Development Of Heart Failure Research Articles

Heart Failure in Diabetes Mellitus: the Pathogenesis and Treatment

People with diabetes mellitus are more likely to develop heart failure, and those with both conditions often experience a worse prognosis compared to heart failure patients without diabetes. This paper will summarize the pathogenesis of diabetic heart failure and propose treatment and prevention options for diabetic patients with heart failure based on the existing literature and data results. Both types of diabetes lead to high blood sugar levels, which, along with diabetes itself, exert different effects on the heart. As time goes on, it causes heart failure. The outcome demonstrates how chronically elevated blood sugar levels can lead to inflammation and accelerate the development of heart failure. Significant roles are also played by oxidative damage, insulin resistance, and other variables. It has been demonstrated that altering one's lifestyle can avoid diabetic heart failure and improve the quality of life for individuals with asymptomatic diastolic dysfunction and heart failure with preserved ejection fraction (HFpEF).

Calcific aortic stenosis: omics-based target discovery and therapy development.

Calcific aortic valve disease (CAVD) resulting in aortic stenosis (AS) is the most common form of valvular heart disease, affecting 2% of those over age 65. Those who develop symptomatic severe AS have an average further lifespan of <2 years without valve replacement, and three-quarters of these patients will develop heart failure, undergo valve replacement, or die within 5 years. There are no approved pharmaceutical therapies for AS, due primarily to a limited understanding of the molecular mechanisms that direct CAVD progression in the complex haemodynamic environment. Here, advances in efforts to understand the pathogenesis of CAVD and to identify putative drug targets derived from recent multi-omics studies [including (epi)genomics, transcriptomics, proteomics, and metabolomics] of blood and valvular tissues are reviewed. The recent explosion of single-cell omics-based studies in CAVD and the pathobiological and potential drug discovery insights gained from the application of omics to this disease area are a primary focus. Lastly, the translation of knowledge gained in valvular pathobiology into clinical therapies is addressed, with a particular emphasis on treatment regimens that consider sex-specific, renal, and lipid-mediated contributors to CAVD, and ongoing Phase I/II/III trials aimed at the prevention/treatment of AS are described.

Pathophysiology of Angiotensin II-Mediated Hypertension, Cardiac Hypertrophy, and Failure: A Perspective from Macrophages.

Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among the various regulatory systems that impact on these heterogeneous pathological processes, angiotensin II (Ang II)-activated macrophages play a pivotal role in the induction of subcellular defects and cardiac adverse remodeling during the progression of heart failure. Ang II stimulates macrophages via its AT1 receptor to release oxygen-free radicals, cytokines, chemokines, and other inflammatory mediators in the myocardium, and upregulates the expression of integrin adhesion molecules on both monocytes and endothelial cells, leading to monocyte-endothelial cell-cell interactions. The transendothelial migration of monocyte-derived macrophages exerts significant biological effects on the proliferation of fibroblasts, deposition of extracellular matrix proteins, induction of perivascular/interstitial fibrosis, and development of hypertension, cardiac hypertrophy and heart failure. Inhibition of macrophage activation using Ang II AT1 receptor antagonist or depletion of macrophages from the peripheral circulation has shown significant inhibitory effects on Ang II-induced vascular and myocardial injury. The purpose of this review is to discuss the current understanding in Ang II-induced maladaptive cardiac remodeling and dysfunction, particularly focusing on molecular signaling pathways involved in macrophages-mediated hypertension, cardiac hypertrophy, fibrosis, and failure. In addition, the challenges remained in translating these findings to the treatment of heart failure patients are also addressed.

Menopausal age, adipokines, and heart failure incidence in postmenopausal women of the Multi-Ethnic Study of Atherosclerosis.

