Peripartum cardiomyopathy is an idiopathic and nonischemic systolic dysfunction with onset toward the end of pregnancy and up to 5months postpartum. Its clinical phenotype overlaps with pregnancy-associated cardiomyopathy rendering both a continuum of the same disease. Incidence varies geographically and is highest in areas where risk factors are prevalent. The understanding of its pathophysiology is constantly evolving, but a proposed two-hit model of dysfunctional vasculogenesis and genetic predisposition exacerbated by the hemodynamic stressors of pregnancy is widely accepted. The catalysis of the cleavage of prolactin into an anti-angiogenic fragment provoked by unbalanced oxidative stress forms the bedrock of its pathogenesis. Furthermore, miRNA signaling, placenta-produced factors, and a potential underlying genetic susceptibility convene to disrupt cardiac and endothelial metabolic homeostasis. The role of anti-adrenergic and anti-sarcomeric antibodies, nutritional deficiency, and mutated viral cardiotropes are understudied. There are limited randomized controlled trials for disease-specific drugs; however, most trials are targeted at the D2 receptor agonist bromocriptine. Positive primary endpoints in a large German clinical trial led to its approved use in Europe, but the U.S.A. still renders it experimental with ongoing trials evaluating its long-term efficacy and safety. Despite its popularity since the 1900s, multiple gaps in evidence regarding long-term management after myocardial recovery, management of subsequent pregnancies, optimal anticoagulation strategy, and alternative pathophysiological pathways remain unknown.

Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease, affecting 1:200 to 1:500 individuals worldwide. Guidelines on the diagnosis and management of HCM have been recently published by the European Society of Cardiology (ESC) and American societies. The ESC guidelines cover a broad range of cardiomyopathies, including HCM, with 119 recommendations, whereas the American guidelines focus exclusively on HCM with 141 specific recommendations. Both guidelines emphasize a comprehensive diagnostic approach, including imaging and genetic testing, but differ in some specific aspects. For example, sudden cardiac death (SCD) risk assessment is a primary point of divergence. The ESC guidelines advocate for the use of a validated Risk-SCD calculator, while the American guidelines rely on specific risk markers for individualized risk evaluation. Management strategies also vary: both guidelines prioritize beta-blockers and calcium channel blockers in patients with resting or provocable left ventricular outflow tract (LVOT) obstruction. If beta-blockers (or verapamil/diltiazem) are ineffective, either disopyramide or the myosin inhibitor mavacamten may be an option with slightly different indications among the two guidelines. Septal reduction therapy is recommended in ESC guidelines for symptomatic patients with significant LVOT gradients, while American guidelines suggest earlier myectomy for certain clinical factors and emphasize shared decision-making. The ESC guidelines recommend sequential atrioventricular pacing and dual-chamber defibrillators for reducing LVOT gradients. The American guidelines focus on genetic testing for risk assessment and suggest periodic cardiac magnetic resonance imaging. This paper provides a detailed comparison of these guidelines, highlighting key differences and areas needing further research and expert debate.

Heart failure with preserved ejection fraction (HFpEF) presents a challenge in clinical practice due to its complexity and impact on morbidity and mortality. The aim of this systematic review and meta-analysis (SR/MA) was to evaluate the value of B-Type Natriuretic Peptide (BNP) and NT-proBNP in predicting overall adverse outcomes, cardiovascular events, and mortality, in patients with HFpEF. This SR/MA included observational studies and randomized controlled trials (RCTs) that reported the use of BNP and NT-proBNP as prognostic biomarkers for adverse outcomes in HFpEF patients. A comprehensive literature search was conducted using PubMed, EMBASE, and Google, without language restrictions, from inception until June 2024. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. The quality and risk of bias of the included studies were assessed using the Newcastle-Ottawa Scale (NOS). Twenty-two studies involving 10,158 HFpEF patients were included. The analysis showed that BNP is a significant predictor of overall adverse events in HFpEF patients, with an overall HR of 1.34 (95% CI: 1.20-1.52). Similarly, BNP was a significant predictor of cardiovascular events and mortality in HFpEF patients with a HR of 1.36 (95% CI 1.12-1.64) and HR of 1.44 (95% CI: 1.04-1.84), respectively. When analyzing data for NT-proBNP predictive potential, 3 studies confirmed that NT-proBNP is a significant independent prognostic indicator for adverse events, with an overall HR of 1.80 (95% CI: 1.38-2.35). Comparable results were seen for mortality, with higher NT-proBNP levels associated with increased mortality risk and the MA showing a HR of 1.65 (95% CI: 1.55-1.76). This systematic review highlights the valuable prognostic role of BNP and NT-proBNP in predicting overall adverse outcome, cardiovascular events, and mortality in HFpEF patients. Our findings underscore the importance of further research to establish standardized thresholds and investigate BNP and NT-proBNP's potential in predicting morbidity and mortality.

