Emergency department clinical performance of ADVIA Centaur n-terminal prohormone of B-type natriuretic peptide assay.

BACKGROUND: Natriuretic peptide testing is guideline recommended as an aid to the diagnosis of heart failure (HF). We sought to evaluate the performance of the ADVIA Centaur (Siemens Healthcare Diagnostics, Tarrytown, NY) NT-proBNPII assay (PBNPII) in emergency department (ED) dyspneic patients. METHODS: Eligible patients presented to the ED with dyspnea, with their gold standard diagnosis determined by up to 3 cardiologists blinded to the PBNPII results. Patients were stratified into 3 groups based on PBNPII resultsa rule out group of NT-proBNP<300  pg/mL, an age-specific rule in group using cutoffs of 450, 900, and 1800 pg/mL, for <50, 50-75, and > 75 years respectively, and an intermediate cohort for results between the rule out and rule in groups. RESULTS: Of 3128 eligible patients, 1148 (36.7 %) were adjudicated as acute heart failure (AHF). The gold standard AHF diagnosis rate was 3.7, 24.3, and 67.2 % for patients with NTproBNPII in the negative, indeterminate, and positive groups, respectively. Overall likelihood ratios (LR) were 0.07 (95 % CI: 0.05,0.09), 0.55 (0.45,0.67), and 3.53 (3.26,3.83) for the same groups, respectively. Individual LR+for age dependent cutoffs were 5.01 (4.25,5.91), 3.71 (3.25,4.24), and 2.38 (2.10,2.69), respectively. NTproBNPII increased with increasing severity of HF when stratified by NYHA classification. CONCLUSIONS: The ADVIA Centaur PBNPII assay demonstrates acceptable clinical performance using the recommended single rule out and age dependent rule in cutoffs for an AHF diagnosis in dyspneic ED patients.

Image-Based Estimation of Left Ventricular Myocardial Stiffness.

Elevation in left ventricular (LV) myocardial stiffness is a key remodeling-mediated change that underlies the development and progression of heart failure (HF). Despite the potential diagnostic value of quantifying this deterministic change, there is a lack of enabling techniques that can be readily incorporated into current clinical practice. To address this unmet clinical need, we propose a simple protocol for processing routine echocardiographic imaging data to provide an index of left ventricular myocardial stiffness, with protocol specification for patients at risk for heart failure with preserved ejection fraction. We demonstrate our protocol in both a preclinical and clinical setting, with representative findings that suggest sensitivity and translational feasibility of obtained estimates.

Exosomal miRNAs in patients with chronic heart failure and hyperuricemia and the underlying mechanisms.

Chronic heart failure (CHF) combined with hyperuricemia (HUA) is a comorbidity that is hard to diagnose by a single biomarker. Exosomal miRNAs are differentially expressed in cardiovascular diseases and are closely associated with regulating most biological functions. This study aimed to provide evidence for miRNA as a new molecular marker for precise diagnosis of the comorbidity of CHF with HUA and further analyze the potential targets of differentially expressed miRNA. This controlled study included 30 CHF patients combined with HUA (Group T) and 30 healthy volunteers (Group C). 6 peripheral blood samples from Group T and Group C were analyzed for exosomal miRNAs by high-throughput sequencing and then validated in the remaining 24 peripheral blood samples from Group T and Group C by applying real-time PCR (RT-PCR). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using R software to predict the differential miRNAs' action targets. 42 differentially expressed miRNAs were detected (18 upregulated and 24 downregulated), in which miR-27a-5p was significantly upregulated (P<0.01), and miR-139-3p was significantly downregulated (P<0.01) in Group T. The combination of miR-27a-5p and miR-139-3p predicted the development of CHF combined with HUA with a maximum area under the curve (AUC) of 0.899 (95 % CI: 0.812-0.987, SEN=79.2 %, SPE=91.7 %, J value = 0.709). GO and KEGG enrichment analysis revealed that the differentially expressed miRNAs had a role in activating the AMPK-mTOR signaling pathway to activate the autophagic response. Collectively, our findings suggest that upregulated exosomal miR-27a-5p combined with downregulated exosomal miR-139-3p can be used as a novel molecular marker for precise diagnosis of CHF combined with HUA and enhanced autophagy by AMPK-mTOR signaling pathway may be one pathogenesis of the differentially expressed miRNAs.

