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Aim: Determination of the phenotype of adult human atrial and ventricular myocytes based on gene expression and morphology. Methods: Atrial and ventricular cardiomyocytes were obtained from patients undergoing cardiac surgery using a modified isolation procedure. Myocytes were isolated and cultured with or without serum. The relative cell attachment promoting efficiency of several reagents was evaluated and compared. Morphological changes during long-term culture were assessed with phase contrast microscopy, morphometric analysis and immunocytochemistry or RT-PCR of sarcomeric markers including α-actinin, myosin light chain-2 (MLC-2) and the adhesion molecule, cadherin. Results: The isolation method produced viable rod-shaped atrial (16.6±6.0%, mean±S.E.; n=5) and ventricular cells (22.4±8.0%, mean±S.E.; n=5) in addition to significant numbers of apoptotic and necrotic cells. Cell dedifferentiation was characterized by the loss of sarcomeric structure, condensation and extrusion of sarcomeric proteins. Cells cultured with low serum recovered and assumed a flattened, spread form with two distinct morphologies apparent. Type I cells were large, had extensive sarcolemmal spreading, with stress fibers and nascent myofibrils, whilst type II cells appeared smaller, with more mature myofibril organisation and focal adhesions. Conclusion: Characterization of the redifferentiation capabilities of cultured adult cardiac myocytes in culture, provides an important system for comparing cardiomyocytes differentiating from human stem cells and provides the basis for an in vitro transplantation model to study interaction and communication between primary adult and stem cell-derived cardiomyocytes. [Copyright &y& Elsevier]

Aims To determine the impact of paroxysmal atrial fibrillation on quality of life and to determine the predictors of quality of life, particularly the role of symptomatology and autonomic function.Methods and Results The study group comprised 73 patients with paroxysmal atrial fibrillation (mean age 54·1 years, 51 males). On average, patients had a 3-year history of one paroxysm per week lasting 2h. Quality of life was assessed using the SF-36 (Medical Outcomes Study Short-Form Health Survey) and compared with age-matched controls. Autonomic function was assessed using Holter monitoring with analysis of heart rate variability and autonomic function tests. Symptoms during paroxysms of atrial fibrillation were also scored. Multivariate analysis was performed to identify independent predictors of quality of life. Quality of life scores were markedly lower in patients than in controls in four of the eight subscales (P<0·001): physical role function, emotional role function, vitality and general health. Structural heart disease did not predict quality of life, whereas frequency of paroxysms was predictive only of physical role function. In contrast, autonomic variables (baroreflex-sensitivity, total power (heart rate variability), response to deep breathing, 30–15 ratio (standing up)) were predictive in all four respective subscales (P<0·05), depressed vagal function being predictive of low scores. Symptoms, particularly severe perspiration, were also predictive of low scores (P<0·05).Conclusions This study shows that paroxysmal atrial fibrillation causes significant impairment of quality of life. Further, symptomatology and autonomic function are important predictors of quality of life in this patient group. [ABSTRACT FROM PUBLISHER]

As atrial fibrillation (AF) progresses from initial paroxysmal episodes to the persistent phase, maintaining sinus rhythm for an extended period through pharmacotherapy and catheter ablation becomes difficult. A major cause of the deteriorated treatment outcome is the atrial structural and electrophysiological heterogeneity, which AF itself can exacerbate. This heterogeneity exists or manifests in various dimensions, including anatomically segmental structural features, the distribution of histological fibrosis and the autonomic nervous system, sarcolemmal ion channels, and electrophysiological properties. All these types of heterogeneity are closely related to the development of AF. Recognizing the heterogeneity provides a valuable approach to comprehending the underlying mechanisms in the complex excitatory patterns of AF and the determining factors that govern the seemingly chaotic propagation. Furthermore, substrate modification based on heterogeneity is a potential therapeutic strategy. This review aims to consolidate the current knowledge on structural and electrophysiological atrial heterogeneity and its relation to the pathogenesis of AF, drawing insights from clinical studies, animal and cell experiments, molecular basis, and computer-based approaches, to advance our understanding of the pathophysiology and management of AF. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that when the cyclin D2 (CCND2), a cell-cycle regulatory protein, is overexpressed in human-induced pluripotent stem cells (hiPSCs), cardiomyocytes (CMs) differentiated from these CCND2-overexpressing hiPSCs can proliferate after transplantation into infarcted hearts, which significantly improves the cells' potency for myocardial regeneration. However, persistent CM proliferation could lead to tumor growth or the development of arrhythmogenic complications; thus, the goal of the current study was to generate a line of hiPSCs in which CCND2 overexpression could be tightly controlled. First, we transfected hiPSCs with vectors coding for a doxycycline-inducible Tet-On transactivator and S. pyogenes dCas9 fused to the VPR activation domain; then, the same hiPSCs were engineered to express guide RNAs targeting the CCND2 promotor. Thus, treatment with doxycycline (dox) activated dCas9-VPR expression, and the guide RNAs directed dCas9-VPR to the CCND2 promoter, which activated CCND2 expression. Subsequent experiments confirmed that CCND2 expression was dox-dependent in this newly engineered line of hiPSCs (doxCCND2-hiPSCs): CCND2 protein was abundantly expressed after 48 h of treatment with dox and declined to near baseline level ~96 h after dox treatment was discontinued. [ABSTRACT FROM AUTHOR]

