Cardiac Failure Review最新文献

Frailty is common among heart failure (HF) patients and linked to increased risk of adverse outcomes. Contributing factors include inflammation, sarcopenia and neurohormonal issues which diminish physiological reserves and accelerate the decline of health. Managing frailty in HF requires a multidisciplinary approach to address physical, nutritional and pharmacological needs. Structured exercise and dietary support can improve physical function, while careful medication management, especially with polypharmacy, reduces frailty-related risks. Telemedicine and wearable tech facilitate continuous monitoring and timely intervention, especially for those in remote areas. Future research should develop standardised frailty assessment tools specific to HF, enhancing risk stratification and personalised care. Studies on underlying mechanisms, such as inflammation and mitochondrial dysfunction, could lead to new therapies. Addressing socioeconomic factors can also improve care equity. This review summarises the mechanisms, clinical characteristics and impact of frailty on HF, highlighting challenges in treatment and opportunities for improving patient outcomes.

Background: Increased BMI is paradoxically associated with improved survival among patients with acute heart failure (AHF). However, the impact of different nutritional status on this obesity paradox on 1-year mortality is underreported. The prognostic nutritional index is a simple tool to assess nutrition status.

Methods: From 10,027 emergency department admissions at the Amager and Hvidovre Hospital, Copenhagen University Hospital in Denmark, all patients with AHF were identified. Patients were categorised by BMI (normal: 18.5-24.9 kg/m², overweight: 25-29.9 kg/m², obese: ≥30 kg/m²) and nutritional status using the prognostic nutritional index (malnourished: <38, well-nourished: ≥38). Kaplan- Meier curves analysed cumulative survival, and Cox regression examined associations between BMI, nutritional status and outcomes, expressed as HR and 95% CI.

Results: Among 383 AHF patients (median age 76 years), 41.3% were malnourished and 58.7% well nourished. In the well-nourished group, obesity was inversely associated with 1-year mortality (adjusted HR 0.48; 95% CI [0.24-0.95]; p=0.035). However, this correlation disappeared in the malnourished group (adjusted HR 1.08; 95% CI [0.59-2.00]; p=0.798). Mortality rates were significantly lower in the well-nourished group among patients with overweight and obesity.

Conclusion: Obesity was associated with reduced 1-year mortality only in AHF patients with good nutritional status, while in malnourished patients, obesity was not associated with 1-year mortality. The prognosis in patients with AHF depends on both the presence of obesity and their nutritional status, highlighting the need for nutritional assessment for risk stratification.

Introduction: Percutaneous ventricular assist devices (pVADs) are increasingly used in cardiogenic shock but are associated with complications including haemolysis. The aim of this study was to investigate patient characteristics associated with haemolysis in cardiogenic shock patient population.

Methods: Consecutive patients were identified using Current Procedural Terminology (CPT) codes for pVAD insertion. Patient characteristics, laboratory and imaging data, and patient outcomes were abstracted manually and using validated automated methods. Laboratory-defined haemolysis required a drop in haemoglobin ≥2 mg/dl with either lactate dehydrogenase ≥250 units/l or undetectable haptoglobin. Clinically significant haemolysis was defined as laboratory-defined haemolysis necessitating transfusion. Primary outcome was the association between haemolysis and on-device and 30-day mortality.

Results: A total of 196 patients underwent pVAD insertion for cardiogenic shock during the study period and were included. Laboratory-defined haemolysis occurred in 46 patients (23.5%), of whom 12 (6.1%) had clinically significant haemolysis. Haemolysis occurred more often following emergency insertion, rather than elective insertion (84.8% versus 40.0%, p<0.001) in patients with elevated lactic acid levels (median 2.5 versus 1.6, p=0.016) and elevated heart rates (92.5 BPM versus 86.5 BPM, p=0.023). After multivariable adjustment, there was no association between laboratory-defined haemolysis and on-device (OR 0.6; 95% CI [0.1-3.4]; p=0.565) or 30-day mortality (OR 2.1; 95% CI [0.4-13.0]; p=0.391).

Conclusion: Laboratory-defined haemolysis was common in patients with cardiogenic shock and pVAD, but clinically significant haemolysis was not. There was no association between haemolysis and on-device or 30-day mortality.

Diuretic therapy is not associated with improved outcomes in heart failure and may cause significant side effects. Counteracting the core pathophysiological mechanisms of heart failure through neurohormonal blockade while reducing reliance on diuretics is potentially the most effective method of decongestion.

Congestion in patients with heart failure (HF) predicts adverse outcomes and is a leading cause of hospitalisation. Understanding congestion mechanisms helps in HF management and underscores the importance of tailored therapies to treat vascular and tissue congestion, improving patient outcomes. In this setting, several tools are available to detect congestion. Biomarker measurement is a simple, valid and affordable method to evaluate congestion in patients with HF. Natriuretic peptides are the most widely available tool in acute and chronic HF, helping diagnosis, risk stratification and management. Novel biomarkers can potentially become reliable allies in diagnosing and monitoring patients with HF. This review aims to assess the current scientific literature on biomarkers for managing HF, evaluate their clinical utility and explore future perspectives in this field.

