Given evidence on the cardiovascular disease (CVD) risk conferred by comorbidity risk factors, the American Heart Association (AHA) recently introduced a novel staging construct, named cardiovascular-kidney-metabolic (CKM) syndrome. This study examined the association of CKM syndrome stages with all-cause and cardiovascular mortality among US adults.

Data were from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 at baseline linked to the 2019 National Death Index records. For each participant, the CKM syndrome was classified into five stages: stage 0 (no CKM risk factors), 1 (excess or dysfunctional adiposity), 2 (metabolic risk factors and chronic kidney disease), 3 (subclinical CVD), or 4 (clinical CVD). The main outcomes were all-cause and cardiovascular mortality.

Among 34,809 participants (mean age: 46.7 years; male: 49.2 %), the prevalence of CKM stages 0 to 4 was 13.2 %, 20.8 %, 53.1 %, 5.0 %, and 7.8 %, respectively. During a median follow-up of 8.3 years, compared to participants with CKM stage 0, those with higher stages had increased risks of all-cause mortality (stage 2: HR 1.43, 95 % 1.13-1.80; stage 3, HR 2.75, 95 % CI 2.12-3.57; stage 4, HR 3.02, 95 % CI 2.35-3.89). The corresponding hazard ratios (95 % confidence interval) of cardiovascular mortality risks were 2.96 (1.39-6.30), 7.60 (3.50-16.5), and 10.5 (5.01-22.2). The population-attributable fractions for advanced (stages 3 or 4) vs. CKM syndrome stages (stages 0, 1, or 2) were 25.3 % for all-cause mortality and 45.3 % for cardiovascular mortality.

Higher CKM syndrome stages were associated with increased risks of all-cause and cardiovascular mortality. These findings emphasize that primordial and primary prevention efforts on promoting CKM health should be strengthened to reduce mortality risk.

Heart failure (HF) is a growing public health concern, with an increasing incidence among younger populations. Traditionally, HF was considered a condition primarily affecting the elderly, but of late, emerging evidence hints at a rapidly rising HF incidence in youth in the past 2 decades. HF in youth has been linked to a complex interaction between emerging risk factors, such as metabolic syndrome, environmental exposures, genetic predispositions, and lifestyle behaviors. This review examines these evolving determinants, including substance abuse, autoimmune diseases, and the long-term cardiovascular effects of coronavirus disease 2019, which disproportionately affect younger individuals. Through a comprehensive analysis, the study highlights the importance of early detection, targeted prevention strategies, and multidisciplinary management approaches to address this alarming trend. Promoting awareness and integrating age-specific interventions could significantly reduce the burden of HF and improve long-term outcomes among younger populations.

Metabolic syndrome (MetS) and elevated high-sensitivity C-reactive protein (hs-CRP) have been identified as risk factors for heart failure (HF) in some studies. However, little was known about the co-exposure of MetS and inflammation to HF. We aimed to investigate the combined effect of MetS and high hs-CRP levels on the risk of incident HF.

The study included 94,841 participants without HF selected from the Kailuan cohort in 2006 (the baseline) and then followed up until 31 December 2020. Participants were divided into four groups based on the presence of MetS and high hs-CRP levels (>3mg/L) at baseline: MetS-CRP- (n=53,937), MetS-CRP+ (n=10,338), MetS+CRP- (n=23,521), MetS+CRP+ (n=7,045). Cox regression models were used to analyze the association of MetS and inflammation with the risk of HF. Statistical significance was defined as a two-tailed P value < 0.05.

The mean age of the participants was 51.5 ± 12.5 years, and 75,976 (80.0%) were male. During 13.1 years of follow-up, 3,058 participants were diagnosed with HF. The HF incidence rate of four groups were 1.69/1000pys, 2.95/1000pys, 3.27/1000pys, 5.33/1000pys. The HR for MetS-CRP+, MetS+CRP-, and MetS+CRP+ were 1.29 (95% CI, 1.15-1.45), 1.40 (95% CI, 1.29-1.53), and 1.85 (95% CI, 1.65-2.06), respectively, compared with MetS-CRP-. After stratification by age (p for interaction < 0.01), compared with the MetS-CRP- group, the HR of the MetS+CRP+ group was 2.17 (95% CI, 1.83-2.57) in participants with < 60 years and 1.53 (95% CI, 1.32-1.78) in participants with ≥ 60 years. There was an interaction between groups and ues of antihypertension medication (p for interaction <0.01). Compared with MetS-CRP-, the risk of HF in the MetS+CRP+ group was increased 1.38-fold (95% CI, 1.12-1.70) in participants with antihypertension medication use and 2.00-fold (95% CI, 1.75-2.27) in participants without antihypertension medication use.

The combination of MetS and elevated hs-CRP was associated with increased risk of HF in the Chinese population.

https://www.chictr.org.cn, identifier ChiCTR-TNRC-11001489.

Current estimates for the lifetime risk to develop heart failure with either a reduced (HFrEF) or preserved ejection fraction (HFpEF) and their associated risk factors are derived from two studies from the USA. The sex-specific lifetime risk and population attributable fraction of potentially modifiable risk factors for incident HFpEF and HFrEF are described in a large European community-based cohort with 25 years of follow-up.

A total of 8558 participants from the PREVEND cohort were studied at baseline from 1997 onwards and followed until 2022 for cases of new-onset HFrEF (ejection fraction < 50%) and HFpEF (ejection fraction ≥ 50%) by assessment of hospital records.

A total of 804 cases of new-onset HF were identified (534 HFrEF and 270 HFpEF) during 25 years of follow-up. The mean age at baseline was 50 years for men and 47 years for women. The mean age at onset of HF was 72.1 years in men and 74.2 years in women. The overall lifetime risk of developing HF was 24.5% in men compared to 23.3% in women. The lifetime risk of HFrEF was lower in women compared with men (11.9% vs. 18.1%), while the lifetime risk of HFpEF was higher in women compared with men (11.5% vs. 6.4%). In women, 71% of incident HFrEF cases were attributable to eight risk factors (hypertension, hypercholesterolaemia, obesity, smoking, atrial fibrillation, chronic kidney disease, myocardial infarction, and diabetes mellitus) and 60% in men. In women, 64% of incident HFpEF cases were attributable to those risk factors, whereas this was 46% in men. More specifically, in both men and women, hypertension and hypercholesterolaemia were the strongest risk factors for HFrEF, whereas hypertension and obesity were the strongest risk factors for HFpEF.

In this European cohort, the lifetime risk of developing HFrEF was greater in men than in women, while women were at greater risk of developing HFpEF. Eight directly and indirectly modifiable risk factors substantially accounted for the risk of developing HFrEF and HFpEF, particularly in women.

