Over the past few decades, the rising burden of metabolic disease, including type 2 diabetes, prediabetes, obesity, and metabolic dysfunction-associated steatotic liver disease, has corresponded with fundamental shifts in the landscape of heart failure (HF) epidemiology, including the rising prevalence of HF with preserved ejection fraction. It has become increasingly important to understand the role of extracardiac contributors and interorgan communication in the pathophysiology and phenotypic heterogeneity of HF. Whereas traditional epidemiological strategies have separately examined individual contributions of specific comorbidities to HF risk, these approaches may not capture the shared mechanisms and more complex, bidirectional relationships between cardiac and noncardiac comorbidities. In this review, we highlight the cardiac, kidney, liver, and metabolism multiorgan interactions and pathways that complicate HF development and progression and propose research strategies to further understand HF in the context of multiple organ disease. This includes evolving epidemiological approaches such as multiomics and machine learning which may better capture common underlying mechanisms and interorgan crosstalk. We review existing preclinical models of HF and how they have enhanced our understanding of the role of multiorgan disease in the development of HF subtypes. We suggest recommendations as to how clinical practice across multiple specialties should screen for and manage multiorgan involvement in HF. Finally, recognizing the advent of novel combinatorial therapeutic agents that may have multiple indications across the cardiac-kidney-liver metabolism continuum, we review the current clinical trials landscape. We specifically highlight a pressing need for the design of more inclusive trials that examine the contributions of multimorbidity and incorporate multiorgan end points, which we propose may lead to outcomes that are evermore clinically relevant today.

The liver and heart are closely interconnected organs, and their bidirectional interaction plays a central role in cardiometabolic disease. In this review, we summarize current evidence linking liver dysfunction-particularly metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, and cirrhosis-with an increased risk of heart failure and other cardiovascular diseases. We discuss how these liver conditions contribute to cardiac remodeling, systemic inflammation, and hemodynamic stress and how cardiac dysfunction in turn impairs liver perfusion and promotes hepatic injury. Particular attention is given to the molecular mediators of liver-heart communication, including hepatokines and cardiokines, as well as the emerging role of advanced research methodologies, including omics integration, proximity labeling, and organ-on-chip platforms, that are redefining our understanding of interorgan cross talk. By integrating mechanistic insights with translational tools, this review aims to support the development of multiorgan therapeutic strategies for cardiometabolic disease.

Hospital admission for heart failure (HF) is associated with increased mortality risk. Patients admitted with HF can be divided into those with a known previous diagnosis of HF and de novo cases. However, few studies have compared these groups. We compared long-term outcomes of patients with de novo versus acute decompensated HF (ADHF).

We included data from two London hospitals, King's College Hospital and Princess Royal University Hospital. Data from all admissions were collected from the National Institute for Cardiovascular Outcomes and Research (NICOR) National Heart Failure Audit (NHFA) between 2020 and 2021. The outcome measure was all-cause mortality. A total of 561 patients were included in the study. One third (29 %) were de novo hospitalisations. Over a median follow-up of 15 (interquartile range 4-21) months, 257 (46 %) patients died. Hospitalisation for ADHF was associated with higher all-cause mortality during follow-up (51 % vs 34 %, p < 0.001). In adjusted models, hospitalisation for ADHF remained independently associated with higher all-cause mortality during follow-up (HR 0.60, 95 % CI 0.38-0.96; p = 0.03).

Amongst patients hospitalised for HF, having a history of HF is associated with a higher risk of all-cause mortality than de novo cases. This may have implications for randomised studies that do not routinely document patients' HF history. Prospective studies are needed to elucidate the risk profiles of these two distinct populations for better risk stratification.

The assessment of left ventricular (LV) diastolic function based on the American Society of Echocardiography and the European Association of Cardiovascular Imaging (ASE/EACVI) guidelines requires measurement of several echocardiographic indices. However, these assessments often yield inconclusive results owing to the absence of measurable parameters. Multiple B-lines on lung ultrasound have been proposed as a method for evaluating pulmonary congestion. We aimed to evaluate the association between B-lines and LV diastolic function and to examine whether B-lines show potential as an alternative to conventional indices for assessing LV diastolic function.

This prospective study included 172 patients with pre-heart failure (HF) or HF. We investigated (i) the relationship between B-lines and LV diastolic function using echocardiography, (ii) the diagnostic accuracy of B-lines compared to echocardiography indices for estimating LV filling pressures and (iii) the relationship between B-lines and risk of hospitalisation for HF.

Among patients for whom the ASE/EACVI guideline algorithm for LV diastolic dysfunction was available (n = 89), the number of B-lines typically increased with the severity of diastolic dysfunction grade. In patients who underwent left heart catheterisation (n = 20), the LV filling pressure was significantly correlated with B-lines (r = 0.690, P < 0.001). The diagnostic accuracy of B-lines for detecting high LV filling pressure was comparable to that of tricuspid regurgitation peak gradient (TRPG). When TRPG was replaced with B-lines to diagnose grade II or III diastolic dysfunction using the ASE/ESCVI algorithm, sensitivity remained comparable (0.80); however, specificity improved (0.80 vs. 0.50). In patients who underwent lung ultrasound while they were hemodynamically stable and were followed up for prognosis (median, 730 days; n = 75), 14 hospitalisations for HF were observed. Kaplan-Meier analysis revealed that the high B-line group had a significantly higher incidence of hospitalisation events for HF (P = 0.036, log-rank test).

B-lines have shown potential as an alternative to conventional indices for assessing LV diastolic dysfunction.

