Explore the vast range of titles available.

Acute heart failure (AHF) is a syndrome defined as the new onset (de novo heart failure (HF)) or worsening (acutely decompensated heart failure (ADHF)) of symptoms and signs of HF, mostly related to systemic congestion. In the presence of an underlying structural or functional cardiac dysfunction (whether chronic in ADHF or undiagnosed in de novo HF), one or more precipitating factors can induce AHF, although sometimes de novo HF can result directly from the onset of a new cardiac dysfunction, most frequently an acute coronary syndrome. Despite leading to similar clinical presentations, the underlying cardiac disease and precipitating factors may vary greatly and, therefore, the pathophysiology of AHF is highly heterogeneous. Left ventricular diastolic or systolic dysfunction results in increased preload and afterload, which in turn lead to pulmonary congestion. Fluid retention and redistribution result in systemic congestion, eventually causing organ dysfunction due to hypoperfusion. Current treatment of AHF is mostly symptomatic, centred on decongestive drugs, at best tailored according to the initial haemodynamic status with little regard to the underlying pathophysiological particularities. As a consequence, AHF is still associated with high mortality and hospital readmission rates. There is an unmet need for increased individualization of in-hospital management, including treatments targeting the causative factors, and continuation of treatment after hospital discharge to improve long-term outcomes. Acute heart failure (AHF) is a syndrome characterized by signs and symptoms of heart failure (typically systemic congestion) that occurs in the presence of an underlying cardiac dysfunction (previously diagnosed, undiagnosed or new-onset) and precipitating factors. AHF is associated with high mortality and hospital readmission rates.

Congestion (i.e., backward failure) is an important culprit mechanism driving disease progression in heart failure. Nevertheless, congestion remains often underappreciated and clinicians underestimate the importance of congestion on the pathophysiology of decompensation in heart failure. In patients, it is however difficult to study how isolated congestion contributes to organ dysfunction, since heart failure and chronic kidney disease very often coexist in the so-called cardiorenal syndrome. Here, we review the existing relevant and suitable backward heart failure animal models to induce congestion, induced in the left- (i.e., myocardial infarction, rapid ventricular pacing) or right-sided heart (i.e., aorta-caval shunt, mitral valve regurgitation, and monocrotaline), and more specific animal models of congestion, induced by saline infusion or inferior vena cava constriction. Next, we examine critically how representative they are for the clinical situation. After all, a relevant animal model of isolated congestion offers the unique possibility of studying the effects of congestion in heart failure and the cardiorenal syndrome, separately from forward failure (i.e., impaired cardiac output). In this respect, new treatment options can be discovered.

In heart failure (HF), acute decompensation can occur quickly and unexpectedly because of worsening of chronic HF or to new‐onset HF diagnosed for the first time (‘de novo’). Patients presenting with acute HF (AHF) have a poor prognosis comparable with those with acute myocardial infarction, and any delay of treatment initiation is associated with worse outcomes. Recent HF guidelines and recommendations have highlighted the importance of a timely diagnosis and immediate treatment for patients presenting with AHF to decrease disease progression and improve prognosis. However, based on the available data, there is still uncertainty regarding the optimal ‘time‐to‐treatment’ effect in AHF. Furthermore, the immediate post‐worsening HF period plays an important role in clinical outcomes in HF patients after hospitalization and is known as the ‘vulnerable phase’ characterized by high risk of readmission and early death. Early and intensive treatment for HF patients in the ‘vulnerable phase’ might be associated with lower rates of early readmission and mortality. Additionally, in the chronic stable HF outpatient, treatments are often delayed or not initiated when symptoms are stable, ignoring the risk for adverse outcomes such as sudden death. Consequently, there is a dire need to better identify HF patients during hospitalization and after discharge and treating them adequately to improve their prognosis. HF is an urgent clinical scenario along all its stages and disease conditions. Therefore, time plays a significant role throughout the entire patient's journey. Therapy should be optimized as soon as possible, because this is beneficial regardless of severity or duration of HF. Time lavished before treatment initiation is recognized as important modifiable risk factor in HF.

The importance of physical activity has become evident since a sedentary lifestyle drives cardiovascular disease progression and is associated with increased morbidity and mortality. The favorable effects of exercise training in chronic heart failure (HF) and chronic kidney disease (CKD) are widely recognized and exercise training is recommended by European and American guidelines. However, the application of exercise intervention in HF patients hospitalized for acute decompensation or acute worsening in cardiac function has not been explored extensively and, as a result, knowledge about the effects of exercise training in the inpatient setting of acute HF is limited. Acute HF is often accompanied by signs and symptoms of congestion, termed acute decompensated heart failure (ADHF), which leads to worsening renal function (WRF) and eventually negatively affects both thoracic and abdominal organs. Therefore, we first provide a comprehensive overview of the impact of exercise training in hospitalized patients demonstrating acute decompensating HF. In the second part, we will focus on the effects of exercise training on congestion in a setting of ADHF complicated by renal dysfunction. This review suggests that exercise intervention is beneficial in the inpatient setting of acute HF, but that more clinical studies focusing on the application of exercise training to counteract venous congestion are needed.