The mechanisms through which menopausal age influences heart failure (HF) development are controversial. Adiposity increases after menopause and could affect HF risk by influencing serum adipokine secretion. We investigated the associations of early menopause, and serum adipokines with incident HF in postmenopausal women. We included 746 postmenopausal women from the Multi-Ethnic Study of Atherosclerosis who reported their menopausal age and had data on adipokines and incident HF at the end of follow-up. Multivariable Cox proportional hazards models were used for analysis. The mean age was 65.1 years. Over a median follow-up period of 17.8 years, 45 HF events occurred. After adjusting for waist circumference, other cardiovascular disease risk factors and myocardial infarction, the hazard ratios (95% confidence intervals) of incident HF attributable to early menopause were 4.50 (1.41-14.3), 4.64 (1.46-14.7), and 5.16 (1.59-16.7) in models that additionally included adiponectin, leptin, and resistin, respectively. In adjusted analyses, adiponectin was independently associated with incident HF 2.20 (1.35-3.57), while leptin and resistin were not. The interaction terms of early menopause with adiponectin, leptin, and resistin for incident HF were not significant ( Pint = 0.08-0.82). Early menopause was significantly associated with incident HF. This association did not differ by serum adipokine levels. Only adiponectin was independently associated with incident HF in postmenopausal women when waist circumference, body mass index, and waist-hip ratio were used as the adiposity metric.

Role of Multimodality Imaging in Cardiac Sarcoidosis: A Retrospective Single-Center Experience.

Background/Objectives: Cardiac sarcoidosis (CS) is a rare entity characterized by granulomatous infiltration of the myocardium, which can lead to myocardial fibrosis, conduction abnormalities, and the development of heart failure, thereby elevating the risk of sudden cardiac death (SCD). While endomyocardial biopsy (EMBx) is regarded as the gold standard for diagnosis, its low sensitivity and inherent procedural risks may limit its practical application. Methods: This study retrospectively explored the role of advanced imaging modalities, specifically cardiovascular magnetic resonance imaging (CMR) and fluorodeoxyglucose positron emission tomography (FDG-PET), in the diagnosis and management of CS within a single center. In this retrospective study, we aimed to assess the utility of advanced imaging modalities in the clinical diagnosis of CS and the monitoring of treatment. Results: A total of 92 patients were identified as having cardiac sarcoidosis, with males constituting 66.3% of the sample and a mean age of 62 years (±11.9). Among these patients, 80 (87%) underwent FDG-PET. Here, the basal inferolateral segment was the most frequently observed segment of the heart with FDG uptake. A total of 77 patients (84%) underwent CMR, with 51 demonstrating late gadolinium enhancement (LGE). The basal inferolateral segment exhibited the highest frequency of LGE (26%). Logistic regression analysis indicated that patients presenting with a combination of LGE, FDG uptake on PET, and a "mismatch pattern" faced a two-fold increase in the risk of experiencing major adverse cardiac events (odds ratio = 2.311, p = 0.077). Conclusions: This study underscores the importance of multimodality imaging as a non-invasive alternative for CS diagnosis and management, reducing reliance on EMBx.

Association Between Plasma ADAMTS-7 Levels and Diastolic Dysfunction in Patients with Type 2 Diabetes Mellitus.

A disintegrin and metalloproteinase with thrombospondin motifs-7 (ADAMTS-7) belongs to the family of metalloproteinases that contributes to tissue homeostasis during morphogenesis and reproduction. These metalloproteinases regulate various cell functions such as cell proliferation, are important regulators in tissue regeneration, and play a role in vascular remodelling, which is involved in atherosclerosis development. Despite the well-established association between ADAMTS-7 and atherosclerotic disease, data regarding the metalloproteinase's association with LV function remain scarce. The aim of this study was to investigate the association of ADAMTS-7 levels with diastolic dysfunction and various echocardiographic parameters in patients with type 2 diabetes mellitus. All patients underwent a clinical, vascular, and echocardiographic examination during their visit. Plasma ADAMTS-7 levels were measured in all patients. The results showed that diastolic dysfunction was strongly associated with age, but had no statistically significant association with ADAMTS-7. When individual echocardiographic parameters were examined, ADAMTS-7 levels showed a positive tendency only with deceleration time (DT), with the other echocardiographic parameters being positively associated only with age. The possible role of ADAMTS-7 in diastolic dysfunction and in the development and progression of heart failure in patients with type 2 diabetes mellitus deserves further investigation.

Factors Associated With the Development of Heart Failure Following Acute Coronary Syndrome: A Systematic Review and Meta-Analysis.