Heart failure poses a significant health concern globally, and despite advancements in treatment, the search for additional, supportive therapeutic options remains crucial. This systematic review and meta-analysis studied the impact of probiotics and polyphenols on heart failure biomarkers, focusing on potential improvements in heart function and inflammation.

We analyzed studies published in Embase, PubMed and Cochrane library from 2012 to 2024, focusing on randomized controlled trials. Our findings are drawn from 5 studies on probiotics, involving 401 participants, and 3 studies on polyphenols with a total of 140 participants. The analysis included assessments of LVEF, hs-CRP, creatinine and NT-proBNP levels in intervention and control groups.

The probiotics or polyphenols from the included studies did not demonstrate significant changes in the health indicators analyzed for heart failure patients compared to placebo.

The systematic review suggested that while the concept of dietary management for heart failure is promising, further research is necessary to validate the efficacy of probiotics and polyphenols as supplementary therapies in heart failure care, by analyzing more diverse health outcomes and patient populations.

The growing morbidity, mortality, and health care costs related to heart failure (HF) underscore the urgent need to prioritize its primary prevention. Whereas a risk-based approach for HF prevention remains in its infancy, several key opportunities exist to actualize this paradigm in clinical practice. First, the 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America HF guidelines provided recommendations, for the first time, on the clinical utility of multivariable risk equations to estimate risk of incident HF. Second, the American Heart Association recently developed the PREVENT (Predicting Risk of Cardiovascular Disease Events) equations, which not only enable prediction of incident HF separately, but also include HF in the prediction of total cardiovascular disease. Third, the predominant phenotype of HF risk has emerged as the cardiovascular-kidney-metabolic syndrome. Fourth, the emergence of novel therapies that prevent incident HF (eg, sodium-glucose cotransporter-2 inhibitors) and target multiple cardiovascular-kidney-metabolic axes demonstrate growing potential for risk-based interventions. Whereas the concept of risk-based prevention has been established for decades, it has only been operationalized for atherosclerotic cardiovascular disease prevention to date. Translating these opportunities into a conceptual framework of risk-based primary prevention of HF requires implementation of PREVENT-HF (Predicting Risk of Cardiovascular Disease Events-Heart Failure) equations, targeted use of cardiac biomarkers (eg, natriuretic peptides) and echocardiography for risk reclassification and earlier detection of pre-HF, and definition of therapy-specific risk thresholds that incorporate net benefit and cost-effectiveness. This scientific statement reviews the current evidence for accurate risk prediction, defines strategies for equitable prevention, and proposes potential strategies for the successful implementation of risk-based primary prevention of HF.

Because heart failure (HF) with preserved ejection fraction (HFpEF) is mainly a disease of elderly, there are a few reports focusing young patients. This study aims to elucidate characteristics of comparatively young HFpEF patients. We divided HFpEF patients in PURSUIT-HFpEF registry into younger HFpEF group (age ≤ 65 years) and older HFpEF group and compared the all-cause mortality and HF readmission (HFR) between the two groups and identified discharge factors correlated with HFR among younger HFpEF patients. The younger HFpEF group comprised 51 patients (4.1%). In this group, body mass index and smoking were significantly higher, while hypertension was significantly lower compared to older HFpEF group. Kaplan-Meier analysis indicated no significant difference in HFR between the groups, although all-cause mortality was significantly lower in younger HFpEF group (p < 0.001). Multivariable Cox proportional hazards analysis indicated that angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB) were inversely correlated with HFR, whereas mineralocorticoid receptor antagonists (MRA) were positively correlated with HFR in younger HFpEF patients (p = 0.004 and p = 0.007, respectively). In conclusion, younger HFpEF is rare (approximately 4%), with obesity and smoking being significant modifiable factors. HFR was similar between younger and older HFpEF patients. Administration of ACEI/ARB and unnecessity of MRA at discharge may be associated with reducing HFR in younger HFpEF patients.

Patients with heart failure (HF) and their caregivers are a dyad inextricably linked that exert influence on patients' quality of life (QoL).

The aim of this study was to explore factors affecting HF patients' QoL. Factors were: (a) HF patients' characteristics, (b) anxiety/depression of the dyad (patient-caregiver) and (c) caregivers' QoL.

In this cross-sectional study, we enrolled 340 patients and 340 caregivers. Data collection was performed by the method of an interview using "The Hospital Anxiety and Depression Scale", HADS) to assess anxiety and depression (patient-caregiver) as well as the "Minnesota Living with Heart Failure" and the "SF-36 Health Survey (SF-36)" to assess QoL (patient-caregiver, respectively).

From the 340 dyads who comprised the sample, 81.3% and 77.5% of patients experienced anxiety and depression, respectively, while 79.3% and 62.2% of caregivers experienced anxiety and depression, respectively. A statistically significant difference between patients and caregivers was only detected for depression (p = 0.001) and not for anxiety (p = 0.567). Patients with scores in HADS that indicate anxiety and depression had a worse QoL (total, physical, and mental). All subscales of the caregiver's QoL were significantly associated with the patient's QoL (p < 0.001) apart from the physical functioning scale. The correlation coefficients were all negative, indicating that a better caregiver's QoL (higher SF36 scores) is associated with a better patient's QoL (lower Minnesota scores). After controlling for the patient's characteristics, the anxiety and depression of caregivers did not affect the patient's QoL (confounding effect) whereas the patient's anxiety/depression remained significant factors. Patients with anxiety and depression had 5.58 and 6.49 points, respectively, higher QoL score, meaning a worse QoL, compared to those with no anxiety/depression.

Evaluating the impact of HF on patients' QoL and anxiety/depression along with their caregivers permits acknowledgment of this dyadic relationship.

Heart failure (HF) is a leading cause of hospitalization and mortality worldwide, emphasizing the critical role of optimal medical therapy (OMT) in improving patient outcomes. Despite extensive research, most scientific evidence regarding HF is gathered and studied in developed countries, leaving substantial knowledge gaps regarding HF in Latin America and the Caribbean.

To characterize the sociodemographic and clinical profiles of HF patients and to assess their adherence to OMT in the Americas.

The AMERICCAASS Registry is a prospective, observational, multicenter study, including patients aged 18 and older, both hospitalized and ambulatory, and diagnosed with HF. Sociodemographic and clinical data were collected from the first 2,500 patients to characterize the study population. Adherence to OMT was subsequently evaluated according to left ventricular ejection fraction (LVEF).