Congestion is a key clinical feature of heart failure (HF), contributing to hospitalizations, disease progression, and poor outcomes. While traditionally considered a hemodynamic issue, congestion is now recognized as a systemic process affecting multiple organs. Renal dysfunction arises from impaired perfusion and sodium retention, leading to maladaptive left ventricular remodeling. Hepatic congestion contributes to cholestatic liver injury, while metabolic disturbances drive anemia, muscle wasting, and systemic inflammation. Additionally, congestion disrupts the intestinal barrier and immune function, exacerbating HF progression. Given its widespread impact, effective congestion management requires a shift from a cardiovascular-centered approach to a comprehensive, multidisciplinary strategy. Targeted decongestive therapy, metabolic and nutritional optimization, and immune modulation are crucial in mitigating congestion-related organ dysfunction. Early recognition and intervention are essential to slow disease progression, preserve functional capacity, and improve survival. Addressing HF congestion through personalized, evidence-based strategies is vital for optimizing long-term care and advancing treatment paradigms.

Heart failure (HF) is a major health problem because of its high prevalence, morbidity, mortality, and cost of care. An important contributor to morbidity and mortality in patients with advanced HF is kidney dysfunction. Almost half of HF patients develop cardiorenal syndrome (CRS). The management of advanced HF complicated by CRS is challenging. Two main strategies have been widely accepted for the management of CRS, namely improving cardiac output and relieving congestion. Diuretics remain the cornerstone and first-line therapy for decongestion; however, a substantial number of CRS patients develop diuretic resistance. In the face of persistent congestion and the progressive deterioration of kidney function, the implementation of kidney replacement therapy may become the only solution. In the review the current evidence on extracorporeal and peritoneal-based kidney replacement techniques for the therapy of CRS patients are presented.

Central venous pressure (CVP) monitoring is critical for fluid management in critically ill patients. This study evaluated the impact of CVP monitoring on 1-year mortality in intensive care unit (ICU) patients with congestive heart failure (CHF).

Data from the Medical Information for Critical Care IV (MIMIC-IV) database were analyzed for ICU patients admitted for the first time with a stay > 24 h. Patients were categorized into CVP and no-CVP groups based on CVP measurement. Logistic regression analyses were performed, with propensity score matching (PSM) and overlap weighting (OW) to minimize confounding. Inflection point analysis using logistic regression was conducted in the CVP group. Patients were further stratified into early (≤ 24 h) and late (> 24 h) CVP monitoring groups for additional analysis.

Among 4,479 patients, 919 were in the CVP group and 3,560 in the no-CVP group. CVP monitoring was associated with lower 1-year mortality (odds ratio [OR] = 0.75, 95% confidence interval [CI] = 0.62-0.91, p = 0.003). Early CVP monitoring (≤ 24 h) independently reduced 1-year mortality (OR = 0.68, 95% CI = 0.47-0.97, p = 0.032). Predictors of mortality included the lowest diastolic blood pressure, lowest blood glucose, highest blood chloride, and Acute Physiology Score III (APSIII) score within 24 h of admission.

Early CVP monitoring significantly improves 1-year survival in ICU patients with congestive heart failure. These findings underscore the value of timely hemodynamic assessments in critical care and warrant further prospective validation in diverse settings.

Interactions between the heart and other organs have been a focus in acute decompensated heart failure (ADHF). However, the association between ADHF and pancreatic exocrine insufficiency (PEI), which may lead to malnutrition, remains unclear. We investigated the relationship between exocrine pancreatic enzymes and ADHF.

We enrolled 155 and 46 patients with and without ADHF, respectively. Serum amylase and lipase levels were compared between the two groups. In the ADHF group, factors correlating with serum amylase or lipase levels were assessed using multiple regression analysis, and changes in their levels throughout the hospital course were determined.

Patients with ADHF exhibited significantly lower amylase and lipase levels. In the same group, the significant independent correlates of lower amylase levels included a lower blood urea-nitrogen level (partial correlation coefficient, 0.530; p < 0.001), lower albumin level (partial correlation coefficient, 0.252; p = 0.015), and higher uric acid level (partial correlation coefficient, -0.371; p < 0.001). The significant independent correlates of lower lipase levels included coexisting atrial fibrillation (coefficient, 0.287; p = 0.026), lower creatinine level (coefficient, 0.236; p = 0.042), and higher B-type natriuretic peptide level (coefficient, -0.257; p = 0.013). Both amylase and lipase levels significantly increased following the improvement in ADHF.

In patients with ADHF, decreased serum amylase and lipase levels were associated with the congestion severity, suggesting that PEI may occur in patients with ADHF, potentially due to ADHF-related congestion.

This chapter focuses on currently underappreciated aspects of the maternal circulation: blood pressure phenotypes, venous hemodynamics, intra-abdominal pressure, and body water homeostasis. Based on the hemodynamic balance between cardiac output and total peripheral resistance, flow-dominant and resistance-dominant phenotypes of normotension and hypertension exist, with different impacts on gestational outcome. Cardiac diastolic function and venous hemodynamics play a prominent role in gestational changes in cardiac output. An increase in intra-abdominal pressure during pregnancy interferes with body water volume homeostasis, similar to syndromes of multi-organ dysfunctions in non-pregnant individuals. Today, non-invasive maternal hemodynamics assessment allows for obtaining important information on these ignored circulatory functions in addition to conventional sphygmomanometric blood pressure measurement. This offers perspectives to improve current strategies for screening, diagnosis, and management of gestational hypertension disorders, a path, however, to be paved first by intensified multifaceted and multidisciplinary research.