Background: Artificial intelligence (AI) can radically change almost every aspect of the human experience. In the medical field, there are numerous applications of AI and subsequently, in a relatively short time, significant progress has been made. Cardiology is not immune to this trend, this fact being supported by the exponential increase in the number of publications in which the algorithms play an important role in data analysis, pattern discovery, identification of anomalies, and therapeutic decision making. Furthermore, with technological development, there have appeared new models of machine learning (ML) and deep learning (DP) that are capable of exploring various applications of AI in cardiology, including areas such as prevention, cardiovascular imaging, electrophysiology, interventional cardiology, and many others. In this sense, the present article aims to provide a general vision of the current state of AI use in cardiology. Results: We identified and included a subset of 200 papers directly relevant to the current research covering a wide range of applications. Thus, this paper presents AI applications in cardiovascular imaging, arithmology, clinical or emergency cardiology, cardiovascular prevention, and interventional procedures in a summarized manner. Recent studies from the highly scientific literature demonstrate the feasibility and advantages of using AI in different branches of cardiology. Conclusions: The integration of AI in cardiology offers promising perspectives for increasing accuracy by decreasing the error rate and increasing efficiency in cardiovascular practice. From predicting the risk of sudden death or the ability to respond to cardiac resynchronization therapy to the diagnosis of pulmonary embolism or the early detection of valvular diseases, AI algorithms have shown their potential to mitigate human error and provide feasible solutions. At the same time, limits imposed by the small samples studied are highlighted alongside the challenges presented by ethical implementation; these relate to legal implications regarding responsibility and decision making processes, ensuring patient confidentiality and data security. All these constitute future research directions that will allow the integration of AI in the progress of cardiology. [ABSTRACT FROM AUTHOR]

Ischemic heart disease, which is one of the top killers worldwide, encompasses a series of heart problems stemming from a compromised coronary blood supply to the myocardium. The severity of the disease ranges from an unstable manifestation of ischemic symptoms, such as unstable angina, to myocardial death, that is, the immediate life-threatening condition of myocardial infarction. Even though patients may survive myocardial infarction, the resulting ischemia-reperfusion injury triggers a cascade of inflammatory reactions and oxidative stress that poses a significant threat to myocardial function following successful revascularization. Moreover, despite evidence suggesting the presence of cardiac stem cells, the fact that cardiomyocytes are terminally differentiated and cannot significantly regenerate after injury accounts for the subsequent progression to ischemic cardiomyopathy and ischemic heart failure, despite the current advancements in cardiac medicine. In the last two decades, researchers have realized the possibility of utilizing stem cell plasticity for therapeutic purposes. Indeed, stem cells of different origin, such as bone-marrow- and adipose-derived mesenchymal stem cells, circulation-derived progenitor cells, and induced pluripotent stem cells, have all been shown to play therapeutic roles in ischemic heart disease. In addition, the discovery of stem-cell-associated paracrine effects has triggered intense investigations into the actions of exosomes. Notwithstanding the seemingly promising outcomes from both experimental and clinical studies regarding the therapeutic use of stem cells against ischemic heart disease, positive results from fraud or false data interpretation need to be taken into consideration. The current review is aimed at overviewing the therapeutic application of stem cells in different categories of ischemic heart disease, including relevant experimental and clinical outcomes, as well as the proposed mechanisms underpinning such observations. [ABSTRACT FROM AUTHOR]

