Non-traditional risk factors for atrial fibrillation: epidemiology, mechanisms, and strategies.

Atrial fibrillation (AF) has become the pre-dominant arrhythmia worldwide and is associated with high morbidity and mortality. Its pathogenesis is intricately linked to the deleterious impact of cardiovascular risk factors, emphasizing the pivotal imperative for early detection and mitigation strategies targeting these factors for the prevention of primary AF. While traditional risk factors are well recognized, an increasing number of novel risk factors have been identified in recent decades.

Characterization of a novel mitophagy-related 5-genes signature for diagnosis of acute myocardial infarction.

Myocardial infarction (MI) and the ensuing heart failure (HF) remain the main cause of morbidity and mortality worldwide. One of the strategies to combat MI and HF lies in the ability to accurately predict the onset of these disorders. Alterations in mitochondrial homeostasis have been reported to be involved in the pathogenesis of various cardiovascular diseases (CVDs).

Algorithms of Electrocardiographic Changes for Quantitative and Localization Analysis of Thrombus Burden in Patients with Acute Pulmonary Thromboembolism.

Background: Various electrocardiographic (ECG) abnormalities are associated with the severity of pulmonary thromboembolism (PTE). The utility of evaluating the clot burden of PTE based on ECG findings alone has yet to be thoroughly investigated in Chinese patients. The aim of this study was therefore to use ECG signs to establish novel models for quantitative and localization analysis of clot burden in patients with acute PTE.

Thrombospondin 1 and Reelin act through Vldlr to regulate cardiac growth and repair.

Adult mammalian cardiomyocytes have minimal cell cycle capacity, which leads to poor regeneration after cardiac injury such as myocardial infarction. Many positive regulators of cardiomyocyte cell cycle and cardioprotective signals have been identified, but extracellular signals that suppress cardiomyocyte proliferation are poorly understood. We profiled receptors enriched in postnatal cardiomyocytes, and found that very-low-density-lipoprotein receptor (Vldlr) inhibits neonatal cardiomyocyte cell cycle.

Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis.

Epigenetic mechanisms and cell crosstalk have been shown to play important roles in the initiation and progression of cardiac fibrosis. This review article aims to provide a thorough overview of the epigenetic mechanisms involved in fibroblast regulation. During fibrosis, fibroblast epigenetic regulation encompasses a multitude of mechanisms, including DNA methylation, histone acetylation and methylation, and chromatin remodeling.

Large animal models of cardiac ischemia-reperfusion injury: Where are we now?

Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless, current cardioprotective strategies/interventions formulated in preclinical cardiovascular research are often limited to small animal models, which are not transferable or reproducible in large animal models due to different factors such as: (i) complex and varied features of human ischemic cardiac disease (ICD), which are challenging to mimic in animal models, (ii) significant differences in surgical techniques applied, and (iii) differences in cardiovascular anatomy and physiology between small versus large animals. This article highlights the advantages and disadvantages of different large animal models of preclinical cardiac ischemic reperfusion injury (IRI), as well as the different methods used to induce and assess IRI, and the obstacles faced in using large animals for translational research in the settings of cardiac IR.

Prognostic Significance of Coronary Microvascular Dysfunction in Patients With Heart Failure With Preserved Ejection Fraction.

Background: The prognostic impact of coronary microvascular dysfunction (CMD) has been scarcely addressed in heart failure with preserved ejection fraction (HFpEF). This study investigated the prevalence and prognostic significance of CMD as measured by a novel pressure wire-free coronary angiography-derived index of microcirculatory resistance (caIMR) on clinical outcomes.

Methods: Patients diagnosed with HFpEF from 2019 to 2021 were enrolled retrospectively.

Jmjd4 Facilitates Pkm2 Degradation in Cardiomyocytes and Is Protective Against Dilated Cardiomyopathy.

Background: A large portion of idiopathic and familial dilated cardiomyopathy (DCM) cases have no obvious causal genetic variant. Although altered response to metabolic stress has been implicated, the molecular mechanisms underlying the pathogenesis of DCM remain elusive. The JMJD family proteins, initially identified as histone deacetylases, have been shown to be involved in many cardiovascular diseases.

Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP.

Background: Myocardial infarction (MI) elicits cardiac fibroblast activation and extracellular matrix (ECM) deposition to maintain the structural integrity of the heart. Recent studies demonstrate that Fap (fibroblast activation protein)-a prolyl-specific serine protease-is an important marker of activated cardiac fibroblasts after MI.

Methods: Left ventricle and plasma samples from patients and healthy donors were used to analyze the expression level of FAP and its prognostic value.

Plasma GAS6 predicts mortality risk in acute heart failure patients: insights from the DRAGON-HF trial.

Background: Growth arrest-specific 6 (GAS6) is a vitamin K-dependent protein related to inflammation, fibrosis, as well as platelet function. Genetic ablation of GAS6 in mice protects against cardiac hypertrophy and dysfunction. Nonetheless, the association between plasma GAS6 levels and acute heart failure (AHF) patients is still unknown.

The Calcineurin-Drp1-Mediated Mitochondrial Fragmentation Is Aligned with the Differentiation of c-Kit Cardiac Progenitor Cells.

Objective: The heart contains a pool of c-kit progenitor cells which is believed to be able to regenerate. The differentiation of these progenitor cells is reliant on different physiological cues. Unraveling the underlying signals to direct differentiation of progenitor cells will be beneficial in controlling progenitor cell fate.