Among the 2,500 patients in the study, 36% were hospitalized and 64% were ambulatory. The median ages of the patients were 66.9 (hospitalized) and 66.3 years (ambulatory). Males made up 60.8% of hospitalized and 59.3% of ambulatory patients. The majority had HF with reduced LVEF (≤40%): 60.7% for hospitalized and 58.5% for ambulatory. The New York Heart Association (NYHA) functional class II predominated among ambulatory patients (67.9%), while NYHA functional class III predominated among hospitalized patients (46.6%). Only 21% of patients with reduced LVEF were receiving quadruple therapy, whereas 12.3% of patients with mildly reduced LVEF (41-49%) were on this treatment.

The findings demonstrate that the sociodemographic and clinical profiles of HF patients in the Americas are broadly consistent with international reports. However, the low use of OMT observed in this population underscores gaps in adherence to current guidelines. These results highlight the need for targeted strategies to improve pharmacological treatment adherence to optimize health outcomes in this region.

Evidence on the longitudinal association of serum uric acid (SUA) with the risk of heart failure (HF) was limited and controversial. This study aimed to investigate the associations of cumulative SUA (cumSUA), incorporating its time course of accumulation, with the risk of HF.

This prospective study enrolled 54 606 participants from the Kailuan study. The magnitude of SUA accumulation was expressed as cumSUA, exposure duration, and cumulative burden from baseline to the third survey, with cumSUA, calculated by multiplying mean values between consecutive examinations by time intervals between visits, as the primary exposure.During a median follow-up of 10 years, 1260 cases of incident HF occurred. A higher risk of HF was observed in participants with the highest vs. the lowest quartile of cumSUA [adjusted hazard ratio (aHR), 1.54; 95% confidence interval (CI), 1.29-1.84], 6-year vs. 0-year exposure duration (aHR, 1.87; 95% CI, 1.43-2.45), cumulative burden >0 vs. = 0 (aHR, 1.55; 95 CI, 1.29-1.86), and those with a negative vs. positive SUA slope (aHR, 1.12; 95% CI, 1.02-1.25). When cumSUA was incorporated with its time course, those with cumSUA ≥median and a negative SUA slope had the highest risk of HF (aHR, 1.55; 95% CI, 1.29-1.86).

Incident HF risk was associated with the magnitude and time course of cumSUA accumulation. Early accumulation resulted in a greater risk of HF compared with later accumulation, indicating the importance of optimal SUA control earlier in life.

Congestive heart failure (CHF) represents an important health issue characterised by considerable morbidity and mortality. This study sought to identify risk factors for CHF and to evaluate clinical outcomes between CHF patients and control subjects.

Data were obtained through interviews, physical examinations, and medical records. Risk variables encompassed hypertension, diabetes, dyslipidaemia, tobacco use, alcohol use, sedentary lifestyle, dietary practices, age, gender, and familial history of cardiovascular disease. The outcomes were all-cause mortality, cardiovascular mortality, hospitalisation, major adverse cardiovascular events (MACE), quality of life as measured by the Minnesota Living with Heart Failure Questionnaire (MLHFQ), and functional level according to the New York Heart Association (NYHA) classification. Statistical analyses including t-tests, Chi-square tests, logistic regression and Cox regression.

The findings indicated that hypertension (71.8% vs. 38.5%, p < 0.001), diabetes (47.9% vs. 28.2%, p = 0.002), dyslipidaemia (54.7% vs. 41.0%, p = 0.04), smoking (42.7% vs. 29.1%, p = 0.03), and physical inactivity (65.8% vs. 41.9%, p < 0.001) were more prevalent in cases. Cases exhibited increased hospitalisations (1.8 ± 1.2 vs. 0.7 ± 0.9, p < 0.001), prolonged stays (10.5 ± 5.4 vs. 6.2 ± 3.8 days, p < 0.001), elevated 30-day rehospitalisation rates (21.4% vs. 8.5%, p = 0.007), and a greater incidence of intensive care units (ICU) admissions (17.1% vs. 6.0%, p = 0.01). All-cause mortality (35.9% vs. 17.1%, p = 0.001), cardiovascular mortality (25.6% vs. 10.3%, p = 0.003), and MACE (51.3% vs. 25.6%, p < 0.001) were greater in cases. Quality of life (45.8 ± 12.4 vs. 25.6 ± 10.3, p < 0.001) and functional status (55.6% vs. 23.9%, p < 0.001) were inferior in cases.

CHF patients had greater rates of modifiable risk variables and worse clinical outcomes than controls, underscoring the necessity for comprehensive risk management.

Obesity is a global public health crisis, contributing to chronic disease development and poor prognosis. A large body of evidence consistently demonstrates that increased adiposity leads to many cardiovascular diseases (CVDs) and complications, such as coronary artery disease, heart failure, and arrhythmias, via direct and indirect mechanisms. Therefore, weight management is crucial to reduce and prevent cardiovascular risk. The recent emergence of glucose-like peptide-1 receptor agonists shows remarkable weight reduction and cardiovascular prevention. Despite the clear benefits, controversies and challenges on obesity-related CVD remain. This review aims to provide a comprehensive understanding of obesity-related CVD and explore current remaining tasks.

Both the clearance and secretion of prolactin are disrupted in chronic kidney disease (CKD). Evidence indicates that prolactin may play a role in cardiovascular (CV) disturbances. Considering the increased cardiovascular risk associated with CKD, this study investigates the relationship between prolactin levels, CKD, and the risk of CV events in both women and men, with an average follow-up period of 20 years. The study included 2,005 participants from the Tehran Lipid and Glucose Study (TLGS) who met the inclusion criteria. They were reassessed approximately every three years for a median follow-up of 19.0 years (Interquartile range (IQR):16.4-20.2), during which occurrences of CKD and CV events were recorded. A pooled logistic regression model examined the influence of Prolactin on CV events and its interaction with CKD. During follow-up, we identified 156 incident cases of CV events among men and 73 among women. Median (95%CI) PRL levels were 7.4 (5.5-10.5) ng/mL for men and 15.2 (10.3-23) ng/mL for women. The results of analyses showed that a history of CKD was associated with significantly higher odds of CV events for both men 4.2 (95% CI: 2.6-6.8) and women 5.5 (95% CI: 2.6-11.5). Results remained unchanged after adjustment for confounders including age, waist circumference, smoking, education, history of diabetes and hypertension, and family history of CV events. Interaction analyses revealed no statistically significant interaction between CKD and PRL on the odds of CV events in unadjusted and adjusted models. This consistent pattern was observed regardless of gender. Results of population-based data with over a median follow-up period of 20 years showed that CKD independently increases the risk of CV events in both men and women. However, our findings suggest that this elevated risk may not be substantially influenced by prolactin levels. Further investigation may be warranted to confirm these findings.