Aims Implantable pulmonary artery pressure (PAP) sensors have been shown to reduce heart failure hospitalizations (HFH) in selected patients. The goal of this study was to evaluate the safety and efficacy of a novel wireless PAP monitoring system in patients with heart failure (HF). Methods and results This is a prospective, multi‐centre, open‐label, single‐arm trial evaluating the safety and efficacy of the Cordella™ PA Sensor System including the comprehensive Cordella™ Heart Failure System (CHFS) in patients with New York Heart Association (NYHA) Class III heart failure with a heart failure hospitalization and/or increase of N‐terminal pro‐Brain Natriuretic Peptide (NT‐proBNP) within 12 months of enrolment. The primary efficacy endpoint was the accuracy of PA sensor mean PAP measurements, compared with fluid‐filled catheter mean PAP measurements obtained by standard right heart catheterization (RHC) at 90 days post‐implant, assessed in all patients with a successful implant. The primary safety endpoint was freedom from adverse events associated with use of the Cordella PA Sensor System through 30 days post‐implant, assessed in all patients who entered the cath lab for PA sensor implant. The PA sensor was successfully implanted in 70 patients. Equivalence between the PA sensor and RHC for mean pulmonary artery pressures was excellent with measurements confined within the equivalence bounds of −4.0 to 4.0 mmHg (mean PAP: 0.0 to 2.9 mmHg, P = 0.003). The device safety profile was excellent with 98.6% freedom from Device System Related Complications, defined as invasive treatment, device explant or death. There were no pressure sensor failures. Patients' adherence to daily measurement transmissions of PAP and vital signs was 94%. Conclusions This trial supports the safety and efficacy of the Cordella PA Sensor System and in conjunction with the CHFS enables comprehensive HF management in NYHA class III heart failure patients.

[...]congestion does not equal volume overload, and often, pressure and volume changes diverge, which complicates the identification and treatment of HF. [...]it is not surprising that the assessment of congestion through current clinical assessment correlates at best only moderately with the ‘gold standard’ of an invasive assessment.4,5 Therefore, Harjola et al.6 purposed a congestion score related to organ injury assessed through an integrated ultrasonographic assessment evaluating cardiac, lung and abdominal districts. SEE PDF] NPs as HF hallmark A universal accepted threshold for NP's to include and/or exclude HF is far from being achieved.12,13 Although NPs surely have diagnostic and prognostic importance in acute and advanced HF, they are of limited help to guide HF therapies.14,15 In addition, the role of NPs to diagnose patients at risk for HF and those with structural heart disease without clinical evidence of congestion (Stages A and B) is questionable.16 Atrial enlargement and left ventricular dilatation/hypertrophy are a natural attempt to avoid intracardiac pressure elevation in accordance with Laplace law. Whereas most of these drugs have demonstrated faster symptom control and improvement in central haemodynamics, none of these therapies have improved outcome. [...]the prospect of improved long-term prognosis with short-term drug therapy only aimed at congestion relief also has shown to be wrong. [...]a comprehensive diagnostic approach using clinical, laboratory and technical exams will remain important to diagnose and differentiate between signs of congestion and volume overload related to cardiac dysfunction, especially in the preclinical stages of the disease.

Cardiac resynchronization therapy (CRT) improves cardiac hemodynamics. Therefore, the maintenance dose of loop diuretic therapy might be reduced. Consecutive patients who underwent CRT (n = 648) were retrospectively evaluated. Loop diuretic dose was recorded at baseline before implantation and 6 months later with patients classified into 4 groups: (1) no loop diuretic, (2) down-titration, (3) unchanged dose, and (4) up-titration. Afterward total loop diuretic exposure was calculated. Renal function trajectories were evaluated as the difference between implantation and censoring serum creatinine (Cr) value. Clinical outcome was evaluated as the combined end point of heart failure readmissions and all-cause mortality. Independent predictors of successful loop diuretic down-titration were identified. Two hundred ninety-six patients (46%) received no loop diuretic at follow-up, 126 (19%) underwent down-titration, 137 (21%) remained on a stable dose, and 89 (14%) underwent up-titration. In comparison with the group that was free from loop diuretics (Cr = +0.06 mg/dl), renal function deteriorated faster during follow-up in patients on stable doses (Cr = +0.29 mg/dl; p = 0.045) and those underwent up-titration (Cr = +0.44 mg/dl; p = 0.009) but not in patients who were down-titrated (Cr = +0.13 mg/dl; p = 1.00). Patients receiving down-titration had a lower risk for the combined clinical end point (adjusted hazards ratio 0.43; confidence interval 0.22 to 0.83; p = 0.012). Factors associated with successful down-titration after 6 months of CRT included nonischemic cardiomyopathy, higher baseline dose of diuretics, higher ejection fraction at 6 weeks, and lower right ventricular systolic pressure at 6 weeks. In conclusion, after CRT, down-titration of loop diuretics is often feasible and associated with improved outcome and a slower rate of kidney function decline. Patients with nonischemic cardiomyopathy, treated with high doses of loop diuretics before implantation and beneficial left ventricular remodeling with CRT, are most likely to tolerate loop diuretic down-titration.