Prognostic value of plasma sAXL in patients with heart failure: insights from the DRAGON-HF trial.

Background: Little is known about the predictive value of soluble AXL (sAXL) in heart failure (HF). This study aimed to describe the prognostic value of plasma sAXL in patients with symptomatic HF.

Methods: This is a multicentre observational prospective cohort study (Registration No.

Ischemic Preconditioning and Postconditioning Protect the Heart by Preserving the Mitochondrial Network.

Background: Mitochondria fuse to form elongated networks which are more tolerable to stress and injury. Ischemic pre- and postconditioning (IPC and IPost, respectively) are established cardioprotective strategies in the preclinical setting. Whether IPC and IPost modulates mitochondrial morphology is unknown.

Long COVID-19 and the Heart: Is Cardiac Mitochondria the Missing Link?

Although corona virus disease 2019 (COVID-19) has now gradually been categorized as an endemic, the long-term effect of COVID-19 in causing multiorgan disorders, including a perturbed cardiovascular system, is beginning to gain attention. Nonetheless, the underlying mechanism triggering post-COVID-19 cardiovascular dysfunction remains enigmatic. Are cardiac mitochondria the key to mediating cardiac dysfunction post-severe acute respiratory syndrome coronavirus 2 (post-SARS-CoV-2) infection? Cardiovascular complications post-SARS-CoV-2 infection include myocarditis, myocardial injury, microvascular injury, pericarditis, acute coronary syndrome, and arrhythmias (fast or slow).

PLK inhibitors identified by high content phenotypic screening promote maturation of human PSC-derived cardiomyocytes.

Human pluripotent stem cells-derived cardiomyocytes (hPSC-CMs) provide an unlimited source of human cardiomyocytes for disease modeling, cell therapies, and other biomedical applications. However, hPSC-CMs remain developmentally immature which limits their suitability in translational applications. High Content Screening (HCS) is a powerful tool for identifying novel molecules and pathways regulating complex biological processes, but no HCS assay for hPSC-CM maturation has yet been reported.

Efficacy and Dosage Pattern of Sacubitril/Valsartan in Chinese Heart Failure with Reduced Ejection Fraction Patients.

This study aims to investigate the dosage pattern, efficacy, and safety of sacubitril/valsartan (Sac/Val) in Chinese heart failure with reduced ejection fraction (HFrEF) patients regarding real-world settings. Patients from 27 centers with a confirmed diagnosis of HFrEF and initiated Sac/Val treatment were enrolled. The primary objective was to evaluate the dosage pattern and change of heart failure status.

Circulating miR-19b-3p as a Novel Prognostic Biomarker for Acute Heart Failure.

Background Circulating microRNAs are emerging biomarkers for heart failure (HF). Our study aimed to assess the prognostic value of microRNA signature that is differentially expressed in patients with acute HF. Methods and Results Our study comprised a screening cohort of 15 patients with AHF and 5 controls, a PCR-discovery cohort of 50 patients with AHF and 26 controls and a validation cohort of 564 patients with AHF from registered study DRAGON-HF (Diagnostic, Risk Stratification and Prognostic Value of Novel Biomarkers in Patients With Heart Failure).

Association Between Arterial Stiffness and Heart Failure With Preserved Ejection Fraction.

Cardiovascular diseases are the leading cause of mortality in the world. Heart failure with preserved ejection fraction (HFpEF) accounts for about half of all heart failure. Unfortunately, the mechanisms of HFpEF are still unclear, leading to little progress of effective treatment of HFpEF.

Heart Failure With Mid-range Ejection Fraction: Every Coin Has Two Sides.

This review summarizes current knowledge regarding clinical epidemiology, pathophysiology, and prognosis for patients with HFmrEF in comparison to HFrEF and HFpEF. Although recommended treatments currently focus on aggressive management of comorbidities, we summarize potentially beneficial therapies that can delay the process of heart failure by blocking the pathophysiology mechanism. More studies are needed to further characterize HFmrEF and identify effective management strategies that can reduce cardiovascular morbidity and mortality of patients with HFmrEF.

Treatment of Heart Failure With Mid-Range Ejection Fraction: A Summary of Current Evidence.

Heart failure (HF) is a complex syndrome causing heavy burden in public health, and the modern objective assessment of it is based on the left ventricular ejection fraction (LVEF). In 2016, the European Society of Cardiology classified the "gray area" in HF with LVEF of 40-49% as a new HF phenotype (HFmrEF) in an attempt to uncover the specific characteristics and treatment of these patients, which might recover or worsen to HFpEF or HFrEF, respectively, or conversely from these two subtypes. Up to now, many studies have demonstrated that patients with HFmrEF would possibly gain more benefits from some targeted therapies with HFrEF than those with HFpEF.

Single-Cell Transcriptome Analysis Decipher New Potential Regulation Mechanism of ACE2 and NPs Signaling Among Heart Failure Patients Infected With SARS-CoV-2.

COVID-19 patients with comorbidities such as hypertension or heart failure (HF) are associated with poor clinical outcomes. The cellular distribution of Angiotensin-converting enzyme 2 (ACE2), the critical enzyme for SARS-CoV-2 infection, in the human heart is unknown. We explore the underlying mechanism that leads to increased susceptibility to SARS-CoV-2 in patients with cardiovascular diseases and patients of cardiac dysfunction have increased risk of multi-organ injury compared with patients of normal cardiac function.