The American Heart Association (AHA), in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and metabolic syndrome) that contribute to cardiovascular health. The AHA Heart Disease and Stroke Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).

The AHA, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistical Update with review of published literature through the year before writing. The 2025 AHA Statistical Update is the product of a full year's worth of effort in 2024 by dedicated volunteer clinicians and scientists, committed government professionals, and AHA staff members. This year's edition includes a continued focus on health equity across several key domains and enhanced global data that reflect improved methods and incorporation of ≈3000 new data sources since last year's Statistical Update.

Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics.

The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.

Background: The study investigates age-related differences in the prevalence and extent of coronary artery disease (CAD), as well as long-term outcomes in a large cohort of unselected patients undergoing invasive coronary angiography (CA). The aging population, along with an increasing number of older and multi-morbid patients undergoing CA, poses challenges for healthcare systems. Despite this, studies investigating age-related differences in the long-term outcomes of unselected patients undergoing CA are limited. Methods: Consecutive patients undergoing invasive CA from 2016 to 2022 were included from one institution. The prognosis of patients undergoing CA stratified by pre-specified age groups (i.e., 40-<60, 60-<80 and ≥80 years) was investigated with regard to the primary endpoint of rehospitalization for heart failure (HF), as well as the risks of acute myocardial infarction (AMI) and coronary revascularization at 36 months. Results: From 2016 to 2022, 7520 patients undergoing CA were included with a median age of 70 years (mean: 69 years). The prevalence of CAD (61.9% vs. 71.8% vs. 77.3%; p = 0.001), as well as the prevalence of three-vessel CAD (21.0% vs. 31.5% vs. 36.1%) increased with age. At 36 months, patients ≥ 80 years of age had the highest rates of rehospitalization for HF, followed by patients 60-<80 years and patients 40-<60 years (28.4% vs. 23.2% vs. 14.0%; p = 0.001). Consequently, compared to younger patients (i.e., 40-<60 years of age), those ≥80 years of age exhibited the highest risk of HF-related rehospitalization (≥ 80 years: HR = 2.205; 95% CI 1.884-2.579; p = 0.001), followed by those 60-< 80 years (HR = 1.765; 95% CI 1.536-2.029; p = 0.001). The increased risk of rehospitalization for HF at 36 months was still observed after multivariable adjustment (i.e., ≥80 years: HR = 1.265; 95% CI 1.049-1.524; p = 0.014; 60-<80 years: HR = 1.339; 95% CI 1.145-1.565; p = 0.001) and was specifically evident in patients with left ventricular ejection fraction ≥ 35% and in patients without evidence of CAD/single-vessel CAD. In contrast, the rates of AMI and coronary revascularization at 36 months did not differ significantly among different age groups. Conclusions: Advanced age is an independent predictor of rehospitalization for HF in patients undergoing CA, but not AMI and revascularization during long-term follow-up. This highlights the importance of optimizing diagnostic and therapeutic strategies for HF, particularly in older patients undergoing CA.

The global increase in human life expectancy, coupled with an unprecedented rise in the prevalence of obesity, has led to a growing clinical and socioeconomic burden of heart failure with preserved ejection fraction (HFpEF). Mechanistically, the molecular and cellular hallmarks of aging are omnipresent in HFpEF and are further exacerbated by obesity and associated metabolic diseases. Conversely, weight loss strategies, particularly caloric restriction, have shown promise in improving health status in patients with HFpEF and are considered the gold standard for promoting longevity and healthspan (disease-free lifetime) in model organisms. In this review, we implicate fundamental mechanisms of aging in driving HFpEF and elucidate how caloric restriction mitigates the disease progression. Furthermore, we discuss the potential for pharmacologically mimicking the beneficial effects of caloric restriction in HFpEF using clinically approved and emerging caloric restriction mimetics. We surmise that these compounds could offer novel therapeutic avenues for HFpEF and alleviate the challenges associated with the implementation of caloric restriction and other lifestyle modifications to reduce the burden of HFpEF at a population level.

Age is a major risk factor for heart failure, but one that has been historically viewed as non-modifiable. Emerging evidence suggests that the biology of aging is malleable, and can potentially be intervened upon to treat age-associated chronic diseases, such as heart failure. While aging biology represents a new frontier for therapeutic target discovery in heart failure, the challenges of translating Geroscience research to the clinic are multifold. In this review, we propose a strategy that prioritizes initial target discovery in human biology. We review the rationale for starting with human omics, which has generated important insights into the shared (patho)biology of human aging and heart failure. We then discuss how this knowledge can be leveraged to identify the mechanisms of aging biology most relevant to heart failure. Lastly, we provide examples of how this human-first Geroscience approach, when paired with rigorous functional assessments in preclinical models, is leading to early-stage clinical development of gerotherapeutic approaches for heart failure.

Evidence has firmly established the association between superior cardiovascular health (CVH) and reduced susceptibility to cardiometabolic diseases (CMDs). In reality, CVH experiences dynamic fluctuations throughout individuals' lifespans. However, the association between changes in CVH and the impact on CMDs among individuals with different genetic risks remains unclear.

Based on a large-scale community-based cohort, we evaluated the association between baseline CVH (n=289 069), changes in CVH between 2 examinations (n=37 702), and the risk of CMDs and its individual components (ischemic heart disease, type 2 diabetes, and stroke) using Cox proportional hazards models, leveraging detailed repeatedly assessed lifestyle information and genetic data. Estimations were also stratified by age groups (≤65 years, >65 years) and genetic risk groups, defined by the tertiles of the polygenic risk score for CMDs components. Population-attributable fractions and relative risk reduction were calculated to assess the potential benefits of improvement in CVH in preventing CMDs. For participants whose baseline CVH ranged from ideal to poor, an ascending trend was exhibited in the risk of CMDs overall, as well as its individual components. Based on a median of 5.4-year follow-up after the reassessment of CVH, individuals with an enhancement from intermediate to ideal CVH demonstrated a 36% lower risk of CMDs (hazard ratio [HR], 0.64 [95% CI, 0.53-0.77]; P<0.001), compared with those with constantly intermediate CVH, while those deteriorating from intermediate to poor faced a 44% higher risk (HR, 1.44 [95% CI, 1.17-1.78]; P<0.001). Interestingly, changes in CVH exerted a more pronounced impact on CMD risk within younger populations (≤65 years) (Pinteraction=0.006). Notably, among participants with a high genetic risk of ischemic heart disease, those who improved their CVH status from intermediate to ideal exhibited a 50% lower risk of ischemic heart disease (HR, 0.50 [95% CI, 0.34-0.74]; P<0.001), compared with those with constantly intermediate CVH.