Heart failure with preserved ejection fraction (HFpEF) is rapidly growing as the most common form of heart failure. Among HFpEF phenotypes, the cardiometabolic/obese HFpEF — HFpEF driven by cardiometabolic alterations — emerges as one of the most prevalent forms of this syndrome and the one on which recent therapeutic success have been made. Indeed, pharmacological approaches with sodium-glucose cotransporter type 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) have proved to be effective due to metabolic protective effects. Similarly, lifestyle changes, including diet and exercise are crucial in HFpEF management. Increasing evidence supports the important role of diet and physical activity in the pathogenesis, prognosis, and potential reversal of HFpEF. Metabolic derangements and systemic inflammation are key features of HFpEF and represent the main targets of lifestyle interventions. However, the underlying mechanisms of the beneficial effects of these interventions in HFpEF are incompletely understood. Hence, there is an unmet need of tailored lifestyle intervention modalities for patients with HFpEF. Here we present the current available evidence on lifestyle interventions in HFpEF management and therapeutics, discussing their modalities and potential mechanisms.

The latest guidelines advocate for catheter ablation (CA) over standard medical therapy (SMT) for managing atrial fibrillation (AF) in patients with heart failure with reduced ejection fraction (HFrEF). However, significant knowledge gaps exist regarding the effectiveness of CA vs. SMT in patients with heart failure with preserved ejection fraction (HFpEF). PubMed, Scopus, and Embase until February 2024 were systematically searched. Given the limited number of randomized studies, propensity score-matched observational studies comparing CA with SMT in AF patients with HFpEF were also included. The primary outcome was a composite endpoint of all-cause mortality and HF hospitalization. Eight studies that enrolled 17,717 SMT and 2537 CA patients were included. CA was associated with a significantly lower risk of the composite endpoint of all-cause mortality and HF hospitalization (HR 0.61; 95% CI, 0.43-0.85). The risk of HF hospitalization (HR 0.44; 95% CI, 0.23-0.83), cardiovascular mortality (HR 0.43; 95% CI, 0.22-0.84), and AF recurrence (HR 0.53; 95% CI, 0.39-0.73) were also lower in the CA group. CA demonstrated significant cardiovascular morbidity and mortality benefits compared to SMT in the HFpEF population.

Heart failure (HF) is a significant global concern, impacting patient morbidity, mortality, and healthcare costs. Guideline-directed medical therapy and various preventive measures have proven effective in improving clinical outcomes and reducing HF hospitalizations. Recent data indicates that remote HF monitoring facilitates early detection of HF decompensation by observing upstream events and parameters before clinical signs and symptoms manifest. Moreover, these innovative devices have been shown to decrease unnecessary HF hospitalizations and, in some cases, provide predictive insights before an actual HF incident. In this review, we aim to explore the data regarding smart scales and digital biomarkers and summarize both FDA-approved devices and emerging technologies by assessing their clinical utility, mechanism of HF decompensation detection, and ongoing trials. Furthermore, we also discuss the future trend of integrating these devices into routine clinical practice to improve patient clinical outcomes.

