Tachycardia and Atrial Fibrillation-Related Cardiomyopathies: Potential Mechanisms and Current Therapies.

Atrial fibrillation (AF) is associated with an increased risk of new-onset ventricular contractile dysfunction, termed arrhythmia-induced cardiomyopathy (AIC). Although cardioembolic stroke remains the most feared and widely studied complication of AF, AIC is also a clinically important consequence of AF that portends significant morbidity and mortality to patients with AF. Current treatments are aimed at restoring sinus rhythm through catheter ablation and rate and rhythm control, but these treatments do not target the underlying molecular mechanisms driving the progression from AF to AIC.

Chronic kidney disease promotes atrial fibrillation via inflammasome pathway activation.

Chronic kidney disease (CKD) is associated with a higher risk of atrial fibrillation (AF). The mechanistic link between CKD and AF remains elusive. IL-1β, a main effector of NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation, is a key modulator of conditions associated with inflammation, such as AF and CKD.

Cardiac function, structural, and electrical remodeling by microgravity exposure.

Space medicine is key to the human exploration of outer space and pushes the boundaries of science, technology, and medicine. Because of harsh environmental conditions related to microgravity and other factors and hazards in outer space, astronauts and spaceflight participants face unique health and medical challenges, including those related to the heart. In this review, we summarize the literature regarding the effects of spaceflight on cardiac structure and function.

In-depth characterization of a mouse model of postoperative atrial fibrillation.

Introduction: Postoperative atrial fibrillation (POAF), characterized as AF that arises 1-3 days after surgery, occurs after 30%-40% of cardiac and 10%-20% of non-cardiac surgeries, and is thought to arise due to transient surgery-induced triggers acting on a preexisting vulnerable atrial substrate often associated with inflammation and autonomic nervous system dysfunction. Current experimental studies often rely on human atrial tissue samples, collected during surgery prior to arrhythmia development, or animal models such as sterile pericarditis and atriotomy, which have not been robustly characterized.

Aim: To characterize the demographic, electrophysiologic, and inflammatory properties of a POAF mouse model.

Abnormalities in cardiac and inflammatory biomarkers in ambulatory subjects after COVID-19 infection.

Background: Coronavirus-2019 (COVID-19) is known to affect the heart and is associated with a pro-inflammatory state. Most studies to date have focused on clinically sick subjects. Here, we report cardiac and proinflammatory biomarkers levels in ambulatory young adults with asymptomatic or mild COVID-19 infection compared to those without infection 4-8 weeks after severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) testing.

Role of Ca in healthy and pathologic cardiac function: from normal excitation-contraction coupling to mutations that cause inherited arrhythmia.

Calcium (Ca) ions are a key second messenger involved in the rhythmic excitation and contraction of cardiomyocytes throughout the heart. Proper function of Ca-handling proteins is required for healthy cardiac function, whereas disruption in any of these can cause cardiac arrhythmias. This comprehensive review provides a broad overview of the roles of Ca-handling proteins and their regulators in healthy cardiac function and the mechanisms by which mutations in these proteins contribute to inherited arrhythmias.

Mouse models of spontaneous atrial fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia in adults, with a prevalence increasing with age. Current clinical management of AF is focused on tertiary prevention (i.e.

An Integrative Genomic Strategy Identifies sRAGE as a Causal and Protective Biomarker of Lung Function.

Background: There are few clinically useful circulating biomarkers of lung function and lung disease. We hypothesized that genome-wide association studies (GWAS) of circulating proteins in conjunction with GWAS of pulmonary traits represents a clinically relevant approach to identifying causal proteins and therapeutically useful insights into mechanisms related to lung function and disease.

Study Question: Can an integrative genomic strategy using GWAS of plasma soluble receptor for advanced glycation end-products (sRAGE) levels in conjunction with GWAS of lung function traits identify putatively causal relations of sRAGE to lung function?

Study Design And Methods: Plasma sRAGE levels were measured in 6,861 Framingham Heart Study participants and GWAS of sRAGE was conducted to identify protein quantitative trait loci (pQTL), including cis-pQTL variants at the sRAGE protein-coding gene locus (AGER).