Individuals with better baseline CVH exhibited a lower risk of CMDs. Enhancement in CVH significantly mitigates the risk of CMDs, especially when efforts are made before the age of 65 years and within high genetic risk groups. These findings underscore the importance of interventions aimed at promoting cardiovascular well-being across entire populations, offering valuable insights for targeted preventive strategies and healthcare interventions.

Cardiovascular-kidney-metabolic (CKM) syndrome and systemic inflammation significantly contribute to mortality. However, the joint associations of CKM stages and systemic inflammation with all-cause and cardiovascular disease (CVD) mortality remain unclear. This study aimed to evaluate the independent and joint associations of CKM stages and systemic inflammation with all-cause and CVD mortality in a representative cohort of United States adults.

We analyzed data from 29,459 adults aged ≥ 20 years from the National Health and Nutrition Examination Survey (1999-2018). CKM stages were classified based on metabolic risk factors, CVD, and chronic kidney disease. Systemic inflammation was assessed using multiple indicators, and time-dependent ROC analysis identified the systemic inflammatory response index (SIRI) as the most effective inflammatory marker. The associations of CKM stages and SIRI with mortality were evaluated.

Over a median follow-up of 109 months, 5,583 all-cause deaths and 1,843 CVD-specific deaths occurred. Both advanced CKM stages and elevated SIRI were associated with higher risks of all-cause and CVD mortality. Individuals with advanced CKM stages (Stages 3-4) and elevated SIRI (> 0.81) had the highest risks of all-cause (HR: 1.84, 95% CI: 1.65-2.05) and CVD mortality (HR: 2.50, 95% CI: 2.00-3.12). These associations were particularly pronounced in adults aged < 60 years (P for interaction < 0.001).

Advanced CKM stages and elevated SIRI are associated with increased risks of all-cause and CVD mortality, particularly in younger adults. These findings highlight the significance of targeted interventions to address systemic inflammation and CKM progression, potentially improving long-term outcomes in high-risk populations.

There is evidence that heart failure with preserved ejection fraction (HFpEF)-related hospitalizations are increasing in the United States. However, there is a lack of knowledge about HFpEF-related hospitalizations among younger adults.

The aims of this study were to perform a retrospective analysis using the Nationwide Inpatient Sample and to examine age-stratified sex differences in the prevalence, correlates, and outcomes of HFpEF-related hospitalization across the adult life span.

Using the Nationwide Inpatient Sample (2002-2014), patient and hospital characteristics were determined. Joinpoint regression was used to describe age-stratified sex differences in the annual average percent change of hospitalizations with HFpEF. Survey logistic regression was used to estimate adjusted odds ratios representing the association of sex with HFpEF-related hospitalization and in-hospital mortality.

There were 8 599 717 HFpEF-related hospitalizations (2.43% of all hospitalizations). Women represented the majority (5 459 422 [63.48%]) of HFpEF-related adult hospitalizations, compared with men (3 140 295 [36.52%]). Compared with men younger than 50 years, women within the same age group were 6% to 28% less likely to experience HFpEF-related hospitalization. Comorbidities such as hypertensive heart disease, renal disease, hypertension, obstructive sleep apnea, atrial fibrillation, obesity, anemia, and pulmonary edema explained a greater proportion of the risk of HFpEF-related hospitalization in adults younger than 50 years than in adults 50 years or older.

Before the age of 50 years, women exhibit lower HFpEF-related hospitalization than men, a pattern that reverses with advancing age. Understanding and addressing the factors contributing to these sex-specific differences can have several potential implications for improving women's cardiovascular health.

This study explored the effectiveness of a newly constructed frailty index (FI) for predicting short-term and long-term mortality in patients with chronic heart failure (HF).

This retrospective study included inpatients aged ≥60 years diagnosed with chronic HF at a teaching hospital in western China. General data on the patients were collected from the electronic medical record system between January 1, 2017, and July 7, 2022, and death information was obtained from follow-up calls made from July 31, 2022, to August 1, 2022. Receiver operating characteristic (ROC) curves were used to analyze the accuracy of the FI in predicting death in patients with chronic HF. Logistic regression (during hospitalization and within 30 days after discharge) and Cox regression (within 180 days after discharge and one year after discharge) analyses were used to assess associations between frailty and mortality risk in elderly patients with chronic HF.

A total of 432 patients with chronic HF were included in the study. The non-frail group had FI values <0.3, while the FI values in the frail group were ≥0.3. Overall, 130 patients (30.09 %) were diagnosed with frailty, 66 (15.28 %) died during hospitalization or within 30 days after discharge, 55 (12.73 %) died within 180 days after discharge, and 68 (15.74 %) died within one year after discharge. The in-hospital and 30-day mortality rates, the 180-day mortality rates, and the 1-year mortality rates were higher in frail patients than in non-frail patients (in-hospital and 30-day mortality rates, 37.69 % vs. 5.63 %, P < 0.001; within 180 days, 30.61 % vs. 8.45 %, P < 0.001; within 1 year, 34.69 % vs. 11.49 %, P < 0.001). The area under the curve (AUC) values of FI for predicting in-hospital and 30-day mortality after discharge were 0.804, with values of 0.721 for 180-day mortality after discharge and 0.720 for 1-year mortality after discharge. Logistic regression analysis with adjustment for potential confounders indicated that frail HF patients had a higher risk of death during hospitalization and within 30 days than non-frail patients (odds ratio [OR] = 4.98, 95 % confidence interval [CI]: 2.46-10.09). Cox regression analysis with adjustment for potential confounders showed that frail HF patients had a higher risk of death within 180 days (hazard ratio [HR] = 2.63, 95 %CI: 1.47-4.72) and within 1 year (HR = 2.01, 95 %CI: 1.19-3.38).

The results of this study showed that the new FI constructed according to the established construction rules could predict the in-hospital mortality and the risk of death within 30 days after discharge, 180 days after discharge, and 1 year after discharge in patients with chronic HF.