Acute coronary syndrome (ACS) remains a major global health burden, encompassing a spectrum of conditions from unstable angina to acute myocardial infarction.Despite advancements in early detection and management, ACS is often complicated by the development of heart failure. This systematic review and meta-analysis aimed to identify factors associated with the development of heart failure following acute coronary syndrome. A comprehensive search was conducted across PubMed, Embase, Cochrane Library, and Web of Science from January 2018 to November 2024. Studies evaluating clinical or biochemical predictors of heart failure development in adult patients with acute coronary syndrome were included. Out of the initially identified studies, nine studies met the inclusion criteria. The Newcastle-Ottawa Scale was used to assess the quality of included studies, with most studies demonstrating high quality. The pooled analysis revealed that older age, female sex, diabetes, hypertension, chronic obstructive pulmonary disease, atrial fibrillation, multivessel coronary disease, and reduced left ventricular ejection fraction were significant predictors of heart failure development following acute coronary syndrome. The presence of atrial fibrillation emerged as the strongest predictor, followed by reduced left ventricular ejection fraction and chronic obstructive pulmonary disease. While complete revascularization showed a protective trend, this association did not reach statistical significance. The findings were limited by the predominantly retrospective nature of included studies and heterogeneity in the assessment of certain risk factors. Future research should focus on prospective studies with larger cohorts and comprehensive evaluation of additional factors such as treatment delays and revascularization strategies. Understanding these predictors can facilitate early risk stratification and guide targeted interventions, potentially improving outcomes for patients with acute coronary syndrome.

ЛЕЧЕНИЕ ХОРИОАНГИОМЫ ПЛАЦЕНТЫ БОЛЬШИХ РАЗМЕРОВ ПУТЕМ ФЕТОСКОПИЧЕСКОЙ ЛАЗЕРНОЙ КОАГУЛЯЦИИ СОСУДОВ

Lacental chorioangioma is the most common nontrophoblastic tumor of the placenta, occurring in 0.41-1.4 % of examined placentas by microscopy. About half of large chorioangiomas can cause fetal complications such as polyhydramnios, fetal anemia, intrauterine growth retardation, heart failure, fetal hydrops and intrauterine fetal death, complications such as hemolytic anemia, thrombocytopenia, disseminated intravascular coagulation, pregnancy-induced hypertension, maternal mirror syndrome, hemoglobinuria and postpartum bleeding. We performed fetoscopic laser coagulation of blood vessels of the large placental chorioangioma at 23 weeks, which prevented the development of fetal heart failure and other serious pregnancy complications.

Clonal Hematopoiesis and Risk of HeartFailure After Autologous Hematopoietic Cell Transplantation forLymphoma.

Patients with lymphoma are at high risk for developing heart failure (HF) after autologous hematopoietic cell transplantation (HCT). More accurate risk determination pre-HCT may facilitate screening and prevention of HF. The aim of this study was to examine the association between clonal hematopoiesis of indeterminate potential (CHIP) and the risk for HF after HCT for lymphoma. This was a retrospective cohort study of 861 patients who underwent autologous HCT for lymphoma between 2010 and 2016 at City of Hope Comprehensive Cancer Center. Targeted DNA sequencing was performed to determine the presence of CHIP (variant allele frequency≥ 2%). The primary outcome of interest was the 5-year cumulative incidence of de novo HF. Other outcomes of interest included overall and cause-specific mortality. Overall, 186 patients (21.7% of the cohort) had at least 1 CHIP variant, and 59 (6.9%) had≥2 variants. DNMT3A, PPM1D, and TET2 were the most frequently mutated genes. The 5-year incidence of HF was significantly higher in patients with CHIP compared with those without CHIP (13.8% vs 4.7%; P< 0.001; sub-distribution hazard ratio [sHR]: 2.48; 95% CI: 1.32-4.68); the HF incidence increased by variant allele frequency: 0-2% (4.7%), 2-10% (11.7%), and >10% (18.5%), P< 0.001. Patients with CHIP had significantly worse overall survival after HCT, compared with those without (63.4% vs 80.3%; P< 0.001), due primarily to the higher risk for nonrelapse mortality (subdistribution HR: 5.37; 95% CI: 2.34-12.35). CHIP was highly prevalent and associated with risk for HF and nonrelapse mortality after HCT. Thesefindings highlight the role of CHIP as a novel biomarker and potential target for intervention to improve outcomesafter autologous HCT.