Fatal hemoptysis secondary to severe pulmonary veins stenosis and fibrosing mediastinitis is an exceptional late complication of radiofrequency ablation for atrial fibrillation. We report the case of a 53-year-old male with a history of atrial fibrillation treated by radiofrequency ablation and admitted in our center 6 months after the procedure because of aggravating dyspnea and fatigability. Transthoracic echocardiography showed moderate dilation of right heart cavities, severe pulmonary hypertension and a turbulent flow in superior pulmonary veins. The cardiologist suspected pulmonary vein(s) stenosis and so cardiac computed tomography (CT) angiography was performed, with findings of severe stenosis of the right superior, right inferior and left inferior pulmonary veins, near-occlusion of the left superior pulmonary vein and the vein draining the apical segment of the right lower lobe. The CT scan also revealed soft tissue attenuation of the mediastinum posterior to the left atrium suggesting fibrosing mediastinitis together with parenchymal findings consistent with pulmonary veno-oclusive disease and an area of hemorrhagic infarction. Fatal hemoptysis occurred 3 days later, before treatment was attempted. In conclusion, severe pulmonary vein stenosis and fibrosing mediastinitis are rare but devastating complications of radiofrequency ablation. Prevention and early diagnosis are the key elements as these entities are potentially life-threatening. [ABSTRACT FROM AUTHOR]

Primary electrical heart diseases, often considered channelopathies, are inherited genetic abnormalities of cardiomyocyte electrical behavior carrying the risk of malignant arrhythmias leading to sudden cardiac death (SCD). Approximately 54% of sudden, unexpected deaths in individuals under the age of 35 do not exhibit signs of structural heart disease during autopsy, suggesting the potential significance of channelopathies in this group of age. Channelopathies constitute a highly heterogenous group comprising various diseases such as long QT syndrome (LQTS), short QT syndrome (SQTS), idiopathic ventricular fibrillation (IVF), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), and early repolarization syndromes (ERS). Although new advances in the diagnostic process of channelopathies have been made, the link between a disease and sudden cardiac death remains not fully explained. Evolving data in electrophysiology and genetic testing suggest previously described diseases as complex with multiple underlying genes and a high variety of factors associated with SCD in channelopathies. This review summarizes available, well-established information about channelopathy pathogenesis, genetic basics, and molecular aspects relative to principles of the pathophysiology of arrhythmia. In addition, general information about diagnostic approaches and management is presented. Analyzing principles of channelopathies and their underlying causes improves the understanding of genetic and molecular basics that may assist general research and improve SCD prevention. [ABSTRACT FROM AUTHOR]