Background/Objectives: Heart failure (HF) remains a leading cause of hospitalization and morbidity. Arterial stiffness, measured by pulse wave velocity (PWV) and the augmentation index (AIx), has been linked to HF severity and prognosis. This study investigates the relationship between clinical parameters, biochemical indicators, and arterial stiffness in hospitalized patients with HF, aiming to identify predictors of hospitalization and improve patient management. Methods: This cross-sectional study included 98 patients admitted with HF: 53 with acutely decompensated HF (sudden worsening of symptoms) and 45 with chronic HF (stable symptoms of HF). Clinical and biochemical parameters, including ejection fraction (EF), N-terminal prohormone of brain natriuretic peptide (NT-proBNP) levels, and arterial stiffness indicators (PWV and AIx), were measured at admission. During follow-up, 59 patients required re-hospitalization due to acutely decompensated HF, while 39 remained outpatients without further hospitalization. The relationship between these parameters was analyzed using Pearson correlation coefficients, and multiple Cox regression analysis was conducted to identify independent predictors of re-hospitalization. Results: A significant negative correlation between EF and PWV was found (r = -0.853, 95% CI [-0.910, -0.764]), suggesting an association between improved heart function (higher EF) and reduced arterial stiffness (lower PWV). A moderate positive correlation between EF and AIx (r = 0.626, 95% CI [0.473, 0.805]) suggests that, while higher EF is associated with increased AIx, the relationship is weaker compared to EF and PWV. This may reflect differing contributions of vascular and myocardial factors to HF severity. Hospitalized patients exhibited significantly poorer clinical and biochemical profiles, including higher NT-proBNP levels (p < 0.001) and worse blood pressure (BP) measurements (systolic and diastolic, p < 0.01). Multiple Cox regression analysis identified PWV, Aix, and NT-proBNP as independent predictors of re-hospitalization in HF patients, with significant hazard ratios: PWV (HR = 1.15, p = 0.02), AIx (HR = 1.03, p = 0.02), and NT-proBNP (HR = 1.0001, p < 0.01). Conclusions: Arterial stiffness indices (PWV and AIx), EF, and NT-proBNP were identified as significant predictors of re-hospitalization in HF patients. These findings suggest that integrating arterial stiffness measurements into routine clinical assessments may enhance the risk stratification and inform targeted interventions to reduce hospitalizations and improve outcomes.

Transthyretin cardiac amyloidosis (ATTR-CM) may be an underestimated cause of heart failure among geriatric patients and represent a unique phenotype and prognostic profile.

This retrospective, observational, cohort study characterizes cardiac and extracardiac disorders at diagnosis and assesses prognosis among ATTR-CM patients based on age (geriatric vs. non-geriatric) and amyloidosis subtype (wild type, ATTRwt and hereditary, ATTRv). In total, 943 patients with ATTR-CM were included, of which 306 had ATTRv and 637 had ATTRwt. Among these, 331 (35.1%) were non-geriatric (<75 years), and 612 (64.9%) were geriatric (≥75 years). The population exhibited conduction abnormalities, atrial fibrillation and ischaemic heart disease that progressively deteriorated with age. Among ATTRwt patients, peripheral neuropathy, neurovegetative symptoms, and hearing loss were present across all age groups, but reports of carpal tunnel symptoms or surgery decreased with age. Conversely, among ATTRv patients, reports of extracardiac symptoms increased with age and Val122ILe mutation was highly prevalent among geriatric patients. The 3-year survival was higher among non-geriatric ATTR-CM patients (76%) than geriatric patients (55%) and predictors of 3-year mortality differed. Notably, predictors identified among geriatric patients were alkaline phosphatase (ALP) (HR = 1.004, 95% CI: [0.001-1.100)], troponin T hs (HR = 1.005, 95% CI: [1.001-1.120)] and tricuspid insufficiency (HR = 1.194, 95% CI: [1.02-1.230)]. Whereas, among non-geriatric patients, NT-proBNP (HR = 1.002, 95% CI: [1.02-1.04], global longitudinal strain (HR = 0.95, 95% CI: [0.922-0.989], and glomerular filtration rate (HR = 0.984, 95% CI: [0.968-1.00) were identified. We propose a 3-stage prognostic staging system combining troponin T hs (≥44 ng/L) and ALP levels (≥119 UI/L). In the geriatric population, this model discriminated survival more precisely than the National Amyloidosis Centre staging, particularly for classifying between stage 1 (82%), stage 2 (50%) and stage 3 (32%) for ATTRv and ATTRwt.

These diagnostic and prognostic indicators, along with ATTR subtype, highlight the distinct characteristics of this important, geriatric ATTR-CM patient group. Recognizing these mortality markers can be valuable for geriatricians to improve the prognostic quality management of geriatric patients with ATTR-CM.

Heart Failure (HF) and Diabetes Mellitus (DM) often coexist, and each condition independently increases the likelihood of developing the other. While there has been concern regarding the increasing burden of disease for both conditions individually over the last decade, a comprehensive examination of mortality trends and demographic and regional disparities needs to be thoroughly explored in the United States (US).

This study analyzed death certificates from the CDC WONDER database, focusing on mortality caused by the co-occurrence of HF and DM in adults aged 75 and older from 1999 to 2020. Age-adjusted mortality rates (AAMRs) and annual percent changes (APCs) were computed and categorized by year, gender, race, census region, state, and metropolitan status.

A total of 663,016 deaths were reported in patients with coexisting HF and DM. Overall, AAMR increased from 154.1 to 186.1 per 100,000 population between 1999 and 2020, with a notable significant increase from 2018 to 2020 (APC: 11.30). Older men had consistently higher AAMRs than older women (185 vs. 135.4). Furthermore, we found that AAMRs were highest among non-Hispanic (NH) American Indian or Alaskan natives and lowest in NH Asian or Pacific Islanders (214.4 vs. 104.1). Similarly, AAMRs were highest in the Midwestern region and among those dwelling in non-metropolitan areas.

Mortality from HF and DM has risen significantly in recent years, especially among older men, NH American Indian or Alaska Natives, and those in non-metropolitan areas. Urgent policies need to be developed to address these disparities and promote equitable healthcare access.

End-stage hypertrophic cardiomyopathy (ES-HCM) is a disease with severe complications and a poor prognosis. This study aimed to explore the influencing and prognostic factors of ES-HCM.