Heart failure (HF) is a major contributor to hospitalisations and accounts for 7% of cardiovascular-related deaths, with patients who have chronic kidney disease and type 2 diabetes at heightened risk. Existing treatment guidelines inadequately address these comorbidities. Steroidal mineralocorticoid receptor antagonists (MRAs) are commonly used in HF with reduced ejection fraction but pose risks, such as hyperkalaemia and acute kidney injury. Finerenone, a non-steroidal MRA, offers a safer alternative, with higher selectivity, reduced electrolyte disturbances and beneficial effects on heart and kidney tissues. Preclinical studies show anti-inflammatory and anti-fibrotic effects, while phase III trials (ARTS and ARTS-HF) demonstrated fewer hyperkalaemia incidents compared with spironolactone. In phase III trials (FIDELIO-DKD and FIGARO-DKD), finerenone reduced HF hospitalisations by 22% in patients with chronic kidney disease and type 2 diabetes. The FINEARTS-HF trial found that finerenone significantly reduced the risk of worsening HF events or CV death in patients with HF with mildly reduced or preserved ejection fraction. Its combination with therapies, such as sodium-glucose cotransporter 2 inhibitors, shows promise and ongoing trials, such as REDEFINE-HF, FINALITY-HF and CONFIRMATION-HF, are investigating its efficacy in other HF phenotypes. These studies will further establish the role of finerenone in managing cardio-renal-metabolic diseases.

Aldosterone is a key regulator of fluid and electrolyte balance in the body. It is often dysregulated in heart failure (HF) and is a key driver of cardiac remodelling and worse clinical outcomes. Potassium regulation is essential for normal cardiac, gastrointestinal and neuromuscular function. Serum potassium fluctuations are largely determined by aldosterone, the final step of the renin-angiotensin-aldosterone system. Dyskalaemia (i.e. hypokalaemia and hyperkalaemia) is prevalent in HF because of the disease itself, its therapies and related comorbidities such as chronic kidney disease. Prognostic implications of abnormal serum potassium follow a U-shaped curve, where both hypokalaemia and hyperkalaemia are associated with adverse outcomes. Hypokalaemia is associated with increased mortality, starting from potassium <4.0 mmol/l but especially at potassium <3.5 mmol/l. Hyperkalaemia, along with increasing arrhythmia risk, limits the use of lifesaving renin-angiotensin- aldosterone system inhibitors, which may have long-term survival implications. The advent of novel potassium binders aims to manage chronic hyperkalaemia and may allow for uptitration and optimal dosing of guideline-recommended therapy. This review discusses the impacts of dyskalaemia in HF, along with management strategies, including the relevance of potassium binder use in optimising HF treatment. Current and potential future aldosterone-modulating therapies, such as non-steroidal mineralocorticoid receptor antagonists and aldosterone synthase inhibitors, are also discussed.

Activation of the renin-angiotensin-aldosterone system is the ultimate pathophysiological hallmark in heart failure. Though aldosterone primarily appears to regulate electrolyte homeostasis by acting on distal nephrons in the kidneys, its effects are far-reaching across the cardiovascular system as its receptors are also expressed in vascular smooth muscle cells, endothelial cells, macrophages and cardiomyocytes. Aldosterone excess leads to vascular stiffness, vasoconstriction, endothelial dysfunction, inflammation, oxidative stress, cardiac fibrosis and hypertrophy, atherogenesis and thrombosis. Hence, aldosterone antagonism is an attractive proposition for heart failure management. The first-generation non-selective mineralocorticoid receptor antagonist spironolactone produced a spectacular reduction of cardiovascular outcomes in the seminal RALES study, while the selective second-generation congener eplerenone boasts two positive studies: EPHESUS and EMPHASIS-HF. The TOPCAT trial indicated that a specific subgroup of patients with heart failure with preserved ejection fraction may benefit from targeted therapy of mineralocorticoid receptor antagonists. Newer-generation non-steroidal mineralocorticoid antagonists and aldosterone synthase inhibitors are being evaluated in randomised trials.

This review examines the effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on different heart failure phenotypes with preserved ejection fraction (HFpEF). Traditional heart failure treatment modalities have shown limited success in improving outcomes for patients with HFpEF, but new evidence suggests that GLP-1RAs could be beneficial. The positive effects of GLP-1RAs are likely due to their ability to reduce systemic inflammation, enhance metabolism and directly affect the cardiovascular system, addressing critical aspects of HFpEF pathology. However, the exact impact of GLP-1RAs on clinical outcomes for different HFpEF phenotypes is still unclear. This review highlights both the potential benefits and the current limitations of GLP-1RA therapy, suggesting a careful approach for their application in clinical practice.