Unlimited access to ECGs using an over-the-counter smartwatch constitutes a real revolution for our discipline, and the application is rapidly expanding to include patients with cardiac implantable electronic devices (CIEDs) such as pacemakers (PMs) and implantable cardioverter defibrillators (ICDs). CIEDs require periodic evaluation and adjustment by healthcare professionals. In addition, implanted patients often present with symptoms that may be related to their PMs or ICDs. An ECG smartwatch could reveal information about device functioning, confirm normal device function, or aid in the case of device troubleshooting. In this review, we delve into the available evidence surrounding smartwatches with ECG registration and their integration into the care of patients with implanted pacemakers and ICDs. We explore safety considerations and the benefits and limitations associated with these wearables, drawing on relevant studies and case series from our own experience. By analyzing the current landscape of this emerging technology, we aim to provide a comprehensive overview that facilitates informed decision-making for both healthcare professionals and patients. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) in children is a devastating event, often linked to primary electrical diseases (PED) of the heart. PEDs, often referred to as channelopathies, are a group of genetic disorders that disrupt the normal ion channel function in cardiac cells, leading to arrhythmias and sudden cardiac death. This paper investigates the unique challenges of risk assessment and stratification for channelopathy-related SCD in pediatric patients—Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, idiopathic ventricular fibrillation, long QT syndrome, Anderson–Tawil syndrome, short QT syndrome, and early repolarization syndrome. We explore the intricate interplay of genetic, clinical, and electrophysiological factors that contribute to the complex nature of these conditions. Recognizing the significance of early identification and tailored management, this paper underscores the need for a comprehensive risk stratification approach specifically designed for pediatric populations. By integrating genetic testing, family history, and advanced electrophysiological evaluation, clinicians can enhance their ability to identify children at the highest risk for SCD, ultimately paving the way for more effective preventive strategies and improved outcomes in this vulnerable patient group. [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with reduced quality of life and earlier mortality, but its pathogenesis and key genes are still unclear. In this investigation, bioinformatics was used to deeply analyze the pathogenesis of IPF and related key genes, so as to investigate the potential molecular pathogenesis of IPF and provide guidance for clinical treatment. Next-generation sequencing dataset GSE213001 was obtained from Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were identified between IPF and normal control group. The DEGs between IPF and normal control group were screened with the DESeq2 package of R language. The Gene Ontology (GO) and REACTOME pathway enrichment analyses of the DEGs were performed. Using the g:Profiler, the function and pathway enrichment analyses of DEGs were performed. Then, a protein–protein interaction (PPI) network was constructed via the Integrated Interactions Database (IID) database. Cytoscape with Network Analyzer was used to identify the hub genes. miRNet and NetworkAnalyst databaseswereused to construct the targeted microRNAs (miRNAs), transcription factors (TFs), and small drug molecules. Finally, receiver operating characteristic (ROC) curve analysis was used to validate the hub genes. A total of 958 DEGs were screened out in this study, including 479 up regulated genes and 479 down regulated genes. Most of the DEGs were significantly enriched in response to stimulus, GPCR ligand binding, microtubule-based process, and defective GALNT3 causes HFTC. In combination with the results of the PPI network, miRNA-hub gene regulatory network and TF-hub gene regulatory network, hub genes including LRRK2, BMI1, EBP, MNDA, KBTBD7, KRT15, OTX1, TEKT4, SPAG8, and EFHC2 were selected. Cyclothiazide and rotigotinethe are predicted small drug molecules for IPF treatment. Our findings will contribute to identification of potential biomarkers and novel strategies for the treatment of IPF, and provide a novel strategy for clinical therapy. [ABSTRACT FROM AUTHOR]

Over the last decades, the relevance of genetics in cardiovascular diseases has expanded, especially in the context of cardiomyopathies. Its relevance extends to the management of patients diagnosed with heart failure (HF), given its capacity to provide invaluable insights into the etiology of cardiomyopathies and identify individuals at a heightened risk of poor outcomes. Notably, the identification of an etiological genetic variant necessitates a comprehensive evaluation of the family lineage of the affected patients. In the future, these genetic variants hold potential as therapeutic targets with the capability to modify gene expression. In this complex setting, collaboration among cardiologists, specifically those specializing in cardiomyopathies and HF, and geneticists becomes paramount to improving individual and family health outcomes, as well as therapeutic clinical results. This review is intended to offer geneticists and cardiologists an updated perspective on the value of genetic research in HF and its implications in clinical practice. [ABSTRACT FROM AUTHOR]

The reliable operation of power transmission networks depends on the timely detection and localization of faults. Fault classification and localization in electricity transmission networks can be challenging because of the complicated and dynamic nature of the system. In recent years, a variety of machine learning (ML) and deep learning algorithms (DL) have found applications in the enhancement of fault identification and classification within power transmission networks. Yet, the efficacy of these ML architectures is profoundly dependent upon the abundance and quality of the training data. This intellectual explanation introduces an innovative strategy for the classification and pinpointing of faults within power transmission networks. This is achieved through the utilization of variational autoencoders (VAEs) to generate synthetic data, which in turn is harnessed in conjunction with ML algorithms. This approach encompasses the augmentation of the available dataset by infusing it with synthetically generated instances, contributing to a more robust and proficient fault recognition and categorization system. Specifically, we train the VAE on a set of real-world power transmission data and generate synthetic fault data that capture the statistical properties of real-world data. To overcome the difficulty of fault diagnosis methodology in three-phase high voltage transmission networks, a categorical boosting (Cat-Boost) algorithm is proposed in this work. The other standard machine learning algorithms recommended for this study, including Support Vector Machine (SVM), Decision Trees (DT), Random Forest (RF), and K-Nearest Neighbors (KNN), utilizing the customized version of forward feature selection (FFS), were trained using synthetic data generated by a VAE. The results indicate exceptional performance, surpassing current state-of-the-art techniques, in the tasks of fault classification and localization. Notably, our approach achieves a remarkable 99% accuracy in fault classification and an extremely low mean absolute error (MAE) of 0.2 in fault localization. These outcomes represent a notable advancement compared to the most effective existing baseline methods. [ABSTRACT FROM AUTHOR]