A total of 1282 patients with HCM who were hospitalized for the first time at Fujian Medical University Union Hospital between 1 January 2013 and 30 September 2021 were recorded. The patients with HCM and left ventricular ejection fraction (LVEF) < 50% were defined as having ES-HCM, and a control group (LVEF ≥ 50%) was generated from the collected medical records of HCM. The patients were matched in a ratio of 4:1 based on age and sex. Logistic regression analysis was used to determine the influencing factors of ES-HCM. Kaplan-Meier survival analysis was performed to analyse the clinical outcomes of ES-HCM patients. A total of 250 inpatients with HCM were enrolled in the study; 50 patients had ES-HCM, and 200 had HCM with LVEF ≥ 50%. The mean age of the patients at enrolment was 62.5 ± 10.3 years, and 215 patients (215/250, 86.0%) were male. The median follow-up time of the patients was 2.8 (1.4-5.4) years. The incidence of all-cause death and cardiovascular death in patients with ES-HCM was higher than those in patients with HCM and LVEF ≥ 50% (22/50 [44.0%] vs. 13/200 [6.5%]; 12/50 [24.0%] vs. 4/200 [2.0%], all P < 0.001). Multivariate logistic regression analysis showed that the influencing factors associated with ES-HCM included age at first symptom onset (odds ratio [OR] = 0.95, 95% CI [0.90, 1.00], P = 0.042), New York Heart Association (NYHA) class (OR = 7.73, 95% CI [2.93, 20.41], P < 0.001), heart rate (OR = 1.07, 95% CI [1.02, 1.12], P = 0.003), QRS duration (OR = 1.03, 95% CI [1.00, 1.05], P = 0.020), left ventricular end-diastolic diameter (LVEDD) (OR = 1.15, 95% CI [1.04, 1.28], P = 0.006), left atrial anteroposterior diameter (LAD) (OR = 1.13, 95% CI [1.03, 1.24], P = 0.012), and maximum left ventricular wall thickness (MLVWT) (OR = 0.80, 95% CI [0.68, 0.93], P = 0.005). Among the 50 patients with ES-HCM, NYHA class (P < 0.001) and heart rate (P = 0.017) were each associated with a higher likelihood and earlier occurrence of heart transplantation or all-cause mortality in univariate analyses.

The influencing factors for ES-HCM included the age at first symptom onset, NYHA class, heart rate, QRS duration, LVEDD, LAD, and MLVWT. Both NYHA class and heart rate were related to the prognosis of ES-HCM.

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.

Obesity is major cause of heart failure (HF), but it is related with a better prognosis among the elderly. Therefore, we aimed to examine whether metabolically healthy obesity (MHO) in late life increases HF risk and is reflected in impaired left ventricular (LV) function.

The participants were grouped into four metabolic phenotypes based on obesity and metabolic status: metabolically healthy non-obesity (MHN), MHO, metabolically unhealthy non-obesity (MUN), metabolically unhealthy obesity (MUO). Association of metabolic phenotypes with LV function was evaluated using multiple linear regression models. And association between metabolic phenotypes and risk of HF was assessed using multivariable logistic regression models. In addition, we validated the association of metabolic phenotypes and HF risk in a separate longitudinal cohort.

In the primary cohort of 6335 participant, there were 434 participants diagnosed with HF. Compared to MHN participants, the risk of HF was higher among older individuals with MUN (OR = 1.51 [95% CI: 1.14-1.99]) and MUO (OR = 2.01 [95% CI: 1.39-2.91]), but not older individuals with MHO (OR = 0.86 [95% CI: 0.30-2.43). Regarding to LV function, worse LV diastolic function was noted among MUN and MUO individuals rather than MHO individuals. Older adults with MHO were also not associated with risk of HF in the validation cohort.

Among older individuals, the metabolic health status might modify the association of obesity with risk of HF and LV diastolic dysfunction. Worse LV diastolic function and higher risk of HF were just noted in individuals with MUO, but not in those with MHO.

Heart failure (HF) is a common condition that imposes a significant burden on healthcare systems. We aimed to identify subgroups of patients with heart failure admitted to the ICU using routinely measured laboratory biomarkers.

A large dataset (N = 1176) of patients with heart failure admitted to the ICU at the Beth Israel Deaconess Medical Center in Boston, USA, between June 1, 2001, and October 31, 2012, was analyzed. We clustered patients to identify laboratory phenotypes. Cluster profiling was then performed to characterize each cluster, using a binary logistic model.

Two distinct clusters of patients were identified (N = 679 and 497). There was a significant difference in the mortality rate between Clusters 1 and 2 (50 [7.4%] vs. 109 [21.9%], respectively, p < 0.001). Patients in the Cluster 2 were significantly older (mean [SD] age = 72.35 [14.40] and 76.37 [11.61] years, p < 0.001) with a higher percentage of chronic kidney disease (167 [24.6%] vs. 262 [52.7%], respectively, p < 0.001). The logistic model was significant (Log-likelihood ratio p < 0.001, pseudo R2 = 0.746) with an area under the curve of 0.905. The odds ratio for leucocyte count, mean corpuscular volume (MCV), red blood cell (RBC) distribution width, hematocrit (HcT), lactic acid, blood urea nitrogen (BUN), serum potassium, magnesium, and sodium were significant (all p < 0.05).

Laboratory data revealed two phenotypes of ICU-admitted patients with heart failure. The two phenotypes are of prognostic importance in terms of mortality rate. They can be differentiated using blood cell count, kidney function status, and serum electrolyte concentrations.

The aim of this study was to characterize the burden of valvular heart disease (VHD)-related heart failure (HF) in Group of 20 (G20) countries.

Using data from the 2019 Global Burden of Disease Study, we estimated VHD-related HF burdens (cases, age-standardized prevalence rates, and years lived with disabilities rates) in G20 countries from 1990 to 2019 by age, sex, and sociodemographic index. The burden of VHD-related HF increased in G20 countries from 1990 to 2019, exhibiting heterogeneity across VHD subtypes. In 2019, Italy, the United States, and the Russian Federation had the highest age-standardized prevalence rates of nonrheumatic VHD-related HF, whereas India, Brazil, and Mexico had the lowest. Rheumatic VHD-related HF was most prevalent in China, India, and Italy, whereas the Republic of Korea, Brazil, and Turkey had the lowest. Nonrheumatic VHD-related HF prevalence peaked among G20 countries in individuals ≥85 years of age, whereas rheumatic VHD-related HF peaked in those 75 to 84 years of age in several countries, including China, India, the Russian Federation, Mexico, Argentina, and Turkey. Age-standardized prevalence rates of nonrheumatic VHD-related HF showed a decreasing trend, more pronounced in women, whereas rheumatic VHD-related HF increased in both sexes, with a lower increase in men. Nonrheumatic VHD-related HF burden correlated with age and sociodemographic index, whereas rheumatic VHD-related HF burden was highest in middle sociodemographic index countries for those <75 years of age. Years lived with disabilities rates for VHD-related HF represented about 9.0% of the overall burden across populations.

The increasing burden of VHD-related HF in G20 countries highlights the need for timely interventions to mitigate this growing public health challenge.

To evaluate temporal trends, across three decades, in the population attributable fractions (PAFs) of modifiable risk factors for 5-year risk of cardiovascular diseases (CVDs).