PREDICTING HIGH FLOW ARTERIOVENOUS FISTULAS AND CARDIAC OUTCOMES IN HEMODIALYSIS PATIENTS.

Heart failure is common in patients receiving hemodialysis. A high flow arteriovenous fistula (AVF) may represent a modifiable risk factor for heart failure and death. Currently, no tools exist to assess the risk of developing a high flow AVF (>2000 mL/min). The aim of this study was to use machine learning to develop a predictive model identifying patients at risk of developing a high flow AVF and to examine the relationship between blood flow, heart failure, and death. Between 2011 and 2020, serial AVF blood flows were measured in 366 prevalent hemodialysis patients at two tertiary hospitals in Australia. Four prediction models (deep neural network, and 3 separate tree-based algorithms) employing age, first AVF flow, diabetes, and dyslipidemia were compared to predict high flow AVF development. Logistic regression was used to assess the relationship between AVF blood flow, heart failure, and death. High flow AVFs were present in 31.4% of patients. The bootstrap forest predictive model performed best in identifying those at risk of a high flow AVF (AUC 0.94, sensitivity 86%, specificity 83%). Heart failure prior to vascular access creation was identified in 10.2% of patients with an additional 24.9% of patients developing heart failure after AVF creation. Long-term mortality after access formation was 27%, with an average time to death after AVF creation of 307.5 ± 185.6 weeks. No univariable relationship using logistic regression was noted between AVF flow and incident heart failure after AVF creation or death. Age, flow at first measurement >1000 mL/min, time to highest AVF flow, and heart failure predicted death after AVF creation using a general linear model. Predictive modelling techniques can identify patients at risk of developing high flow AVF. No association was seen between AVF blood flow rate and incident heart failure after AVF creation. In those patients who died, time to highest AVF flow was the most important predictor of death after AVF creation.

Safety and effectiveness of ataluren in patients with Duchenne muscular dystrophy: single-center experience from Saudi Arabia

Objective Duchenne muscular dystrophy (DMD) is a rare X-linked neurodegenerative disorder caused by mutations in the DMD gene. This study examined the efficacy and safety of ataluren, the first oral treatment for DMD with nonsense mutations (nmDMD), in patients in the Middle East. Methods This retrospective longitudinal study assessed the outcomes of seven boys with nmDMD who received treatment with ataluren and follow-up at a single center since 2016. Results The median patient age at treatment initiation was 8.04 years (range: 3.3–9.92), and the median duration of exposure was 3.95 years (interquartile range = 4.42 years). Five patients were still ambulatory at the last follow-up. Ataluren was more effective in individuals with baseline 6-min walking distance (6MWD) ≥300 m, as these patients had smaller declines in 6MWD and North Star Ambulatory Assessment scores. Pulmonary function was well preserved in all patients, with no patients having forced vital capacity &lt;60% at their last follow-up. Six patients maintained normal cardiac function, whereas one patient developed heart failure before starting ataluren treatment. Conclusions Our results demonstrated both the efficacy and safety of ataluren. Early initiation of ataluren treatment delayed the loss of ambulation and cardiorespiratory milestones.

Narrative Review of Heart Failure Related to Cocaine Consumption and Its Therapeutic Management.

Background: Cocaine use can cause multiple cardiovascular complications, including heart failure. Aim: This general review of the literature delivers data on the relationship between cocaine consumption and the development of heart failure, as well as the elements of its diagnosis and management. Methods: A literature search was carried out using the PubMed, Web Of Science, and Google Scholar bibliographic databases over the period of 2007-2022 using the following keywords: "cocaine" AND "heart failure" NOT "acute heart disease". The exclusion criteria exempted studies carried out on animals, along with articles not written in English. Results and Discussion: A total of 27 articles (11 reviews, 10 clinical studies, 4 letters to the editor, and 2 clinical cases) were included. The prevalence of heart failure among cocaine users varies from one study to another (2.5%, 5.3%, 6.2%, or even 20%); however, when patients have a history of cocaine consumption, the prevalence of heart failure is higher than that ordinarily found in the young population (<0.1% to 0.5%). Cocaine consumption has a number of serious cardiotoxic effects that can lead to heart failure. According to the studies analysed, heart failure should be treated with beta-blockers, even in the event of long-term cocaine use, with a preference for carvedilol. Conclusions: Despite previous concerns about the use of beta-blockers in cocaine users, treatment with beta-blockers (particularly carvedilol) may actually result in measurable clinical improvement. Cocaine withdrawal remains essential for optimal treatment.