The abnormal neural control of atria has been considered one of the mechanisms of paroxysmal atrial fibrillation (PAF) pathogenesis. The baroreceptor reflex has an important role in cardiovascular regulation and may serve as an index of autonomic function. This study aimed to analyze the baroreceptor reflex's role in heart rate regulation during upright tilt (HUT) in patients with lone PAF. The study included 68 patients with lone PAF and 34 healthy individuals who underwent baroreflex assessment. Parameters such as baroreflex sensitivity (BRS), number of systolic blood pressure (BP) ramps, and the baroreflex effectiveness index (BEI) were evaluated. The study found that PAF patients had comparable resting BPs and heart rates (HRs) to healthy individuals. However, unlike healthy individuals, PAF patients showed a sustained increase in BP with an upright posture followed by the delayed activation of the baroreceptor function with a blunted HR response and lower BEI values. This indicates a pronounced baroreflex impairment in PAF patients, even at rest. Our data suggest that together with BRS, BEI could be used as a marker of autonomic dysfunction in PAF patients, making it important to further investigate its relationship with AF recurrence after ablation and its involvement in cardiovascular autonomic remodeling. [ABSTRACT FROM AUTHOR]

Heart rhythm disorders, arrhythmias, place a huge economic burden on society and have a large impact on the quality of life of a vast number of people. Arrhythmias can have genetic causes but primarily arise from heart tissue remodeling during aging or heart disease. As current therapies do not address the causes of arrhythmias but only manage the symptoms, it is of paramount importance to generate innovative test models and platforms for gaining knowledge about the underlying disease mechanisms which are compatible with drug screening. In this review, we outline the most important features of atrial fibrillation (AFib), the most common cardiac arrhythmia. We will discuss the epidemiology, risk factors, underlying causes, and present therapies of AFib, as well as the shortcomings and opportunities of current models for cardiac arrhythmia, including animal models, in silico and in vitro models utilizing human pluripotent stem cell (hPSC)-derived cardiomyocytes. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is a prevalent cardiac condition predominantly affecting older adults, characterized by irregular heartbeat rhythm. The condition often leads to significant disability and increased mortality rates. Traditionally, two therapeutic strategies have been employed for its treatment: heart rate control and rhythm control. Recent clinical studies have emphasized the critical role of early restoration of sinus rhythm in improving patient outcomes. The persistence of the irregular rhythm allows for the progression and structural remodeling of the atria, eventually leading to irreversible stages, as observed clinically when AF becomes permanent. Cardioversion to sinus rhythm alters this progression pattern through mechanisms that are still being studied. In this review, we provide an in-depth analysis of the pathophysiological mechanisms responsible for maintaining AF and how they are modified during sinus rhythm restoration using existing therapeutic strategies at different stages of clinical investigation. Moreover, we explore potential future therapeutic approaches, including the promising prospect of gene therapy. [ABSTRACT FROM AUTHOR]

Cardiac regeneration is a critical endeavor in the treatment of heart diseases, aimed at repairing and enhancing the structure and function of damaged myocardium. This review offers a comprehensive overview of current advancements and strategies in cardiac regeneration, with a specific focus on regenerative medicine and tissue engineering-based approaches. Stem cell-based therapies, which involve the utilization of adult stem cells and pluripotent stem cells hold immense potential for replenishing lost cardiomyocytes and facilitating cardiac tissue repair and regeneration. Tissue engineering also plays a prominent role employing synthetic or natural biomaterials, engineering cardiac patches and grafts with suitable properties, and fabricating upscale bioreactors to create functional constructs for cardiac recovery. These constructs can be transplanted into the heart to provide mechanical support and facilitate tissue healing. Additionally, the production of organoids and chips that accurately replicate the structure and function of the whole organ is an area of extensive research. Despite significant progress, several challenges persist in the field of cardiac regeneration. These include enhancing cell survival and engraftment, achieving proper vascularization, and ensuring the long-term functionality of engineered constructs. Overcoming these obstacles and offering effective therapies to restore cardiac function could improve the quality of life for individuals with heart diseases. [ABSTRACT FROM AUTHOR]