To explore the molecular mechanism of aerobic exercise to improve heart failure and to provide a theoretical basis and experimental reference for the treatment of heart failure. Nine-week-old male mice were used to establish a left ventricular pressure overload-induced heart failure model by transverse aortic constriction (TAC). The mice were randomly divided into four groups: a sham group (SHAM), heart failure group (HF), heart failure + SKQ1 group (HS) and heart failure + aerobic exercise group (HE). The mice in the HE group were subjected to moderate-intensity aerobic exercise interventions. The mitochondrion-targeting antioxidant (SKQ1) contains the lipophilic cation TPP, which targets scavenging mitochondrial ROS. The HS group was subjected to SKQ1 (100 nmol/kg/d) interventions, which were initiated 1 week after the surgery, and the interventions lasted 8 weeks. Cardiac function was assessed by ultrasound, cardiomyocyte size by H&E and WGA staining, myocardial fibrosis by Masson's staining, and myocardial tissue oxidative stress and apoptosis by DHE and TUNEL fluorescence staining, respectively. Western blotting was used to detect the expression of mitochondrial quality control, inflammation, and apoptosis-related proteins. In the cellular level, an in vitro cellular model was established by isolating primary cardiomyocytes from neonatal mice (2-3 days) and intervening with Ang II (1 μM) to mimic heart failure. Oxidative stress and mitochondrial membrane potential were determined in the cardiomyocytes of each group by DHE and JC-1 staining, respectively. Myocardial fibrosis was increased significantly and cardiac function was reduced significantly in the heart failure mice. Aerobic exercise and SKQ1 intervention improved cardiac function and reduced myocardial hypertrophy and myocardial fibrosis in the heart failure mice significantly. Meanwhile, aerobic exercise and SKQ1 intervention reduced the number of DHE-positive particles (p < 0.01) and inhibited myocardial oxidative stress in the heart failure mice significantly. Aerobic exercise also reduced DRP1, Parkin, and BNIP3 protein expression (p < 0.05, p < 0.01), and increased OPA1 and PINK1 protein expression (p < 0.05, p < 0.01) significantly. Moreover, aerobic exercise and SKQ1 intervention decreased the number of TUNEL-positive particles and the expression of inflammation- and apoptosis-related proteins NLRP3, TXNIP, Caspase-1, IL-1β, BAX, BAK, and p53 significantly (p < 0.05, p < 0.01). In addition, the AMPK agonist AICAR and the mitochondria-targeted ROS scavenger (SKQ1) ameliorated AngII-induced mitochondrial fragmentation and decreased mitochondrial membrane potential in cardiomyocytes significantly. It was shown that inhibition of mitochondrial ROS by aerobic exercise, which in turn inhibits mitochondrial damage, improves mitochondrial quality control, and reduces myocardial inflammatory and apoptosis, may be an important molecular mechanism by which aerobic exercise exerts endogenous antioxidant protective effects to improve cardiac function.

Background/Objectives: Heart failure (HF) can damage organs because of poor perfusion and/or congestion. The interactions between HF and other organs have recently been studied; however, data on the interaction between HF and pancreatic exocrine function, which may affect fat and protein absorption and malnutrition, are scarce. We previously showed that the serum levels of pancreatic exocrine enzymes, as suggestive of pancreatic exocrine function, were low and associated with malnutrition or congestion in hospitalized patients with acute decompensated HF (ADHF). This study investigated the relationship between the serum levels of pancreatic exocrine enzymes and long-term outcomes in patients with ADHF. Methods: We collected serum levels of pancreatic exocrine enzymes (amylase and lipase) from patients who were admitted to the cardiac intensive care unit due to ADHF. Patients undergoing dialysis and those with neoplasms were excluded. Patients were categorized as having high or low pancreatic exocrine enzyme levels in the first quartile upon admission. The association between low serum pancreatic exocrine enzyme levels at admission and the composite of death and ADHF readmission was assessed. Results: Of the 146 patients, 37 (25.3%) and 36 (24.7%) had low amylase and lipase levels, respectively. Patients with low lipase levels showed worse cumulative event-free survival than those with high lipase levels (p < 0.001). A low lipase level was associated with worse outcomes (hazard ratio: 1.96; p = 0.012). Conclusions: These findings suggest that low serum lipase levels may be a predictor of long-term outcomes in patients with ADHF.

Platelet-to-white blood cell ratio (PWR) as a comprehensive indicator of inflammatory response has been widely used to assess the prognosis of various diseases. However, the relationship between PWR and adverse outcomes in patients with acute decompensated heart failure (ADHF) remains unclear. This study aimed to evaluate the association between PWR and all-cause mortality within 30 days of hospitalization in ADHF patients from Jiangxi, China.

A total of 1,453 ADHF patients from the Jiangxi-ADHF study1 cohort were included. The primary outcome measure was all-cause mortality within 30 days of hospitalization. Multivariable Cox proportional hazards regression, restricted cubic spline regression, and receiver operating characteristic curve analysis were employed to explore the association between the inflammatory marker PWR and all-cause mortality in ADHF patients within 30 days of hospitalization.

During the 30-day observation period, a total of 53 subjects experienced mortality events. Multivariable Cox regression showed a negative correlation between PWR and all-cause mortality within 30 days of hospitalization in ADHF patients. Restricted cubic spline regression demonstrated an L-shaped association between PWR and 30-day mortality risk (p for nonlinear = 0.038). Further threshold analysis revealed a threshold point for PWR at 15.88, where a decrease in PWR below this threshold was significantly associated with increased risk of all-cause mortality (p for log-likelihood ratio test = 0.046). Additionally, the results of receiver operating characteristic curve analysis indicated that PWR had high predictive accuracy for mortality events within 30 days of hospitalization in ADHF patients and is significantly better than the traditional HF marker N-Terminal Pro-Brain Natriuretic Peptide (AUC: NT-proBNP 0.69, PWR 0.76; Delong test P < 0.05). Subgroup analysis showed that compared to subjects with reduced or moderately reduced ejection fraction, ADHF patients with preserved ejection fraction had a lower risk of short-term mortality associated with PWR (HR:0.99 vs. 0.98 vs. 0.87, P for interaction = 0.0067).

This study reveals, for the first time, a negative correlation between the inflammatory marker PWR and all-cause mortality within 30 days of hospitalization in ADHF patients. Based on the threshold analysis findings, patients with ADHF and a PWR below 15.88 had a significantly higher risk of death within 30 days.