Effectiveness of the frailty index in predicting short-term and long-term mortality risk in patients with chronic heart failure.

OBJECTIVE: 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). MATERIALS AND METHODS: 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. RESULTS: 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). CONCLUSION: 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.

Hyperuricaemia elevates risk of short-term readmission and mortality in patients with heart failure.

BACKGROUND: Heart failure (HF) is a leading cause of morbidity and mortality worldwide. Serum uric acid (SUA), a product of purine metabolism, has been implicated in HF progression. However, the association between hyperuricaemia and the short-term readmission and mortality in patients with HF remains controversial. METHODS: In this retrospective cohort study, we analysed data from a HF database specific to the Chinese population. The primary endpoint was short-term readmission or all-cause mortality within 90 days. Participants with HF were categorised into normouricaemia group (NUA) and hyperuricaemia group (HUA) based on a SUA threshold of 420 µmol/L. The association between SUA and primary endpoint was evaluated using Kaplan-Meier survival curves and Cox regression analysis. RESULTS: Baseline characteristics revealed significant differences between NUA and HUA groups, with the latter exhibiting a higher prevalence of males, chronic kidney disease (CKD) and elevated levels of various biomarkers. During a 90-day follow-up, 493 (26.6%) participants reached the primary endpoint, with a higher incidence observed in the HUA group at 31.2%, compared with 20.1% in the NUA group. When a threshold effect was identified at 420 µmol/L, a non-linear association was observed between SUA and the primary endpoint. After adjusting for gender, age, New York Heart Association class, CKD, systolic blood pressure (SBP) and potassium, the HUA group exhibited a higher risk for the primary endpoint compared with the NUA group (HR: 1.40, 95% CI: 1.14 to 1.72, p=0.001). Additionally, the risk increased across quartiles of SUA (P for trend=0.002). Furthermore, stratified analyses indicated a stronger association in patients without CKD (P interaction=0.033). CONCLUSION: Hyperuricaemia is independently associated with an increased risk of short-term readmission and mortality in patients with HF. Our findings suggest that monitoring and managing SUA could be crucial in improving patient with HF outcomes.

Association between aspartate aminotransferase to alanine aminotransferase ratio and mortality in critically ill patients with congestive heart failure.

Congestive heart failure (CHF) is a complex clinical syndrome that significantly impacts patient outcomes, especially in critically ill patients admitted to intensive care units (ICUs). The aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio (AST/ALT), has also been reported as a risk factor of cardiovascular diseases. However, few studies investigated the correlations between the AST/ALT ratio and ICU mortality in critically ill patients with CHF. This study investigates the association between the baseline AST/ALT ratio measured within the first 24 h of ICU admission and 28-day ICU all-cause mortality in critically ill patients with CHF. This retrospective cohort study included 4869 critically ill patients with CHF from the eICU Collaborative Research Database. Patients were categorized into tertiles based on their AST/ALT ratio: Tertile 1 (0.13-0.97), Tertile 2 (0.97-1.50), and Tertile 3 (1.50-5.89). Univariate and multivariate Cox proportional hazards regression models were used to evaluate the association between the AST/ALT ratio and 28-day ICU all-cause mortality. Nonlinear threshold effects and subgroup analyses were conducted to assess the robustness of the findings. Kaplan-Meier survival curves were generated to compare survival probabilities across tertiles. Participants with higher AST/ALT ratios were older, had higher illness severity, and experienced worse clinical outcomes. In univariate analysis, the AST/ALT ratio was significantly associated with 28-day ICU mortality (HR: 1.24, 95% CI 1.13-1.37, P < 0.0001). This association remained significant in the fully adjusted multivariate model. The highest tertile of AST/ALT ratio was associated with a significantly higher risk of mortality compared to the lowest tertile across all models (HR: 1.48, 95% CI 1.07-2.03, P = 0.0162 in Model 4). A nonlinear relationship was observed, with a threshold identified at an AST/ALT ratio of 2.08. Below this turning point, the association remained strong (HR: 1.47, 95% CI 1.13-1.91, P = 0.0036), while above it, the association was no longer significant. Subgroup analyses revealed no significant interactions, indicating that the association between AST/ALT ratio and mortality was consistent across various patient characteristics. Survival analysis showed that patients in the highest tertile had the poorest survival outcomes (P < 0.0001). An elevated AST/ALT ratio within the first 24 h of ICU admission is independently associated with increased 28-day ICU all-cause mortality in critically ill patients with CHF.