Obesity Hypoventilation Syndrome (Pickwickian Syndrome): A Literature Review

Obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, is a respiratory disorder characterized by reduced alveolar ventilation and elevated daytime carbon dioxide levels, primarily associated with obesity. If untreated, OHS can progress to pulmonary hypertension (PH) and ultimately heart failure. The exact prevalence of OHS in the general population remains unclear, but studies estimate it to range from 8% to 12.3%, increasing with obesity prevalence. This review discusses the diagnostic criteria for OHS, the utility of the STOP-Bang questionnaire in screening, and advances in understanding the pathophysiology and management of OHS, focusing on heart failure with preserved ejection fraction (HFpEF). Accurate diagnosis of OHS is critical and requires a thorough approach involving an extensive patient medical history and physical examination to differentiate OHS from obstructive sleep apnea (OSA). Key diagnostic tests include serum bicarbonate levels and arterial blood gas (ABG) analysis, to confirm the hypercapnia and identify the severity of hypoventilation. Given the rising prevalence of obesity worldwide and the serious complications associated with untreated OHS, early and accurate identification of OHS is essential, as it can prevent the progression to severe pulmonary hypertension (PH) and the subsequent development of heart failure (HF).

The expression profile analysis and functional prediction of lncRNAs in peripheral blood mononuclear cells in maintenance hemodialysis patients developing heart failure

Heart failure (HF) is the leading cause of death in patients with maintenance hemodialysis (MHD). Biomarkers has an important guiding role in the early diagnosis, risk stratification, and prognostic assessment of HF. Increasing studies have indicated that long non-coding RNAs (lncRNAs) have played an indispensable role in the regulatory network of HF. This study was aiming to explore the expression profiles of lncRNAs in patients treated with MHD developing heart failure. Peripheral blood mononuclear cells were isolated from 4 hemodialysis patients with reduced ejection fraction (HFrEF) and 4 hemodialysis patients with preserved ejection fraction (HFpEF), respectively. The expression profile analysis of lncRNAs was performed by using Illumina Novaseq 6000 sequencer. Quantitative real time polymerase chain reaction (qRT-PCR) was used to verify the expression of representative differentially expressed lncRNAs. Based on lncRNA-miRNA-mRNA-KEGG network analysis, the potential role of candidate lncRNAs and their association with the severity of HF were further evaluated. In total, 1,429 differentially expressed lncRNAs were found between patients with HFrEF and patients with HFpEF, of which 613 were up-regulated and 816 were down-regulated (P < 0.05). Five candidate lncRNAs were screened out by a series of bioinformatic analyses. After being compared with miRBase, ENST00000561762, one of the 5 candidates, was considered the most likely lncRNA to be serving as a precursor for miRNA. Nine predicted target genes were found by further lncRNA-miRNA-mRNA-KEGG network analysis, and among which ITGB5 was enriched in the actin dynamics signaling pathway. In another cohort of hemodialysis patients, the expression of lncRNA ENST00000561762 was verified by qRT-PCR. Further analysis revealed that there was a strong correlation between left ventricular ejection fraction and ENST00000561762, proBNP, and 6-minute walk distance, respectively. LncRNAs expression profile was remarkably different in hemodialysis patients with HFrEF compared to those with HFpEF. Among which, lncRNA ENST00000561762 was considered as a promising biomarker for patients with HFrEF as it was predicted to be a miRNA precursor to regulate the actin dynamics signaling pathway.