As triple-organ transplantation (TOT) has become more common, we evaluate patient characteristics, risk factors, and clinical outcomes of patients undergoing thoracoabdominal TOT.

This retrospective study utilized data from heart-lung-liver (HLL), heart-lung-kidney (HLK), heart-kidney-liver (HKL), and heart-kidney-pancreas (HKP) recipients from the United Network for Organ Sharing registry between 1989 and 2023. Recipient and donor characteristics and risk factors for mortality were analyzed using Cox regression hazard models. Recipient survival up to 10 years was analyzed using the Kaplan-Meier method.

During the study period, 81 TOTs were performed (13 HLLs, 13 HLKs, 46 HKLs, and 9 HKPs). There were no statistically significant differences in long-term survival between TOTs (p = 0.13). However, HLL and HLK recipients had significantly worse (p < 0.0001) and improved (p < 0.0001) survival, respectively, when compared to heart-lung, isolated heart, and lung transplant recipients. HLK was associated with improved survival (hazard ratios [HR]: 0.22, p = 0.033). We found no differences in survival among HKL (p = 0.24) and HKP (p = 0.19) recipients compared to their dual- and single-organ counterparts. TOTs after 2007 (HR: 0.29, p = 0.003) were associated with improved survival, whereas increased recipient age (HR: 1.06, p = 0.037), estimated glomerular filtration rate (HR: 1.02, p = 0.005), and donor age (HR:1.05, p = 0.031) were associated with higher mortality.

The prevalence of TOTs has dramatically increased over the past decade. While overall survival between TOTs appears similar, adding a liver to a heart-lung transplant may be associated with a poorer prognosis compared to adding a kidney. A careful, multidisciplinary approach to patient selection and management remains paramount in optimizing outcomes for high-risk patients undergoing TOTs.

Fulminant myocarditis (FM) is an acute, diffuse inflammatory myocardial disease characterized by abrupt onset and extremely rapid progression. Patients typically exhibit haemodynamic abnormalities that may lead to respiratory failure, liver and renal failure, and subsequent coagulopathy. Collectively, these complications significantly increase the risk of early mortality. Currently, there is limited research on coagulation dysfunction associated with FM; therefore, achieving a rebalancing of the coagulation system is a challenge for successful treatment. We report a case of coagulation disorder secondary to FM, in which the patient recovered successfully and was discharged following comprehensive treatment and correction of coagulation function. By analyzing the etiology of this condition and emphasizing strategies for correcting coagulation disorders, we aim to provide valuable references for clinical diagnosis and management.

In heart failure (HF), congestion is a key pathophysiologic hallmark and a major contributor to morbidity and mortality. However, the presence of congestion is often overlooked in both acute and chronic settings, particularly when it is not clinically evident, which can have important clinical consequences. Ultrasound (US) is a widely available, non-invasive, sensitive tool that might enable clinicians to detect and quantify the presence of (subclinical) congestion in different organs and tissues and guide therapeutic strategies. In particular, left ventricular filling pressures and pulmonary pressures can be estimated using transthoracic echocardiography; extravascular lung water accumulation can be evaluated by lung US; finally, systemic venous congestion can be assessed at the level of the inferior vena cava or internal jugular vein. The Doppler evaluation of renal, hepatic and portal venous flow can provide additional valuable information. This review aims to describe US techniques allowing multi-organ evaluation of congestion, underlining their role in detecting, monitoring, and treating volume overload more objectively.

Background: Pregnant women with congenital heart disease carry a high risk of complications, especially when cardiac function is suboptimal. Increasing evidence suggests that impaired right ventricular (RV) function has a negative effect on placental function, possibly through venous congestion. We report a case series of hepatic and renal venous flow patterns in pregnant women with right ventricular dysfunction after repaired Tetralogy of Fallot (ToF), relative to those observed in normal pregnancy and preeclampsia. Methods: At 20-24 weeks pregnancy, RV function was measured by echocardiography and by cardiovascular magnetic resonance in women with repaired ToF. Combined Doppler-ECG of the hepatic and renal interlobular veins were performed in three women with asymptomatic right ventricular dysfunction. Venous impedance index and pulse transit time were measured and classified as abnormal at >75th and <25th reference percentile, respectively. Results: All three women showed dilated RV and mildly impaired RV function. Both hepatic and intrarenal Doppler flow waves were abnormal and very much resembled the patterns seen in preeclampsia. One of the three women had complications including ventricular tachycardia, intrauterine growth restriction, antenatal bleeding, emergency cesarean section and acute heart failure 2 days postpartum. Conclusions: Pregnant women with mild right ventricular dysfunction after repaired ToF show abnormal venous Doppler flow waves in the liver and kidneys, similar to those observed in preeclampsia. These findings are in line with reported observations on the association between impaired RV function, abnormal return of venous blood, venous congestion and organ dysfunction. The parallel with venous Doppler flow observations in preeclampsia suggest that the venous compartment might play an important role in the etiology of preeclampsia-induced organ dysfunction. Whether this phenomenon directly affects the uteroplacental circulation is to be assessed in future research.

The albumin-bilirubin (ALBI) score has demonstrated prognostic value in a range for liver and heart diseases. However, its association with all-cause mortality in intensive care unit (ICU) patients with heart failure remains uncertain.

This study sought to investigate the relationship between the ALBI score and the risk of all-cause mortality in ICU patients with heart failure.