Cardiotoxicity of venetoclax in patients with acute myeloid leukemia: comparison with anthracyclines.

Venetoclax is a promising drug for patients with acute myeloid leukemia (AML) ineligible for anthracycline-based treatments. In rats, venetoclax is reported to cause myocardial injury. Our objectives were to report the frequency of cardiovascular (CV) events in patients treated with venetoclax, and, subsequently, to compare CV outcomes in matched patients treated with venetoclax or anthracyclines. Patients diagnosed with AML and treated with venetoclax or anthracyclines from January 2017 to July 2021 were identified. Major adverse cardiac events (MACE, including new-onset heart failure (HF), acute myocardial infarction, new onset atrial fibrillation (AF)) were recorded. Propensity-score method was then used to compare patients treated with venetoclax or anthracyclines. Patients treated with venetoclax (n=103) were older, with more hyperlipidemia than patients treated with anthracyclines (n=217). However, only 63% of patients treated with venetoclax underwent echocardiographic screening (vs. 93% of patients treated with anthracyclines, P< 0.001). Eighteen patients with venetoclax (17%) and 27 patients with anthracyclines (12%) developed MACE, including 10 % of new HF in each group. The median time to MACE was 8 days (interquartile range 5-98 days). In the matched cohort (n=132 patients), the cumulative incidence of MACE at one year was not different (17.5 % venetoclax, 9.2% anthracyclines, p =0.27). Thus, MACE incidence is similar in matched patients receiving venetoclax or anthracyclines. Close CV monitoring during the early phase of treatment may be helpful in patients treated with venetoclax.

Early endomyocardial fibrosis mimicking dilated cardiomyopathy.

Endomyocardial fibrosis (EMF) is a poorly understood but common cause of heart failure in sub-Saharan Africa, which typically presents with a restrictive phenotype. We describe a previously unreported presentation of EMF with severe left ventricular dilatation and systolic dysfunction, mimicking dilated cardiomyopathy, in which longitudinal and multimodality imaging was crucial for the diagnosis.

AI derived ECG global longitudinal strain compared to echocardiographic measurements.

Left ventricular (LV) global longitudinal strain (LVGLS) is versatile; however, it is difficult to obtain. We evaluated the potential of an artificial intelligence (AI)-generated electrocardiography score for LVGLS estimation (ECG-GLS score) to diagnose LV systolic dysfunction and predict prognosis of patients with heart failure (HF). A convolutional neural network-based deep-learning algorithm was trained to estimate the echocardiography-derived GLS (LVGLS). ECG-GLS score performance was evaluated using data from an acute HF registry at another tertiary hospital (n = 1186). In the validation cohort, the ECG-GLS score could identify patients with impaired LVGLS (≤ 12%) (area under the receiver-operating characteristic curve [AUROC], 0.82; sensitivity, 85%; specificity, 59%). The performance of ECG-GLS in identifying patients with an LV ejection fraction (LVEF) < 40% (AUROC, 0.85) was comparable to that of LVGLS (AUROC, 0.83) (p = 0.08). Five-year outcomes (all-cause death; composite of all-cause death and hospitalization for HF) occurred significantly more frequently in patients with low ECG-GLS scores. Low ECG-GLS score was a significant risk factor for these outcomes after adjustment for other clinical risk factors and LVEF. The ECG-GLS score demonstrated a meaningful correlation with the LVGLS and is effective in risk stratification for long-term prognosis after acute HF, possibly acting as a practical alternative to the LVGLS.