Integrative Genomic Analysis Reveals Four Protein Biomarkers for Platelet Traits.

Rationale: Mean platelet volume (MPV) and platelet count (PLT) are platelet measures that have been linked to cardiovascular disease (CVD) and mortality risk. Identifying protein biomarkers for these measures may yield insights into CVD mechanisms.

Objective: We aimed to identify causal protein biomarkers for MPV and PLT among 71 CVD-related plasma proteins measured in FHS (Framingham Heart Study) participants.

Lipidomic profiling identifies signatures of metabolic risk.

Background: Metabolic syndrome (MetS), the clustering of metabolic risk factors, is associated with cardiovascular disease risk. We sought to determine if dysregulation of the lipidome may contribute to metabolic risk factors.

Methods: We measured 154 circulating lipid species in 658 participants from the Framingham Heart Study (FHS) using liquid chromatography-tandem mass spectrometry and tested for associations with obesity, dysglycemia, and dyslipidemia.

Genome-wide identification of DNA methylation QTLs in whole blood highlights pathways for cardiovascular disease.

Identifying methylation quantitative trait loci (meQTLs) and integrating them with disease-associated variants from genome-wide association studies (GWAS) may illuminate functional mechanisms underlying genetic variant-disease associations. Here, we perform GWAS of >415 thousand CpG methylation sites in whole blood from 4170 individuals and map 4.7 million cis- and 630 thousand trans-meQTL variants targeting >120 thousand CpGs.

Epigenome-wide association study of DNA methylation and microRNA expression highlights novel pathways for human complex traits.

DNA methylation (DNAm) and microRNAs (miRNAs) have been implicated in a wide-range of human diseases. While often studied in isolation, DNAm and miRNAs are not independent. We analyzed associations of expression of 283 miRNAs with DNAm at >400K CpG sites in whole blood obtained from 3565 individuals and identified 227 CpGs at which differential methylation was associated with the expression of 40 nearby miRNAs (-miR-eQTMs) at FDR<0.

Evidence for a Causal Role of the SH2B3-βM Axis in Blood Pressure Regulation.

Genetic variants at SH2B3 are associated with blood pressure and circulating βM (β-2 microglobulin), a well-characterized kidney filtration biomarker. We hypothesize that circulating βM is an independent risk predictor of hypertension and may causally contribute to its development. The study sample consisted of 7 065 Framingham Heart Study participants with measurements of plasma βM.

Author Correction: Genome-wide mapping of plasma protein QTLs identifies putatively causal genes and pathways for cardiovascular disease.

In the originally published version of this Article, financial support was not fully acknowledged. The sentence "KS was supported by the 'Biomedical Research Program' funds at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation" has been added to the acknowledgement section in both the PDF and HTML versions of the Article.

Genome-wide mapping of plasma protein QTLs identifies putatively causal genes and pathways for cardiovascular disease.

Identifying genetic variants associated with circulating protein concentrations (protein quantitative trait loci; pQTLs) and integrating them with variants from genome-wide association studies (GWAS) may illuminate the proteome's causal role in disease and bridge a knowledge gap regarding SNP-disease associations. We provide the results of GWAS of 71 high-value cardiovascular disease proteins in 6861 Framingham Heart Study participants and independent external replication. We report the mapping of over 16,000 pQTL variants and their functional relevance.

Multigenerational memory and adaptive adhesion in early bacterial biofilm communities.

Using multigenerational, single-cell tracking we explore the earliest events of biofilm formation by During initial stages of surface engagement (≤20 h), the surface cell population of this microbe comprises overwhelmingly cells that attach poorly (∼95% stay <30 s, well below the ∼1-h division time) with little increase in surface population. If we harvest cells previously exposed to a surface and direct them to a virgin surface, we find that these surface-exposed cells and their descendants attach strongly and then rapidly increase the surface cell population. This "adaptive," time-delayed adhesion requires determinants we showed previously are critical for surface sensing: type IV pili (TFP) and cAMP signaling via the Pil-Chp-TFP system.