Performing repeated pulmonary vein isolation (re-PVI) after recurrent atrial fibrillation (AF) following prior PVI is a standard procedure. However, no consensus exists regarding the most effective approach in redo procedures. We assessed the efficacy of re-PVI using wide antral circumferential re-ablation (WACA) supported by high-density electroanatomical mapping (HDM) as compared to conventional re-PVI. Consecutive patients with AF recurrences showing true PV reconnection (residual intra-PV and PV antral electrical potentials within the initial ablation line) or exclusive PV antral potentials (without intra-PV potentials) in the redo procedure were prospectively enrolled and received HDM-guided WACA (Re-WACA group). Conventional re-PVI patients treated using pure ostial gap ablation guided by a circular mapping catheter served as a historical control (Re-PVI group). Patients with durable PVI and no antral PV potentials were excluded. Arrhythmia recurrences ≥30 s were calculated as recurrences. In total, 114 patients were investigated (Re-WACA: n = 56, 68 ± 10 years, Re-PVI: n = 58, 65 ± 10 years). There were no significant differences in clinical characteristics including the AF type or the number of previous PVIs. In the Re-WACA group, 11% of patients showed electrical potentials only in the antrum but not inside any PV. At 402 ± 71 days of follow-up, the estimated freedom from arrhythmia was 89% in the Re-WACA group and 69% in the Re-PVI group (p = 0.01). Re-WACA independently predicted arrhythmia-free survival (HR = 0.39, 95% CI 0.16–0.93, p = 0.03), whereas two previous PVI procedures predicted recurrences (HR = 2.35, 95% CI 1.20–4.46, p = 0.01). The Re-WACA strategy guided by HDM significantly improved arrhythmia-free survival as compared to conventional ostial re-PVI. Residual PV antral potentials after prior PVI are frequent and can be easily visualized by HDM. [ABSTRACT FROM AUTHOR]

Simple Summary: First-line treatment for restoring and maintaining sinus rhythm in patients with symptomatic atrial fibrillation (AF) involves the use of antiarrhythmic drugs. However, these are associated with significant side effects and have limited success rates in terminating AF episodes. In contrast, catheter ablation has been shown to be superior in maintaining sinus rhythm and improving the quality of life of AF patients. These procedures can also be performed via a hybrid set-up involving a minimally invasive surgical approach. These options have shown promise in restoring and maintaining sinus rhythm but are not without risks. Therefore, further studies investigating different ablative strategies are needed. Catheter ablation has been shown to be more effective at maintaining sinus rhythm and improving quality of life when compared to antiarrhythmic drugs. Radiofrequency and cryoablation are two effective methods. However, catheter-only ablation strategies have not consistently produced high success rates in treating longstanding and persistent AF patients. The emerging treatment of choice for such cases is hybrid ablation, which involves a multidisciplinary and minimally invasive approach to achieve surgical ablation of the direct posterior left atrial wall in combination with endocardial catheter ablation. Studies have shown promising results for the hybrid approach when compared with catheter ablation alone, but it is not without risks. Large and randomised studies are necessary to further evaluate these strategies for managing AF. [ABSTRACT FROM AUTHOR]

The electrocardiogram (ECG), considered by some diagnosticians of cardiovascular diseases to be a slightly anachronistic tool, has acquired a completely new face and importance thanks to its three modern features: the digital form of recording, its very frequent use, and the possibility of processing thousands of records by artificial intelligence (AI). In this review of the literature on this subject from the first 3 months of 2023, the use of many types of software for extracting new information from the ECG is described. These include, among others, natural language processing, backpropagation neural network and convolutional neural network. AI tools of this type allow physicians to achieve high accuracy not only in ECG-based predictions of the patient's age or sex but also of the abnormal structure of heart valves, abnormal electrical activity of the atria, distorted immune response after transplantation, good response to resynchronization therapy and an increased risk of sudden cardiac death. The attractiveness of the presented results lies in the simplicity of the examination by the staff, relatively low costs and even the possibility of performing the examination remotely. The twelve studies presented here are just a fraction of the novelties that the current year will bring. [ABSTRACT FROM AUTHOR]