Huangqi-Danshen decoction improves heart failure by regulating pericardial adipose tissue derived extracellular vesicular miR-27a-3p to activate AMPKα2 mediated mitophagy.

BACKGROUND: Huangqi-Danshen decoction (HDD) is a classic traditional Chinese medicine for treating heart failure. Pericardial adipose tissue (PAT) has recently gained increasing attention in cardiovascular diseases. PURPOSE: This study aimed to investigate the effect of pericardial adipose tissue-derived extracellular vesicles on heart failure, the protective effect of HDD on myocardial remodel in heart failure rats, and identify the potential molecular mechanisms involved. METHODS: UPLC-MS/MS identified active components of HDD. Extracellular vesicles (EVs) from pericardial adipose tissue of sham-operated and HF rats were identified through transmission electron microscopy, nanoparticle tracking analysis and western blot. EVs were co-cultured with H9c2 cardiomyocytes in order to examine their uptake and effects. MicroRNA sequencing, dual-luciferase reporter assay and PCR were conducted for exploring specific mechanisms of EVs on hypertrophic cardiomyocytes. In vivo, heart failure was modeled in rats via transverse aortic constriction (TAC). In vitro, the hypertrophic cardiomyocyte model were established using Ang II-induced H9c2 cardiomyocytes. RESULTS: UPLC-MS/MS identified 11 active components in serum of HDD administrated rats. Echocardiography showed HDD improved cardiac function in TAC model rats. HE and Masson staining indicated HDD ameliorated myocardial hypertrophy and fibrosis. MicroRNA sequencing found that HDD treatment resulted in 37 differentially expressed miRNAs (DMEs) (p < 0.05 and |log2FC| ≥ 1). KEGG analysis revealed that DEMs were enriched in the AMPK signaling pathway. PCR identified miR-27a-3p with the greatest difference in AMPK-related DMEs. Dual-luciferase reporter assay and Targetscan website were utilized to identify the target relationship between miR-27a-3p and PRKAA2 (AMPKα2). The miR-27a-3p negatively regulated AMPKα2 to inhibit mitophagy mediated by PINK1/Parkin pathway. HDD inhibited miR-27a-3p secretion from failing heart pericardial adipose tissue-derived extracellular vesicles, thereby improving inflammation, cardiac function, and myocardial remodeling through above pathways. CONCLUSION: HDD inhibited the PAT-derived extracellular vesicular miR-27a-3p in failing hearts to activate AMPK/PINK1/Parkin signaling-mediated mitophagy, which improved cardiomyocyte energy metabolism, myocardial remodeling and heart failure.

Unilateral pulmonary edema in a dog with a large, left-to-right shunting patent ductus arteriosus.

A 4-month-old, 5.0-kg male castrated mixed-breed dog was presented for further evaluation of a heart murmur. A grade 6/6 left basilar, continuous heart murmur, and bounding femoral arterial pulses were observed, consistent with a patent ductus arteriosus (PDA). Transthoracic echocardiography confirmed the diagnosis of a large, left-to-right shunting PDA with severe left heart volume overload. Thoracic radiography revealed severe, alveolar lung disease in the right cranial, right middle, and right caudal lung lobes; no pulmonary infiltrate was observed in the left lung lobes. Unilateral pulmonary edema secondary to the PDA was diagnosed, which later resolved with medical management and transcatheter occlusion of the PDA with an Amplatz Canine Ductal Occluder. Unilateral pulmonary edema secondary to a PDA has not been previously reported in the dog.

Gut dysbiosis and neutrophil extracellular traps in chronic heart failure.