The ICU patients diagnosed with heart failure were selected from the Medical Information Mart for Intensive Care IV database (MIMIC-IV, version 2.2) and stratified into tertiles according to their ALBI scores. The primary outcome of interest was the occurrence of all-cause mortality within 365 days post-discharge. The analysis encompassed a cohort of 4,239 patients, with Kaplan-Meier curves indicating that individuals with higher ALBI levels exhibited an elevated risk of all-cause mortality (log-rank p < 0.001). Multivariate adjusted Cox regression and subgroup analysis demonstrated that individuals in T2 (hazard ratio (HR) 1.09, 95% CI 0.99-1.21) and T3 (HR 1.17, 95% CI 1.02-1.34) had an increased risk of mortality compared to individuals in T1 (p for trend < 0.001), and each incremental tertile in ALBI was linked to a 10% rise in mortality risk, while each individual unit increase in ALBI was associated with a 36% increase in mortality risk. This relationship was consistently observed across most subgroups, except for using or not using inotropes or vasopressors, different ages, different creatinine levels. The restricted cubic spline (RCS) analysis indicated a linear relationship between ALBI levels and the risk of all-cause mortality.

The ALBI scores are independently associated with the risk of all-cause mortality in ICU patients with heart failure, particularly in those not using inotropes or vasopressors, younger patients, and with lower levels of creatinine. ALBI may help identify high-risk patients and optimize risk stratification in this population.

Managing hemodynamic instability in critically ill patients due to cardiovascular disease or, in particular, coronary artery disease requires an integrated and responsive approach. The complexity lies in simultaneously addressing the underlying cardiovascular pathology and managing its systemic effects. The complexity described above involves a careful balance of interventions, including fluid and electrolyte management, pharmacological support, and, in some cases, mechanical circulatory support. The dynamic nature of hemodynamic instability necessitates constant vigilance and rapid adaptation of treatment strategies to align with the evolving clinical picture. So, this study aims to investigate the knowledge, attitude, and practice of Palestinian critical care nurses about hemodynamic instability in patients with cardiovascular diseases.

A cross-sectional design was conducted on 300 nurses in 30 hospitals in the West Bank and East Jerusalem of Palestine. Data were collected using a self-administered questionnaire composed of four sections covering the socio-demographics, knowledge, attitudes, and practices of the sample. Quantitative statistical analysis was done using Statistical Package for Social Sciences (SPSS) software.

The nurses demonstrated an almost low overall level of knowledge about hemodynamic instability, with a mean score of 2.7 on a 7-points scale. Additionally, nurses generally expressed a high positive attitude toward their practice, with a mean score of 3.8 on a 5-point scale. Although; Palestinian nurses showed a low level of knowledge about hemodynamic instability but expressed positive attitudes toward their practice. The practice level was also moderate with a mean score of 2.3 on a 5-point scale. Significant differences were found with a higher attitude of male nurses and higher knowledge with bachelor or higher educational levels. Other variables showed non-significant differences.

Several challenges were identified, including lack of training and resources, within this study context. Educational interventions and improved access to resources could improve nurses' knowledge and practice in managing hemodynamic instability.

Acute failure is a critical condition, encompassed by the sudden or progressive onset of symptoms or signs of congestion. The treatment strategies available are mainly supportive and do not improve mortality or long-term outcomes. Therefore, there is a need for alternative novel treatment strategies. In this narrative review, we explore the role of relaxin agonist as a potential therapeutic strategy in acute heart failure.

We aim to provide an overview of the evidence of preclinical and clinical studies on relaxin as a treatment strategy for acute heart failure. Papers collected in this review are from original research and systematic reviews which have been filtered following Medline and Cochrane Library searches.

Relaxin has shown great potential in both preclinical and clinical studies due to its antifibrotic, anti-inflammatory, and vasodilatory effect on the heart. However, there has been mixed evidence from clinical trials involving relaxin which could be due to patient groups, investigation sites, trial design, and chance. Further studies should focus on developing biomarkers to identify specific population groups who are most likely to benefit from relaxin.

Acute heart failure (AHF) poses significant challenges in clinical practice due to its varied clinical presentations and complex management strategies. Adequate confidence levels among medical residents in diagnosing and managing AHF are crucial for timely and effective patient care.

This cross-sectional study aimed to assess medical residents' knowledge, attitude, and perception levels in diagnosing and managing AHF and explore factors influencing their confidence levels.

A total of 52 medical residents from various specialties participated in the study. Based on different clinical parameters, participants completed a questionnaire assessing their confidence levels in diagnosing AHF. Descriptive statistics were used to summarize confidence levels, while chi-square tests explored associations between demographic/clinical factors and confidence levels.

The majority of residents exhibited high confidence levels in diagnosing heart failure (HF) based on history and physical examination findings alone (22 (42.3%) and 16 (30.8%), respectively). However, confidence levels were lower when relying solely on laboratory tests and imaging modalities for diagnosis (17 (32.7%) and 18 (34.6%), respectively). Factors such as symptoms (e.g., dizziness) and availability of ultrasound equipment were associated with higher confidence levels (p < 0.05). However, demographic factors such as age, gender, and residency year did not significantly influence confidence levels (p > 0.05).

Our study highlights variations in confidence levels among medical residents in diagnosing and managing AHF. While clinical assessment remains paramount, targeted educational interventions focusing on interpreting diagnostic tests and imaging findings are warranted to enhance residents' confidence levels and improve patient care.

Patients with heart failure (HF) often suffer from hepato-renal dysfunction. The associations between hepato-renal function changes and mortality remain unclear. Further, the effect of cardiac rehabilitation (CR) on mortality and motor functions in patients with HF and hepato-renal dysfunction requires investigation.

We reviewed 2522 patients with HF (63.2 % male; median age: 74 years). The association between changes in hepato-renal function assessed by the Model for End-stage Liver Disease eXcluding INR (MELD-XI) score and mortality was examined. The association of CR participation with mortality and physical functions was investigated in patients with HF with decreased, unchanged, and increased MELD-XI scores.