Background A comprehensive disease management programme (DMP) with a central role for general practitioners (GPs) is needed to improve heart failure (HF) care. However, previous research has shown that GPs have mixed experiences with multidisciplinary HF care. Therefore, in this study, we explore the perceptions that GPs have regarding their role in current and future HF care, prior to the design of an HF disease management programme. Methods This was a qualitative semi-structured interview study with Belgian GPs until data saturation was reached. The QUAGOL method was used for data analysis. Results In general, GPs wanted to assume a central role in HF care. Current interdisciplinary collaboration with cardiologists was perceived as smooth, partly because of the ease of access. In contrast, due to less well-established communication and the variable knowledge of nurses regarding HF care, collaboration with home care nurses was perceived as suboptimal. With regard to the future organization of HF care, all GPs confirmed the need for a structured chronic care approach and envisioned this as a multidisciplinary care pathway: flexible, patient-centred, without additional administration and with appropriate delegation of some critical tasks, including education and monitoring. GPs considered all-round general practice nurses as the preferred partner to delegate tasks to in HF care and reported limited experience in collaborating with specialist HF nurses. Conclusion GPs expressed the need for a protocol-driven care pathway in chronic HF care. However, in contrast to the existing care trajectories, this pathway should be flexible, without additional administrative burdens and with a central role for GPs.

Iron deficiency is prevalent in heart failure with reduced ejection fraction and relates to symptomatic status, readmission, and all-cause mortality. The relation between iron status and response to cardiac resynchronization therapy (CRT) remains insufficiently elucidated. This study assesses the impact of iron deficiency on clinical response and reverse cardiac remodeling and outcome after CRT. Baseline characteristics, change in New York Heart Association functional class, reverse cardiac remodeling on echocardiography, and clinical outcome (i.e., all-cause mortality and heart failure readmissions) were retrospectively evaluated in consecutive CRT patients who had full iron status and complete blood count available at implantation, implanted at a single tertiary care center with identical dedicated multidisciplinary CRT follow-up from October 2008 to August 2015. A total of 541 patients were included with mean follow-up of 38 ± 22 months. Prevalence of iron deficiency was 56% at implantation. Patients with iron deficiency exhibited less symptomatic improvement 6 months after implantation (p value <0.001). In addition, both the decrease in left ventricular end-diastolic diameter (−3.1 vs −6.2 mm; p value = 0.011) and improvement in ejection fraction (+11% vs +15%, p value = 0.001) were significantly lower in patients with iron deficiency. Iron deficiency was significantly associated with an increased risk for heart failure admission or all-cause mortality (adjusted hazard ratio 1.718, 95% confidence interval 1.178 to 2.506), irrespectively of the presence of anemia (Hemoglobin <12 g/dl in women and <13 g/dl in men). In conclusion, iron deficiency is prevalent and affects both clinical response and reverse cardiac remodeling after CRT implantation. Moreover, it is a powerful predictor of adverse clinical outcomes in CRT.

Venous congestion is an important contributor to worsening renal function in heart failure and the cardiorenal syndrome. In patients, it is difficult to study the effects of isolated venous congestion on organ function. In this study, the consequences of isolated abdominal venous congestion on morphology and function of the kidneys, liver and heart were studied in a rat model. Twelve sham-operated (SHAM) male Sprague Dawley rats were compared to eleven inferior vena cava-constricted (IVCc) rats for twenty-one weeks. Abdominal venous pressure was significantly higher in the IVCc versus SHAM group (p < 0.0001). Indices of liver and kidney weight, function and morphology, inflammation as well as collagen deposition were significantly increased in the IVCc compared to SHAM group, (p < 0.05). Echocardiographic and hemodynamic parameters were largely unaffected by abdominal venous congestion. In this rat model of isolated abdominal venous congestion, retrogradely conducted glomerular hypertension without a concomitant change in glomerular filtration rate was observed. Adverse short-term hepatic morphological alterations were developed which explain the observed organ function dysfunction. Importantly, cardiac function remained comparable between both groups. This study provides relevant insight in the pathophysiology of abdominal congestion on organ function.