BACKGROUND: Chronic heart failure (HF) patients have reduced microbiota diversity. Leakage of microbes and their metabolites into the bloodstream may activate neutrophils. Neutrophil extracellular traps (NETs) consist of chromatin and proteases, and may contribute to HF pathogenesis. We assessed associations between circulating NETs and 1) cardiac function, 2) the degree of gut microbiota diversity and 3) gut leakage and microbial metabolites in HF patients. METHODS: A cross-sectional study including 124 patients with chronic HF and left ventricular ejection fraction ≤40 %. Severe HF was defined as N-terminal pro-B-type natriuretic peptide concentrations above median. We measured citrullinated histone H3 (CitH3), myeloperoxidase- and double-stranded-DNA in the blood. Gut leakage markers included bacterial lipopolysaccharides and soluble cluster of differentiation 14. The microbial metabolites included circulating trimethylamine N-oxide and butyrate producing capacity. We used the Shannon diversity-index and a dysbiosis-index based on bacteria with altered relative abundance to characterize the gut microbiota profile. RESULTS: Quartile 4 of CitH3 was associated with more severe HF compared to quartiles 1-3, after adjustments for age, gender and hypertension (adjusted odds ratio [95 %CI] 3.21[1.18-8.69], p = 0.022). CitH3 was moderately associated with hypertension (p = 0.04), higher CRP levels (p = 0.016) and lower Shannon diversity index, (p = 0.039). No other NET marker associated with severe HF. CONCLUSIONS: In chronic HF patients with reduced LVEF, high levels of CitH3 were associated with disease severity, inflammation and reduced gut microbiota diversity. Our results suggest that enhanced release of NETs could be involved in progressive HF, although the contribution of the gut microbiota seems limited in this context.

New strategies for the treatment of hyperkalemia.

Renin-angiotensin-aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRAs) are key drugs in the management of patients with cardiovascular diseases (CVD), particularly those with hypertension, diabetes, chronic kidney disease and heart failure (HF), given their demonstrated effectiveness in reducing the risk of both surrogate and hard endpoints. Despite their positive impact on the outcome, patients with RAASi and MRAs are particularly vulnerable to hyperkalaemia, with approximately 50 % of these individuals experiencing two or more recurrences annually. The common practice of reducing the dose or discontinuing the treatment with RAASi and MRAs in conditions of hyperkalaemia results in suboptimal management of these patients, with a potential impact on their mortality and morbidity risk. Recent guidelines from cardiovascular and renal international societies increasingly recognize the need for alternative strategies to manage the risk of hyperkalaemia, allowing the continuation of RAASi and MRA therapies. In this review, we summarise the new potential options available to manage hyperkalaemia in patients with CVD and the recommendations of the most recent guidelines on the topic.

A novel cardioprotective perfusion protocol prevents functional decline during extended normothermic ex situ heart perfusion of porcine hearts.

INTRODUCTION: A common limitation to normothermic ex situ heart perfusion (ESHP) is functional decline. We previously designed a cardioprotective normothermic perfusion protocol, incorporating adenosine-lidocaine cardioplegia, subnormothermic reperfusion, pyruvate and methylprednisolone supplementation, and hemofiltration to prevent myocardial functional decline over 4 hours. In this study, we added continuous catecholamine infusion and protective loading conditions to assess the effectiveness of this enhanced cardioprotective perfusion protocol in preventing functional decline during extended normothermic perfusion in marginal porcine hearts. MATERIALS & METHODS: Six slaughterhouse pig hearts underwent 9 hours of normothermic ESHP using the enhanced cardioprotective protocol. Cardiac function was assessed at 90, 120, 240, 360, 480 and 540 minutes of ESHP. Subsequently, a preload-challenge was conducted after 9 hours to assess preload-responsiveness (mimicking the Frank-Starling principle) and suitability for transplantation. RESULTS: During perfusion, myocardial function remained stable, indicated by consistent mean cardiac index (9.2 L/min/kg at 90; 9.3 L/min/kg at 540 minutes of ESHP), left ventricular stroke work index (6258 mmHg*ml/kg at 90; 6707 mmHg*ml/kg at 540 minutes) and rate of ventricular pressure change over time. In response to a preload-challenge, there was a notable increase of 34% in mean cardiac index and 58% in mean stroke work. CONCLUSION: Our study demonstrates that the implementation of a cardioprotective protocol enables (very) marginal porcine slaughterhouse hearts, subjected to both a warm and cold ischemic insult prior to ESHP, to sustain satisfactory cardiac function without notable decline during 9 hours of normothermic ESHP, while also preserving their preload-responsiveness. The latter finding might indicate suitability for transplantation. This study provides a groundwork for further extending normothermic ESHP, unlocking the full potential of this promising technology.