Laboratory and instrumental parameters associated with the risk of death in the long-term follow-up period in patients after myocardial infarction

BACKGROUND: In patients who successfully survived the 1st year after myocardial infarction, the risk of death remains elevated. AIM: To determine laboratory and instrumental parameters of myocardial remodeling associated with a lethal outcome in the long-term follow-up period in patients 1 year after myocardial infarction. MATERIAL AND METHODS: The study included 184 patients 12 months after myocardial infarction: the first group — living patients at the 5-year follow-up point (n=160), the second group — deceased patients at the 5-year follow-up point (n=24). A comparative analysis of inflammation and myocardial dysfunction biomarkers, as well as echocardiographic parameters reflecting the types of left ventricular remodeling, linear dimensions of the cavities and wall thickness of the heart, chamber volumes, and ventricular systolic function was retrospectively performed. After assessing the distribution of quantitative data, the Student's t-test or Mann–Whitney U-test and the χ2 criterion for categorical data were used. The model was built on the basis of logistic regression. The ROC curve, the Hosmer–Lemeshow test, and the bootstrap method were used to assess the model itself and its reliability. RESULTS: Patients in the second group were older (p=0.007), and more often had myocardial infarction with ST-segment elevation during hospitalization (p 0.001). Twelve months after myocardial infarction, a multidirectional pattern of changes in the level of N-terminal brain natriuretic propeptide was revealed: a decrease was registered in the first group, while an increase was registered in the second group. In the dynamics of the second group, the index of end-diastolic volume (p=0.014) and the size of left ventricular asynergy were higher (p=0.043), and the ejection fraction was lower (p=0.015) than in the first group. The model for predicting 4-year mortality in patients who survived myocardial infarction during the 1st year included such parameters as the index of the left ventricular end-diastolic volume, the content of the N-terminal fragment of the natriuretic peptide and the presence of concentric hypertrophy of the left ventricle. CONCLUSION: In patients who survived 1 year after myocardial infarction, the long-term risk of death is associated with a set of parameters reflecting left ventricular remodeling and the development of heart failure.

Enhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364.

Almost 30% of survivors of myocardial infarction (MI) develop heart failure (HF), in part due to damage caused by the accumulation of dysfunctional mitochondria. Organelle quality control through Parkin-mediated mitochondrial autophagy (mitophagy) is known to play a role in mediating protection against HF damage post-ischaemic injury and remodelling of the subsequent deteriorated myocardium. This study has shown that a single i.p. dose (2 h post-MI) of the selective small molecule Parkin activator PR-364 reduced mortality, preserved cardiac ejection fraction, and mitigated the progression of HF. To reveal the mechanism of PR-364, a multi-omic strategy was deployed in combination with classical functional assays using in vivo MI and in vitro cardiomyocyte models. In vitro cell data indicated that Parkin activation by PR-364 increased mitophagy and mitochondrial biogenesis, enhanced adenosine triphosphate production via improved citric acid cycle, altered accumulation of calcium localization to the mitochondria, and initiated translational reprogramming with increased expression of mitochondrial translational proteins. In mice, PR-364 administered post-MI resulted in widespread proteome changes, indicating an up-regulation of mitochondrial metabolism and mitochondrial translation in the surviving myocardium. This study demonstrates the therapeutic potential of targeting Parkin-mediated mitophagy using PR-364 to protect surviving cardiac tissue post-MI from progression to HF.

Hepatocardial relationships in non-alcoholic fatty liver disease: issues of epidemiology, diagnosis, prognosis