Within population-based Rotterdam Study, we defined three time groups of individuals without established CVD at 'baseline' with a mean age of 70 years, and followed for five years: Epoch 1990s (1989-93, n = 6195), Epoch 2000s (1997-2001, n = 5572), and Epoch 2010s (2009-14, n = 5135). The prevalence of risk factors and related relative risks were combined to quantify PAFs. The PAF of the six risk factors combined for global CVD was 0.57 [95% confidence interval (CI) 0.47-0.65], 0.52 (0.39-0.62), and 0.39 (0.18-0.54) in three respective epochs. Hypertension contributed the highest PAF to global CVD in Epoch 1990s (0.37, 95% CI: 0.28-0.44) and 2000s (0.34, 95% CI: 0.22-0.43), while smoking was the largest contributor in Epoch 2010s (0.20, 95% CI: 0.06-0.32). Dyslipidaemia changed population-level coronary heart disease risk over time. For stroke, hypertension became a less significant contributor over time, but smoking became a larger contributor. For heart failure, all risk factors showed non-significant PAFs in Epoch 2010s. PAFs related to individual risk factor varied among women and men.

Six modifiable risk factors to population-level global CVD risk decreased over time, but still explained 39% of total CVD in the latest decade. PAFs changed considerably for hypertension, dyslipidaemia, and smoking. Risk factors had different PAFs for different CVDs with pronounced sex differences.

Atrial fibrillation (AF) is often accompanied by comorbidities. Not only cardiovascular but also non-cardiovascular comorbidities have been associated with AF. Multimorbidity is therefore a common finding in patients with AF, especially in elderly patients. Multimorbidity is associated with adverse outcomes, adds complexity to AF management, and poses a significant burden on healthcare costs. It is expected that the prevalence of elderly patients with multimorbidity will increase significantly. It is therefore crucial to outline implications for clinical practice and guide comprehensive multimorbidity management.

This perspective article outlines multimorbidity in AF and the importance of comprehensive comorbidity management. It addresses current clinical practice guided by international guidelines and the need for integrated care including a patient-centered focus, comprehensive AF management, coordinated multidisciplinary care, and supporting technology. Moreover, it proposes a novel model of care delivery following a systematic approach to multimorbidity management.

Providing comprehensive care by means of a multidisciplinary team and patient engagement is crucial to provide optimal personalized care for elderly patients with AF and multimorbidity. A systematic integrated care approach seems promising, but further studies are needed to investigate the feasibility of a systematic approach and prioritization of comorbidity management in patients with multimorbidity.

Heart failure is a resource-intensive condition to manage and typically involves a multi-disciplinary and multi-modality approach leading to an expensive treatment paradigm. It is worth noting that hospital admissions constitute over 80% of heart failure management costs. In the past two decades, healthcare systems have developed new ways of following patients remotely to prevent them from being readmitted to the hospital. However, despite these efforts, hospital admissions have still increased. Many successful readmission reduction programs prioritize education and self-care to increase patients' awareness of their disease and promote lasting lifestyle changes. While socioeconomic factors impact success, interventions tend to be effective when medication adherence and guideline-directed medical therapy are emphasized. Monitoring intracardiac pressure can improve resource allocation efficiency and has demonstrated significant reductions in readmissions with improved quality of life in outpatient and remote settings. Data from several studies focused on remote monitoring devices strongly suggest that understanding congestion using physiological biomarkers is an effective management strategy. Since most cases of heart failure are first presented in acute hospitalization settings, immediate access to intracardiac pressure for treatment and decision-making purposes could result in substantial management improvements. However, a notable technology gap needs to be addressed to enable this at a low cost with less reliability on scarce specialist care resources. Contemporary evidence is conclusive that direct hemodynamic are the vital signs in heart failure with the highest clinical utility. Therefore, future ability to obtain these insights reliably using non-invasive methods will be a paradigm-changing technology.

Metabolic syndrome (MetS) is not a disease but a constellation of metabolic abnormalities that together increase the risk of developing cardiovascular disease (CVD) [...].

The genetic landscape of cardiometabolic risk factors has been explored extensively. However, insight in the effects of genetic variation on these risk factors over the life course is sparse. Here, we performed genome-wide interaction studies (GWIS) on different cardiometabolic risk factors to identify age-specific genetic risks. This study included 270,276 unrelated European-ancestry participants from the UK Biobank (54.2% women, a median age of 58 [interquartile range (IQR): 50, 63] years). GWIS models with interaction terms between genetic variants and age were performed on apolipoprotein B (ApoB), low-density lipoprotein-cholesterol (LDL-C), log-transformed triglycerides (TG), body mass index (BMI) and systolic blood pressure (SBP). Replication was subsequently performed in the Copenhagen General Population Study (CGPS) and the Estonian Biobank (EstBB). Multiple lead variants were identified to have genome-wide significant interactions with age (Pinteraction < 1e - 08). In detail, rs429358 (tagging APOE4) was identified for ApoB (Pinteraction = 9.0e - 14) and TG (Pinteraction = 5.4e - 16). Three additional lead variants were identified for ApoB: rs11591147 (R46L in PCSK9, Pinteraction = 3.9e - 09), rs34601365 (near APOB, Pinteraction = 8.4e - 09) and rs17248720 (near LDLR, Pinteraction = 2.0e - 09). Effect sizes of the identified lead variants were generally closer to the null with increasing age. No variant-age interactions were identified for LDL-C, SBP and BMI. The significant interactions of rs429358 with age on ApoB and TG were replicated in both CGPS and EstBB. The majority of genetic effects on cardiometabolic risk factors remain relatively constant over age, with the noted exceptions of specific genetic effects on ApoB and TG.

Limited data are available regarding the effect of metabolic syndrome on heart failure (HF) development in young individuals. Utilizing data from the Korean National Health Insurance Service, we included a total of 1,958,284 subjects in their 40s who underwent health screening between January 2009 and December 2009 in Korea. Subjects were classified into three groups: normal, pre-metabolic syndrome (Pre-MetS), and metabolic syndrome (MetS). MetS was identified in 10.58% of males and 5.21% of females. The hazard ratio for HF in subjects with MetS was 1.968 (95% CI: 1.526-2.539) for males and 2.398 (95% CI: 1.466-3.923) for females. For those with Pre-MetS, the hazard ratio was 1.607 (95% CI: 1.293-1.997) in males and 1.893 (95% CI: 1.43-2.505) in females. Additionally, acute myocardial infarction and low hemoglobin levels were identified as significant risk factors for HF in both genders. MetS approximately doubled the risk of developing HF in individuals in their 40s. Pre-MetS was also a significant risk factor for HF in this population.