DAPAGLIFLOZIN EFFECTS ON LEFT VENTRICULAR REMODELING AND FILLING PRESSURES IN HEART FAILURE WITH REDUCED EJECTION FRACTION.

AIMS: The benefits of sodium glucose cotransporter 2 inhibitors in patients with heart failure with reduced ejection fraction (HFrEF) have been clearly demonstrated in randomized clinical trails. However, the mechanisms of the observed beneficial effects remain incompletely understood. This study aimed to assess morpho-functional cardiac changes following dapagliflozin introduction in stable outpatients with HFrEF and to investigate whether these changes were determinants of the improved clinical outcome. METHODS AND RESULTS: In this multicenter, prospective observational study, 300 consecutive HFrEF patients ≥ 18 years old on optimized medical therapy (OMT) and eligible for dapagliflozin therapy were enrolled between april 2022 and January 2023. Laboratory and echocardiographic assessments were performed at baseline and after a median of 6 months. Following dapagliflozin initiation, 47% of patients achieved a target of improvement in left ventricular end-diastolic volume (Δ EDVi < -10%) and/or end-systolic volume (Δ ESVi <-15%) and/or ejection fraction (Δ EF% > 10%) at 6 months. The proportion of patients with elevated left ventricular filling pressures decreased from 26% to 3% at 6 months (p<0.001). The combination of left ventricular remodeling (LVRR) and filling pressures improvements was associated with absence of HF-related hospitalizations and significant natriuretic peptides (NPs) reduction at 12 months. CONCLUSIONS: Dapagliflozin detemined LVRR and improved left ventricular filling pressures in a high proportion of patients with stable HFrEF patients already on OMT. These improvements were associated with absence of HF-related hospitalizations and a significant NPs reduction at 12 months.

Benefits of a comprehensive care model in patients with heart failure and chronic obstructive pulmonary disease: UMIPIC Program.

BACKGROUND: Patients with heart failure (HF) and chronic obstructive pulmonary disease (COPD) have a high risk of hospital admission and mortality. This study evaluated the benefit of a care model, characterized by comprehensive and continuous care (UMIPIC program) in patients with HF and a history of COPD. METHODS: A total of 5644 patients were prospectively recruited, of which 1320 had a history of COPD between March 2008 and March 2020. They were divided into 2 follow-up groups at the time of discharge, one in follow-up in the UMIPIC program (435 patients) and another treated conventionally (885 patients). The baseline characteristics of each group were analyzed and patients in each group were selected by propensity score matching and admissions and mortality were evaluated during 12 months of follow-up, after an episode of hospitalization for HF. RESULTS: The UMIPIC group, compared to the conventional group in the matched cohort, had a lower rate of admissions for HF (21% vs 30 respectively; hazard ratio [HR] = 0.64; 95% confidence interval [95% CI]: 0.54-0.84; p = 0.002) and mortality (28% vs. 36%, respectively; HR = 0.68; 95% CI: 0.51-0.90; p = 0.008). From a therapeutic point of view, patients with HF and a history of COPD who were followed in the UMIPIC program received a higher percentage of beta-blockers (64% vs 54%; p < 0.05) and direct-acting anticoagulants (17% vs 9%: p < 0.05) than those followed conventionally. CONCLUSIONS: The implementation of the UMIPIC care program for patients with HF and a history of COPD, based on comprehensive and continuous care, reduces both admissions and mortality at one year of follow-up. The prescription of beta-blockers and direct-acting anticoagulants was also higher during follow-up in the UMIPIC program.