During the follow-up period, 519 (20.6 %) patients died. Worsened MELD-XI score was independently associated with all-cause death [adjusted hazard ratio (aHR): 1.099; 95 % confidence interval (CI): 1.061-1.138; p < 0.001]. CR participation was associated with low mortality, even in the increased MELD-XI score group (aHR: 0.498; 95 % CI: 0.333-0.745; p < 0.001). Trajectory of the MELD-XI score was not associated with physical function changes. There were no time by MELD-XI score interaction effects on handgrip strength (p = 0.084), leg strength (p = 0.082), walking speed (p = 0.583), and 6-min walking distance (p = 0.833) in patients participating in outpatient CR.

Hepato-renal dysfunction predicts high mortality. CR participation may be helpful for a better prognosis of patients with HF and hepato-renal dysfunction.

To investigate the changes in retinal microvasculature by contemporary imaging techniques during episodes of acute decompensated heart failure (ADHF) and following recompensation compared to age-matched controls without known cardiac or retinal disease.

Adult patients hospitalized with a primary diagnosis of ADHF, regardless of left ventricular ejection fraction (LVEF) and treated with a minimum dose of 40 mg of intravenous furosemide or equivalent were included. Transthoracic echocardiography was conducted in all patients. Eye examinations were performed out within the initial 24 h after admission and after recompensation before discharge. All eyes underwent a general examination, including a best corrected visual acuity test, dilated fundoscopy, spectral-domain optical coherence tomography (OCT) as well as OCT angiography (OCT-A). In addition, 40 participants without documented cardiac or retinal diseases served as controls. Forty patients with ADHF (mean age 78.9 ± 8.8 years; 32% female) with a mean LVEF of 43 ± 12.8% were included. All patients were treated with intravenous diuretics for a median of 4.3 ± 2.8 days. There was a significant reduction in N-terminal pro-B-type natriuretic peptide from baseline up to discharge (10 396 [interquartile range 6410] vs. 6380 [interquartile range 3933] pg/ml, p ≤ 0.001) and inferior vena cava diameters (2.13 ± 0.4 vs. 1.63 ± 0.3 cm, p = 0.003). Compared to the control group, patients with ADHF showed on admission impaired visual acuity (0.15 ± 0.1 vs. 0.35 ± 0.1 logMAR, p < 0.001), reduced macular vessel density (18.0 ± 1.9 vs. 14.3 ± 3.6 mm/mm2, p < 0.001) and perfusion density (42.6 ± 3.2 vs. 35.2 ± 9.7%, p < 0.001). After recompensation, the mean overall vessel density and mean overall perfusion density were markedly increased at discharge (14.3 ± 3.6 vs. 19.7 ± 2.6 mm/mm2, p = 0.001, and 35.2 ± 9.7 vs. 39.2 ± 6.5%, p = 0.005, respectively). The mean diameter of the superior temporal retinal vein at admission was significantly larger compared to the control group (136 ± 19 vs. 124 ± 22 μm, p = 0.008) and decreased significantly to 122 ± 15 μm at discharge (p < 0.001).

This analysis revealed a remarkable reversible change in retinal microvasculature after ADHF. This could provide a valuable evidence for use of OCT-A in the assessment of overall microperfusion and haemodynamic status in patients with acute heart failure.

Recent research has focused on the relationship between heart failure (HF) symptom clusters and outcomes, including mortality, hospitalization, functional status, and quality of life. No known studies to date have explored the role of physical HF symptom clusters and delays in seeking treatment.

Describe physical symptom clusters in a population of HF patients and determine if a specific cluster is predictive of delay in seeking treatment for HF symptoms.

We analyzed combined data from two studies ( n = 406) collected during acute HF hospitalization. The Heart Failure Somatic Awareness Scale quantified physical HF symptoms. Delay, measured in days, was collected from the medical record and confirmed by interview. Hierarchical agglomerative clustering techniques determined physical HF symptom clusters. Hierarchical multiple regression analysis was computed to explore predictors of delay.

Participants were primarily White, male sex older adults. Three physical HF symptom clusters were identified: discordant, edema-related, and dyspnea-related symptoms. Hierarchical multiple regression analysis revealed in Step 1 that age was a significant predictor of delay.

Our findings provide valuable insight into the role of physical symptom clusters on delay in persons with HF. Through agglomerative hierarchical clustering techniques, we found three physical HF symptom clusters that were then used to determine differences in cluster membership by demographic and clinical variables. Significant age differences were noted by cluster membership with youngest older adults in a discordant symptom cluster.

Patients after surgical correction of Tetralogy of Fallot (ToF) often show adverse cardiac remodeling. To better understand the underlying biological processes, we studied the relation between changes in blood biomarkers and changes in biventricular size and function as assessed by cardiac magnetic resonance imaging (CMR).

This study included 50 ToF patients, who underwent blood biomarker and CMR analysis at least twice between 2002 and 2018.34 (68 %) of these patients were male. Patients had an average age of 16.1 at first visit. Biomarkers were chosen based on earlier research by our group and included: NT-proBNP, ST2, GDF-15, DLK-1, IGFBP-1/7, and FABP-4. Pearson correlations coefficients (rpearson) were determined to quantify the relationship between changes in biomarkers and CMR measurements.

For changes in parameters of right ventricular (RV) size significant correlations were observed with changes in NT-proBNP, ST-2, GDF-15, IGFBP7 and FABP-4 (rpearson between 0.28 and 0.51). Correlations with NT-proBNP were driven by changes in RV size induced by pulmonary valve replacement (n = 9). For LV serial size changes, significant correlations were noted with changes in NT-pro-BNP, ST-2, GDF-15 and FABP-4 (rpearson between 0.32 and 0.52).

In clinically stable ToF patients changes in right and left ventricular size and function correlated with alterations in blood biomarkers of inflammation and immune response to stress.