In this study, we sought to investigate the occurrence of appropriate implantable cardioverter-defibrillator (ICD) therapies and inappropriate shocks in secondary prevention ICD recipients with ventricular arrhythmia of unclear cause and ventricular arrhythmia in the context of underlying heart disease. In this retrospective study, consecutive patients with an ICD implanted for secondary prevention in the University Medical Center Groningen (UMCG), the Netherlands between 1 January 2012 and 31 December 2018 were included. Patients were classified as having ventricular arrhythmia of unclear cause if no clear cause was found which could explain the index ventricular arrhythmia. The primary outcome was appropriate ICD therapy. The study population consisted of 257 patients. In 220 patients, an underlying heart disease could be identified as the cause of ventricular arrhythmia, while 37 patients had an unclear cause of ventricular arrhythmia. The median age was 64 years (interquartile range (IQR) 53–72 years). Forty-five (18%) patients were women. During a median duration of follow-up of 6.2 years (IQR 4.8–7.8 years), appropriate ICD therapy occurred in 95 (37%) patients. This number was 90 (41%) in the group with a clear etiology and 5 (14%) in the group with an unclear etiology. In multivariable analysis, index ventricular arrhythmia of unclear cause was associated with fewer appropriate ICD therapies (HR 0.37 [95% CI 0.14–0.99]; p = 0.048), as well as an increased risk of inappropriate ICD shocks (HR 3.71 [95% CI 1.17–11.80]; p = 0.026). Index ventricular arrhythmia of unclear cause was significantly associated with fewer appropriate ICD therapies. [ABSTRACT FROM AUTHOR]

Maintenance of normal cardiac rhythm requires coordinated activity of ion channels and transporters that allow well-ordered propagation of electrical impulses across the myocardium. Disruptions in this orderly process provoke cardiac arrhythmias that may be lethal in some patients. Risk of common acquired arrhythmias is increased markedly when structural heart disease caused by myocardial infarction (due to fibrotic scar formation) or left ventricular dysfunction is present. Genetic polymorphisms influence structure or excitability of the myocardial substrate, which increases vulnerability or risk of arrhythmias in patients. Similarly, genetic polymorphisms of drug-metabolizing enzymes give rise to distinct subgroups within the population that affect specific drug biotransformation reactions. Nonetheless, identification of triggers involved in initiation or maintenance of cardiac arrhythmias remains a major challenge. Herein, we provide an overview of knowledge regarding physiopathology of inherited and acquired cardiac arrhythmias along with a summary of treatments (pharmacologic or non-pharmacologic) used to limit their effect on morbidity and potential mortality. Improved understanding of molecular and cellular aspects of arrhythmogenesis and more epidemiologic studies (for a more accurate portrait of incidence and prevalence) are crucial for development of novel treatments and for management of cardiac arrhythmias and their consequences in patients, as their incidence is increasing worldwide. [ABSTRACT FROM AUTHOR]