Cardio-oncological dialogue: Understanding the mechanistic correlation between heart failure and cancer.

AIMS: This review aims to elucidate the bidirectional relationship between heart failure and cancer by identifying their common and reciprocal risk factors. It seeks to provide a comprehensive understanding of the mechanistic interactions between these two conditions, supported by evidence from preclinical and clinical investigations. MATERIALS AND METHODS: A thorough review of peer-reviewed articles was conducted to identify all possible interactions between cancer and heart failure. Multiple search engines were utilized with queries incorporating terms such as cardio-oncology, heart failure, cancer, risk factors, and mechanistic interactions. Selected studies were analysed to identify shared risk factors and to explore the mechanistic junctions that link the two diseases. KEY FINDINGS: The review identified several common risk factors, including, inflammation, smoking, obesity, clonal haematopoiesis of indeterminate potential, and reduced exercise potential. The pathophysiological mechanisms linking heart failure with cancer include metabolic reprogramming in cancer, cancer-induced thrombosis, cardiac metastasis, paraneoplastic syndrome, cancer-associated cachexia, and anorexia. Additionally, it was found that cancer therapies, such as anthracyclines and radiation, can induce cardiotoxicity, leading to heart failure. The pathophysiological mechanisms that contribute to cancer in heart failure patients were identified as neurohormonal activation, state of hypoxia, secretion of Cardiokines, heart failure medication, innate immune reprograming & cardiac remodelling and coronary atherosclerotic disease. SIGNIFICANCE: By highlighting the interconnected nature of heart failure and cancer, this review promotes a cardio-oncologic discourse, encouraging cardiologists and oncologists to consider these diseases as interrelated rather than separate entities. This perspective can lead to the development of novel therapeutic strategies and improve patient management by addressing the dual disease burden. Future research should focus on exploring the translational potential of existing drugs and developing new interventions to target the shared characteristics of heart failure and cancer.

Left ventricular size and heart failure: A cardiac MRI assessment of 38,129 individuals from the UK Biobank.

BACKGROUND: Previous studies suggest that prevalent heart failure (HF) differs based on left ventricular ejection fraction (LVEF) and left ventricular (LV) chamber size. Furthermore, the prevalence of HF with preserved ejection fraction (HFpEF) is often considered approaching, or exceeding that of HF with reduced ejection fraction in the community. AIM: The aim of this study was to evaluate prevalent and incident HF based on LVEF and CMR-determined LV size within a large community-dwelling cohort. METHODS: Individuals from the United Kingdom Biobank (UKB) who underwent CMR and had available health record linkage to allow ascertainment of HF diagnosis were included. The cohort was analysed according to LVEF, LV end-diastolic volume (LVEDV) quartiles and LVEDV indexed to body surface area (LVEDVi). RESULTS: 38,129 individuals were included, comprising those with reduced LVEF (LVEF<50 %, n = 5096) and preserved LVEF (LVEF 50-60 %, n = 22,907, LVEF≥60 %, n = 10,126). Prevalent HF was highest in males with LVEF<50 %, and participants with reduced LVEF had higher rates of incident HF (p < 0.001) during the follow-up period (median = 2.46 years from CMR). Mean LVEDV and LVEDVi were largest in individuals with EF < 50 % (146.9 ±â€¯36.2 ml and 76.8 ±â€¯16.4 ml/m2 respectively). Compared to the smallest quartiles, the largest quartiles for LVEDV were associated with increased odds of HF (odds ratio 2.14 [95 % confidence interval 1.47-3.12], p < 0.001). CONCLUSIONS: Over 50 % of HF cases occur in individuals with LVEF ≥50 %, however HF prevalence is highest in those with reduced LVEF, particularly in males. Larger LV size is associated with increased HF across the LVEF spectrum.