World statistics indicate a steady increase in the prevalence of non-alcoholic fatty liver disease, which correlates with the pandemics of obesity and diabetes, which are quite common in Russia. The commonality of cardiometabolic risk factors, the high global prevalence of non-alcoholic fatty liver disease and atherosclerotic cardiovascular diseases generates the interest of researchers in studying hepatocardial relationships. Currently, non-alcoholic fatty liver disease is positioned as a hepatic manifestation of a multisystem disorder, heterogeneous in underlying causes, manifestations, course and outcomes. The purpose of this review was to analyze hepatocardial relationships based on publications. 76 sources on the epidemiology of non-alcoholic fatty liver disease, published from 2011–2023 in journals indexed in Pubmed and eLibrary, were analyzed. Age and gender aspects of the development of non-alcoholic fatty liver disease were considered. The pathogenetic mechanisms of hepatocardial relationships, which were closely related to systemic inflammation, insulin resistance, metabolic syndrome and its components, were highlighted. The criteria and methods for diagnosing non-alcoholic fatty liver disease and metabolic-associated liver disease were outlined. Recent studies demonstrated the presence of hepatocardial connections, characterized by an increased risk of developing atherosclerosis, cardiomyopathy and rhythm disturbances, changes in the structural and functional parameters and geometry of the heart, as well as diastolic dysfunction, which may precede and/or contribute to the development of chronic heart failure in patients with non-alcoholic fatty liver disease. The article presents data on non-alcoholic fatty liver disease as a new factor associated with the development of adverse cardiovascular events to a greater extent than the outcome of liver diseases themselves, which confirms the need for primary and secondary prevention of cardiovascular diseases in this cohort of patients.

Kill two birds with one stone: Hapatologist's approach to metabolic dysfunction-associated steatotic liver disease and heart failure.

Heart failure (HF) is a major global public health concern, and one of the less commonly known risk factors for HF development is metabolic dysfunction-associated steatotic liver disease (MASLD), as they share a similar pathophysiological background. In this article, we evaluated a recently published review article by Arriola-Montenegro et al. This article briefly summarizes the common pathophysiology of HF and MASLD development and evaluates the available therapeutic options to treat both conditions. Clinical practice guidelines highlight the importance of initiating and titrating guideline-directed medication therapy (GDMT) for patients with HF with reduced ejection fraction. GDMT is comprised of the four pillars currently proposed in most clinical practice guidelines, namely angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose co-transporter 2 inhibitors (SGLT-2i). Given the similarity of pathophysiology and risk factors, recent studies for GDMT regarding ACEIs, ARBs, mineralocorticoid receptor antagonists, and SGLT-2i have shown beneficial effects on MASLD. Nonetheless, other medications for both conditions and novel therapies require more robust data and well-designed clinical studies to demonstrate their efficacies in both conditions.

Sex and Age Differences in the Impact of Metabolic Syndrome on Heart Failure Development.

Metabolic syndrome (MetS), a cluster of metabolic dysregulations, is recognized as a significant risk factor for the development of heart failure (HF). The pathophysiological mechanisms linking MetS to HF are complex and multifaceted, with the components of MetS contributing to cardiac deterioration through impaired myocardial energy metabolism, increased inflammation, and endothelial dysfunction. Numerous clinical studies have confirmed the relationship between MetS and HF. Multiple studies have demonstrated that the impact of MetS on HF varies by sex and age. Metabolic disorders, including MetS, have a greater impact on HF incidence in younger adults compared to the elderly population and in women compared to men. Although the reasons for these differences are not yet fully understood, recognizing the sex- and age-related variations is crucial for developing targeted strategies to prevent HF in individuals with MetS. Future research should continue to investigate the underlying mechanisms behind these variations and identify optimal management approaches that account for both sex and age in reducing HF risk.

Prevention of New-Onset Heart Failure in Atrial Fibrillation: The Role of Pharmacological Management.

Atrial fibrillation (AF) is the most common type of chronic arrythmia, with a lifetime prevalence of one in every three to five individuals above the age of 45 years. The higher heart rate, abnormal rhythm and inflammation caused by AF lead to changes in the function and structure of the heart. This, over time, can culminate in heart failure. In patients with AF, the lifetime prevalence of new-onset heart failure is twice that of stroke. The development of new-onset heart failure in AF is associated with high mortality. Despite the emphasis that AF guidelines put on preventing cardiovascular comorbidities, there is limited evidence regarding pharmacological therapies to prevent incident heart failure in individuals with AF. Specifically, the association between the use of rate control agents and incident heart failure in this population is unknown. Whilst rhythm control may reduce the risk of heart failure, the comparative effect of each pharmacological agent is not clear. In select subgroups of patients with AF, the choice of direct-acting oral anticoagulants and their optimal dosing has been attributed to a lower risk of new-onset heart failure. Future research is needed to identify an evidence-based approach to minimizing the development of heart failure in patients with AF.