Preterm birth is a risk factor for cardiometabolic disease. The preterm heart before terminal differentiation is in a phase that is crucial for the number and structure of cardiomyocytes in further development, with adverse effects of hypoxic and hyperoxic events. Pharmacological intervention could attenuate the negative effects of oxygen. Dexmedetomidine (DEX) is an α2-adrenoceptor agonist and has been mentioned in connection with cardio-protective benefits. In this study, H9c2 myocytes and primary fetal rat cardiomyocytes (NRCM) were cultured for 24 h under hypoxic condition (5% O2), corresponding to fetal physioxia (pO2 32–45 mmHg), ambient oxygen (21% O2, pO2 ~150 mmHg), or hyperoxic conditions (80% O2, pO2 ~300 mmHg). Subsequently, the effects of DEX preconditioning (0.1 µM, 1 µM, 10 µM) were analyzed. Modulated oxygen tension reduced both proliferating cardiomyocytes and transcripts (CycD2). High-oxygen tension induced hypertrophy in H9c2 cells. Cell-death-associated transcripts for caspase-dependent apoptosis (Casp3/8) increased, whereas caspase-independent transcripts (AIF) increased in H9c2 cells and decreased in NRCMs. Autophagy-related mediators (Atg5/12) were induced in H9c2 under both oxygen conditions, whereas they were downregulated in NRCMs. DEX preconditioning protected H9c2 and NRCMs from oxidative stress through inhibition of transcription of the oxidative stress marker GCLC, and inhibited the transcription of both the redox-sensitive transcription factors Nrf2 under hyperoxia and Hif1α under hypoxia. In addition, DEX normalized the gene expression of Hippo-pathway mediators (YAP1, Tead1, Lats2, Cul7) that exhibited abnormalities due to differential oxygen tensions compared with normoxia, suggesting that DEX modulates the activation of the Hippo pathway. This, in the context of the protective impact of redox-sensitive factors, may provide a possible rationale for the cardio-protective effects of DEX in oxygen-modulated requirements on survival-promoting transcripts of immortalized and fetal cardiomyocytes. [ABSTRACT FROM AUTHOR]

Introduction. Atrial fibrillation (AF) is more prevalent in men than in women. However, women with AF are more symptomatic, have a worse quality of life, a higher stroke risk and may therefore benefit most from ablation. In this study we aim to identify the risk of recurrent AF after thoracoscopic ablation, and assess the differential impact of the risk factors for recurrence between women and men. Method. This is a single center cohort study, including patients undergoing thoracoscopic ablation for advanced AF between 2008 and 2019. All patients were clinically followed up for two years with quarterly 24 h Holter monitoring and ECGs for the detection of recurrent AF. Left atrial appendage (LAA) tissue was collected for collagen analysis. Results. We included 571 patients, of whom 143 (25%) were women. Women were older than men (63 ± 8.3 y vs. 59 ± 8.5, p < 0.001), but had fewer cardiovascular risk factors, myocardial infarctions (1.4% vs. 6.5%, p = 0.03) and, in particular, vascular disease (7.0% vs. 16.1%, p = 0.01). Women suffered more from AF recurrence, driven by more atrial tachycardias, and sex was an independent risk factor for recurrence (HR1.41 [1.04–1.91], p = 0.028]). The presence of vascular disease was associated with an increased risk for AF recurrence in women, but not in men. In LAA histology, women had more collagen than men, as had patients with persistent compared to paroxysmal AF. Conclusion. Women had 15% more recurrences, driven by more atrial tachycardias, which may be explained by a more fibrotic atrial substrate. What's new? Women undergoing thoracoscopic AF ablation have a higher risk of recurrent AF, driven by more atrial tachycardias. Among patients with left atrial enlargement or persistent AF, women have worse outcomes than men. Vascular disease was a risk factor for recurrence in women, but not in men. In a histopathologic analysis of the left atrial appendage, women had more collagen than men, as had patients with persistent compared to paroxysmal AF. [ABSTRACT FROM AUTHOR]

Arrhythmogenic cardiomyopathy (ACM) is largely an autosomal dominant genetic disorder manifesting fibrofatty infiltration and ventricular arrhythmia with predominantly right ventricular involvement. ACM is one of the major conditions associated with an increased risk of sudden cardiac death, most notably in young individuals and athletes. ACM has strong genetic determinants, and genetic variants in more than 25 genes have been identified to be associated with ACM, accounting for approximately 60% of ACM cases. Genetic studies of ACM in vertebrate animal models such as zebrafish (Danio rerio), which are highly amenable to large-scale genetic and drug screenings, offer unique opportunities to identify and functionally assess new genetic variants associated with ACM and to dissect the underlying molecular and cellular mechanisms at the whole-organism level. Here, we summarize key genes implicated in ACM. We discuss the use of zebrafish models, categorized according to gene manipulation approaches, such as gene knockdown, gene knock-out, transgenic overexpression, and CRISPR/Cas9-mediated knock-in, to study the genetic underpinning and mechanism of ACM. Information gained from genetic and pharmacogenomic studies in such animal models can not only increase our understanding of the pathophysiology of disease progression, but also guide disease diagnosis, prognosis, and the development of innovative therapeutic strategies. [ABSTRACT FROM AUTHOR]