Malnutrition is classified into marasmus and kwashiorkor in children. However, the clinical significance of these aspects is unclear in adult patients with heart failure (HF). We divided 2308 adult patients with HF into four groups according to marasmus type (body mass index < 18.5 kg/m2) and kwashiorkor type (serum albumin < 3.4 g/dL) malnutrition: Group C (no malnutrition, n = 1511, 65.5%), Group M (marasmus type malnutrition, n = 133, 5.8%), Group K (kwashiorkor type malnutrition, n = 554, 24.0%) and Group MK (marasmic-kwashiorkor type malnutrition, n = 110, 4.8%). Group M showed the lowest blood pressure. Groups K and MK showed higher levels of B-type natriuretic peptide. Right atrial pressure was lowest in Groups M and MK. Kaplan-Meir analysis demonstrated that Group MK had the lowest event-free rate of all-cause death and cardiac death. In the multivariable Cox proportional hazard analysis, Groups M, K, and MK were associated with all-cause death (hazard ratio 1.790, 1.657 and 2.313, respectively) and cardiac death (hazard ratio 2.053, 1.855 and 3.001, respectively) compared to Group C as a reference. Marasmus type and kwashiorkor type malnutrition are associated with distinct profiles and high mortality, and marasmic-kwashiorkor type malnutrition has the poorest prognosis.

Model for end-stage liver disease (MELD) is an effective predictive marker for renal, hepatic, and cardiac dysfunctions. In this study, we explore the correlation between MELD scores and the outcomes of patients undergoing cardiac valve surgery.

We conducted a retrospective analysis of clinical data from patients who underwent cardiac valve surgery, encompassing procedures on the aortic valve, mitral valve, and tricuspid valve, using the Informative Surgical Patient dataset for Innovative Research Environment (INSPIRE) database, we conducted receiver operating characteristic (ROC) analyses on the study participants and chose MELD as the primary scoring tool for our study due to its optimal area under the curve (AUC), patients were stratified into high (MELD ≥18) and low (MELD <18) groups based on the determined cutoff value. The perioperative clinical data of the two groups were compared.

The analysis revealed 751 patients in the low MELD group (75.5%) and 244 patients (24.5%) in the high MELD group. Patients in the high MELD group exhibited a lower body mass index (BMI) compared to those in the low MELD group. In comparison to the low MELD group, the high MELD group exhibited a higher rate of emergency surgery (10.66% vs. 5.99%, P=0.01), along with prolonged anesthesia time, surgery time, and cardiopulmonary bypass (CPB) time. Regarding clinical prognosis, the high MELD group demonstrated a higher 28-day mortality rate (10.66% vs. 0.8%, P<0.001), as also observed in the analysis of three valve subgroups. Additionally, the high MELD group experienced longer hospitalization and intensive care unit (ICU) stay, and a higher proportion of patients requiring mechanical circulatory support, including intra-aortic balloon pump (IABP) assist (14.75% vs. 3.86%, P<0.001), extracorporeal membrane oxygenation (ECMO) assist (7.38% vs. 0.8%, P<0.001), and continuous renal replacement therapy (CRRT) (27.87% vs. 1.46%, P<0.001) post-surgery. The Kaplan-Meier survival curves illustrated a significantly lower mortality rate in the low MELD group compared to the high MELD group, with highly significant statistical differences (P<0.001).

The MELD score demonstrates a robust predictive value for clinical outcomes following cardiac valve surgery, underscoring its utility as a viable metric for disease stratification research.

Acute kidney injury (AKI) is one of the most frequent and prognostic-relevant complications of cardiogenic shock (CS) complicating myocardial infarction (MI). Mechanical circulatory assist devices (MCS) like left ventricular Impella microaxial pump have increasingly been used in the last decade for stabilization of hemodynamics in those patients. Moreover, a protective effect of Impella on renal organ perfusion could recently be demonstrated. However, data identifying early risk predictors for developing AKI during Impella support in CS are rare. Data of hemodynamics and renal function from 50 Impella patients (January 2020 and February 2022) with MI-related CS (SCAI stage C), were retrospectively analyzed using e.g. multivariate logistic regression analysis as well as Kaplan-Meier curves and Cox regression analysis. 30 patients (60%) developed AKI. Central venous pressure as an indicator for venous congestion (OR 1.216, p = 0.02), GFR at admission indicating existing renal damage (OR 0.928, p = 0.002), and reduced central venous oxygen saturation (SvO2) as a marker for decreased tissue perfusion (OR 0.930, p = 0.029) were independently associated with developing an AKI. The 30-day mortality rate was significantly higher in patients with AKI stage 3 (Stage 1: 0%, Stage 2: 0%, Stage 3; 41.6%, p = 0.014) while AKI stage 3 (HR 0.095, p = 0.026) and norepinephrine dosage (HR 1.027, p = 0.008) were independent predictors for 30-day mortality. AKI as a complication of MI-related CS occurs frequently with a major impact on prognosis. Venous congestion, reduced tissue perfusion, and an already impaired renal function are independent predictors of AKI. Thus, timely diagnostics and a focused treatment of the identified factors could improve prognosis and outcome.

Heart failure is hemodynamically characterized as congestion and/or end-organ hypoperfusion, and is associated with increased morbidity and mortality. Underlying pathophysiology, such as neuro-hormonal activation, exacerbates heart failure and leads to functional deterioration of other organs. We have been conducting clinical research to study the pathophysiology of heart failure and discover prognostic factors. In this review article, we report the results and implications of our clinical research on heart failure.

7 T cardiac magnetic resonance imaging (MRI) studies may enable higher precision in clinical metrics like cardiac function, ventricular mass, and more. Higher precision may allow early detection of functional impairment and early evaluation of treatment responses in clinical practice and pre-clinical studies.

Seven female German Landrace pigs were scanned prior to and at three time points (3-4 days, 7-10 days, and ~60 days) post myocardial infarction using a whole body 7 T system and three radiofrequency (RF) coils developed and built in-house to accompany animal growth.

