-2, IL-6, IL-7, IL-22, CXCL10, and TNFα. Whilst the lungs are the primary site of infection for SARS-CoV-2, in more severe cases its effects can be detected in multiple organ systems. Indeed, many COVID-19 positive patients develop cardiovascular complications, such as myocardial injury, myocarditis, cardiac arrhythmia, and thromboembolism, which are associated with higher mortality. Drug and cell therapies targeting immunosuppression have been suggested to help combat the cytokine storm. In particular, mesenchymal stromal cells (MSCs), owing to their powerful immunomodulatory ability, have shown promise in early clinical studies to avoid, prevent or attenuate the cytokine storm. In this review, we will discuss the mechanistic underpinnings of the cytokine storm on the cardiovascular system, and how MSCs potentially attenuate the damage caused by the cytokine storm induced by COVID-19. We will also address how MSC transplantation could alleviate the long-term complications seen in some COVID-19 patients, such as improving tissue repair and regeneration.

Vascular Manifestations of COVID-19 - Thromboembolism and Microvascular Dysfunction.

The coronavirus pandemic has reportedly infected over 31.5 million individuals and caused over 970,000 deaths worldwide (as of 22nd Sept 2020). This novel coronavirus, officially named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), although primarily causes significant respiratory distress, can have significant deleterious effects on the cardiovascular system. Severe cases of the virus frequently result in respiratory distress requiring mechanical ventilation, often seen, but not confined to, individuals with pre-existing hypertension and cardiovascular disease, potentially due to the fact that the virus can enter the circulation via the lung alveoli. Here the virus can directly infect vascular tissues, via TMPRSS2 spike glycoprotein priming, thereby facilitating ACE-2-mediated viral entry. Clinical manifestations, such as vasculitis, have been detected in a number of vascular beds (e.g., lungs, heart, and kidneys), with thromboembolism being observed in patients suffering from severe coronavirus disease (COVID-19), suggesting the virus perturbs the vasculature, leading to vascular dysfunction. Activation of endothelial cells via the immune-mediated inflammatory response and viral infection of either endothelial cells or cells involved in endothelial homeostasis, are some of the multifaceted mechanisms potentially involved in the pathogenesis of vascular dysfunction within COVID-19 patients. In this review, we examine the evidence of vascular manifestations of SARS-CoV-2, the potential mechanism(s) of entry into vascular tissue and the contribution of endothelial cell dysfunction and cellular crosstalk in this vascular tropism of SARS-CoV-2. Moreover, we discuss the current evidence on hypercoagulability and how it relates to increased microvascular thromboembolic complications in COVID-19.

A meta-analytic evaluation of the diagnostic accuracy of the electrocardiographic Peguero-Lo Presti criterion for left ventricular hypertrophy.

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.

Implication of ventricular pacing burden and atrial pacing therapies on the progression of atrial fibrillation: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Atrial fibrillation (AF) is common after pacemaker implantation. However, the impact of pacemaker algorithms in AF prevention is not well understood. OBJECTIVE: The purpose of this study was to evaluate the role of pacing algorithms in preventing AF progression. METHODS: A systematic search of articles using the PubMed and Embase databases resulted in a total of 754 references. After exclusions, 21 randomized controlled trials (8336 patients) were analyzed, comprising studies reporting ventricular pacing percentage (VP%) (AAI vs DDD, n = 1; reducing ventricular pacing [RedVP] algorithms, n = 2); and atrial pacing therapies (atrial preference pacing [APP], n = 14; atrial antitachycardia pacing [aATP]+APP, n = 3; RedVP+APP+aATP, n = 1). RESULTS: Low VP% (<10%) lead to a nonsignificant reduction in the progression of AF (hazard ratio [HR] 0.80; 95% confidence interval [CI] 0.57-1.13; P = .21; I2 = 67%) compared to high VP% (>10%). APP algorithm reduced premature atrial complexes (PAC) burden (mean difference [MD] -1117.74; 95% CI -1852.36 to -383.11; P = .003; I2 = 67%) but did not decrease AF burden (MD 8.20; 95% CI -5.39 to 21.80; P = .24; I2 = 17%) or AF episodes (MD 0.00; 95% CI -0.24 to 0.25; P = .98; I2 = 0%). Similarly, aATP+APP programming showed no significant difference in AF progression (odds ratio 0.65; 95% CI 0.36-1.14; P = .13; I2 = 61%). No serious adverse events related to algorithm were reported. CONCLUSION: This meta-analysis of randomized controlled trials demonstrated that algorithms to reduce VP% can be considered safe. Low burden VP% did not significantly suppress AF progression. The atrial pacing therapy algorithms could suppress PAC burden but did not prevent AF progression.

Progression and reversibility of stretch induced atrial remodeling: Characterization and clinical implications.

Atrial fibrillation (AF) is the most common sustained arrhythmia and across the developed nations, it contributes to increasing hospitalizations and healthcare burden. Several comorbidities and risk factors including hypertension, heart failure, obstructive sleep apnoea and obesity are known to play an important role in the initiation and perpetuation of AF and atrial stretch or dilatation may play a central mechanistic role. The impact of atrial stretch in the development of AF can vary dependent on the underlying disease. This review focuses on understanding the substrate for AF in conditions of acute and chronic stretch and in the presence of common co-morbidities or risk factors through the review of findings in both animal and human studies. Additionally, the reversibility of atrial remodeling following stretch release will also be discussed. Identification of clinical conditions associated with increased atrial stretch as well as the treatment or prevention of these conditions may help to prevent AF progression and improve sinus rhythm maintenance.