Heart failure (HF) is considered one of a leading cause of cardiovascular morbidity and mortality worldwide. The association between HF and venous thromboembolism (VTE) has been reported in several studies owing to many physiological and thromboembolic risk factors. Thus, the need for extended thromboprophylaxis during the post-discharge period in HF patients has been evaluated. Most guidelines do not recommend extended thromboprophylaxis because of its uncertain benefits and increased risk of bleeding. However, recent evidence in HF patients revealed no increased risk of bleeding with extended thromboprophylaxis, which highlights the importance of identifying ideal candidates who might benefit from extended thromboprophylaxis. Several risk assessment models (RAMs) have been developed to identify patients at a high risk of VTE who would benefit from in-hospital and post-discharge prophylactic anticoagulation therapy based on the risk-benefit principle. However, their accuracy in predicting VTE is questionable, and none have a standardized approach for evaluating the risk of VTE in HF patients. In this review, we provided an overview of the incidence and pathophysiology of VTE in HF patients, a summary of guideline recommendations for VTE prevention, and a summary of studies evaluating the use of extended thromboprophylaxis, with a focus on subgroup or post-hoc analyses of HF patients. We also discussed the need to design an ideal RAM that can identify candidate patients for extended thromboprophylaxis by stratifying the risk of VTE and identifying the key risk factors for bleeding in medically ill patients, including those with HF.

Cancer is the leading cause of death worldwide, and the number of cancer-related deaths is expected to increase. Common types of cancer include skin, breast, lung, prostate, and colorectal cancers. While clinical research has improved cancer therapies, these treatments often come with significant side effects such as chronic fatigue, hair loss, and nausea. In addition, cancer treatments can cause long-term cardiovascular complications. Doxorubicin (DOX) therapy is one example, which can lead to decreased left ventricle (LV) echocardiography (ECHO) parameters, increased oxidative stress in cellular level, and even cardiac fibrosis. The apelinergic system, specifically apelin and its receptor, together, has shown properties that could potentially protect the heart and mitigate the damages caused by DOX anti-cancer treatment. Studies have suggested that stimulating the apelinergic system may have therapeutic benefits for heart damage induced by DOX. Further research in chronic preclinical models is needed to confirm this hypothesis and understand the mechanism of action for the apelinergic system. This review aims to collect and present data on the effects of the apelinergic system on doxorubicin-induced cardiotoxicity.

Cardiac disorders exhibit considerable heterogeneity, and understanding their genetic foundations is crucial for their diagnosis and treatment. Recent genetic analyses involving a growing number of participants have uncovered novel mutations within both coding and non-coding regions of DNA, contributing to the onset of cardiac conditions. The NEXN gene, encoding the Nexilin protein, an actin filament-binding protein, is integral to normal cardiac function. Mutations in this gene have been linked to cardiomyopathies, cardiovascular disorders, and sudden deaths. Heterozygous or homozygous variants of the NEXN gene are associated with the development of endocardial fibroelastosis (EFE), a rare cardiac condition characterized by excessive collagen and elastin deposition in the left ventricular endocardium predominantly affecting infants and young children. EFE occurs both primary and secondary to other conditions and often leads to unfavorable prognoses and outcomes. This review explores the role of NEXN genetic variants in cardiovascular disorders, particularly EFE, revealing that functional mutations are not clustered in a specific domain of Nexilin based on the cardiac disorder phenotype. Our review underscores the importance of understanding genetic mutations for the diagnosis and treatment of cardiac conditions.

Heart failure imposes a significant global health burden, standing as a primary contributor to mortality. Various indicators and physiological shifts within the body may hint at distinct cardiac conditions. Specific biosensors have the capability to identify these changes. Integrating or embedding these biosensors into mechanical circulatory support devices (MCSDs), such as left ventricular assist devices (LVADs), becomes crucial for monitoring alterations in biochemical and physiological factors subsequent to an MCSD implantation. Detecting abnormal changes early in the course of disease progression will allow for improved patient outcomes and prognosis following an MCSD implantation. The aim of this review is to explore the available biosensors that may be coupled or implanted alongside LVADs to monitor biomarkers and changes in physiological parameters. Different fabrication materials for the biosensors are discussed, including their advantages and disadvantages. This review also examines the feasibility of integrating feedback control mechanisms into LVAD systems using data from the biosensors. Challenges facing this emerging technology and future directions for research and development are outlined as well. The overarching goal is to provide an overview of how implanted biosensors may improve the performance and outcomes of LVADs through continuous monitoring and closed-loop control.Graphical