The combination of dedicated RF hardware and 7 T MRI enables a longitudinal study in a pig model of acute and chronic infarction, providing consistent blood tissue contrast and high signal-to-noise ratio (SNR) in measurements of cardiac function, as well as low coefficients of variation (CoV) for ejection fraction (CoVintra-observer: 2%, CoVinter-observer: 3.8%) and infarct size (CoVintra-observer: 8.4%, CoVinter-observer: 3.8%), despite drastic animal growth.

Best results are achieved via manual segmentation. We define state-of-the-art procedures for large animal studies at 7 T.

Systolic Heart failure is a complex clinical syndrome characterized by a decrease in cardiac contractility and a reduction in organ perfusion. Current pharmacologic inotropes attempt to improve contractility via indirect mechanisms but are limited in terms of safety and effectiveness. Omecamtiv mecarbil is a novel agent in a new class of drugs known as cardiac myosin activators; their unique mechanism of action involves directly activating the enzymatic pathway in the cardiac myocyte as a way to improve ventricular contraction. Preclinical and clinical trials have found that omecamtiv mecarbil improves cardiac contractility without increasing the risk of any of the harmful effects that are associated with the currently available inotropic agents. Omecamtiv mecarbil is a worthwhile advance and patients with systolic heart failure would benefit from pharmacological use of this drug.

Cardiovascular disease is a worldwide health problem and a leading cause of morbidity and mortality. Preclinical cardiovascular research using animals is needed to explore potential targets and therapeutic options. Compared with rodents, pigs have many advantages, with their anatomy, physiology, metabolism and immune system being more similar to humans. Here we present an overview of the available pig models for cardiovascular diseases, discuss their advantages over other models and propose the concept of standardized models to improve translation to the clinical setting and control research costs.

Shear wave elastography (SWE) is a noninvasive method for measuring organ stiffness. Liver stiffness measured using SWE reflects hepatic congestion in patients with heart failure (HF). However, little is known about the use of SWE to assess other organ congestions. This study aimed to evaluate the utility of SWE for assessing not only the liver but also thyroid congestion in patients with HF. This prospective study included 21 patients with HF who have normal thyroid lobes (age: 77.0 ± 11.0, men: 14). Thyroid and liver stiffness were measured by SWE using the ARIETTA 850 ultrasonography system (Fujifilm Ltd., Tokyo, Japan). SWE of the thyroid was performed on B-mode ultrasonography; a target region was identified within a region of interest. SWE was performed in each lobe of the thyroid gland. Five measurements were taken at the same location and the averages were recorded for comparison. We investigated the relationship between SWE for evaluating thyroid stiffness and the clinical characteristics of patients with HF. SWE of the thyroid was significantly correlated with SWE of the liver (R = 0.768, P < .001), thyroid stimulation hormone (R = 0.570, P = .011), free thyroxine (R = 0.493, P = .032), estimated right atrial pressure (RAP; R = 0.468, P = .033), and composite congestion score (R = 0.441, P = .045). SWE may be useful for evaluating thyroid stiffness and assessing the degree of thyroid congestion. Thyroid congestion may reflect the elevation of RAP and cause thyroid dysfunction through organ congestion.

To evaluate the prognostic value (total mortality + repeated hospitalization for heart failure (HF)) of ultrasound diagnostic methods in patients with acute decompensated HF (ADHF).

The subjects were patients with chronic HF, who were hospitalized for ADHF. Using ultrasound methods-lung ultrasound, ultrasound assessment of hepatic venous congestion as per the venous excess ultrasound (VExUS) protocol, and indirect elastometry-we assessed the number of B-lines, hepatic venous congestion, and liver density of the patients. Clinical outcomes were assessed using a structured telephone survey method at 1, 3, 6, and 12 months after discharge. Combined overall mortality and readmission rates associated with HF were assessed. Threshold values for different methods for detecting congestion were set as follows: the number of B-lines in ultrasound data > 5; liver density > 6.2 kPa.

The subjects were 207 patients (54.1% male; mean age = 70.7 ± 12.8 years). A total of 63 (30.4%) endpoints and 23 (11.1%) deaths were detected within 364 days (IQR = 197-365). Liver density > 6.2 kPa had a hazard ratio (HR) of 1.9 (95% CI: 1.0-3.3; p = 0.029). Hepatic venous congestion (VExUS protocol) had HR of 2.8 (95% CI: 1.3-5.7; p = 0.004). There was a significant increase in the risk of overall prognostic value in the presence of congestion, identified by liver fibroelastometry + lung ultrasound (HR = 10.5, 95% CI: 2.3-46.2; p = 0.002). The ultrasound assessment of hepatic venous congestion (VExUS + lung ultrasound protocol) yielded HR of 16.7 (95% CI: 3.9-70.7; p < 0.001). For all three methods combined, the overall HR was 40.1 (95% CI: 6.6-243.1; p < 0.001).

A combination of ultrasound diagnostic methods that include the number of B-lines, presence of hepatic venous congestion according to the VExUS protocol, and liver density according to indirect elastometry at discharge may have an independent prognostic value for patients with ADHF.

The delayed titration of guideline-directed drug therapy (GDMT) is a complex event influenced by multiple factors that often result in poor prognosis for patients with heart failure (HF). Individualized adjustments in GDMT titration may be necessary based on patient characteristics, and every clinician is responsible for promptly initiating GDMT and titrating it appropriately within the patient's tolerance range. This review examines the current challenges in GDMT implementation and scrutinizes titration considerations within distinct subsets of HF patients, with the overarching goal of enhancing the adoption and effectiveness of GDMT. The authors also underscore the significance of establishing a novel management strategy that integrates cardiologists, nurse practitioners, pharmacists, and patients as a unified team that can contribute to the improved promotion and implementation of GDMT.