ESC Heart Failure最新文献

Aims: The prognostic significance of left ventricular (LV) diastolic dysfunction (LVDD) severity in patients with dilated cardiomyopathy (DCM) remains uncertain. This study aimed to evaluate the association of LVDD severity and elevated left atrial pressure (eLAP) with patient outcomes in stable, non-acutely decompensated patients with DCM.

Methods: This single-centre, retrospective, observational study involved 740 DCM patients (either inpatients or outpatients) managed at our tertiary cardiac centre between 2010 and 2021. Due to incomplete data, 96 patients were excluded. LVDD and eLAP were assessed using echocardiography according to the 2016 guidelines of the European Association of Cardiovascular Imaging (EACVI). The primary outcomes were all-cause mortality and heart failure (HF)-related mortality.

Results: The final cohort comprised of 644 DCM patients [mean age: 52 ± 12 years, LV ejection fraction (LVEF): 26 ± 10%]. Over a median follow-up period of 41 (18.5-66.7) months, 105 (16.3%) patients died: 8 (5.3%) patients in the normal left atrial pressure (nLAP) group and 97 (19.6%) patients in the eLAP group. eLAP was identified as an independent prognostic factor for both all-cause mortality [hazard ratio (HR) 2.0; 95% confidence interval (CI) 1.1-3.7; P = 0.01] and HF-related mortality (HR 2.5; 95% CI 1.01-6.5; P = 0.04), even after adjusting for LVEF and atrial fibrillation (AF) presence. Additionally, HF-related mortality rates were significantly higher in patients with moderate to severe LVDD compared with those with mild LVDD [5 (3.3%) vs. 67 (13.6%), P < 0.05].

Conclusions: This study's findings highlight the importance of assessing the severity of LVDD in patients with DCM, which provides incremental prognostic information over LVEF.

The main purpose of this project was to capture experts' opinion on hyperkalaemia management and form best practice recommendations for cardiorenal patients in Greece. A steering committee of nephrologists and cardiologists developed 37 statements. An online questionnaire completed by 32 experts in cardiorenal management in Greece. Median score used to determine the level of agreement and disagreement index (DI) used to determine the level of consensus for each statement. Statements divided in four sectors: hyperkalaemia risk management, preventative measures, treatment and collaboration between specialties. The rate of the first round of the consensus was 94.6%. Median score was >7 for 36 of 37 statements and DI ≤ 1 for 35 of 37. Among other statements, consensus reached for recognizing levels K+ > 5.0 mEq/L as associated with elevated mortality risk; retaining renin-angiotensin-aldosterone system inhibitors (RAASi) on maximum recommended dose for cardiorenal patients; and using novel K+ binders to help enabling guideline-recommended doses of RAASi therapy. Cardiologists compared to nephrologists showed higher reluctance to discontinue down-titrate RAASi and MRA in patients with K+ levels above 5 mEq/L. Additionally, 88.9% of nephrologists and 71.4% of cardiologists agreed that cross-specialty alignment on a serum K+ concentration level (K > 5.5 mEq/L) is needed to initiate hyperkalaemia treatment. Both cardiologists and nephrologists showed disagreement with the statement on keeping titration in cardiorenal patients with K+ > 5.5 mEq/L or preserving fruit and vegetable consumption when moderate or severe hyperkalaemia exhibits. This Delphi project pointed out nephrologists' and cardiologists' agreement on hyperkalaemia management in cardiorenal patients; thus, it can help a cross-specialty optimal management of cardiorenal patients, with hyperkalaemia not being an obstacle for disease-optimizing therapy. Novel potassium binding agents can enable guideline-recommended doses of potassium-sparing medication.

Cardiac amyloidosis due to transthyretin (ATTR) remains an underdiagnosed cause of cardiomyopathy. As awareness of the disease grows and referrals for ATTR increase, clinicians are likely to encounter more atypical forms of the condition in clinical practice. Therefore, physicians and treating cardiologists should be aware of the full phenotypic spectrum of ATTR. The phenotypic manifestation of ATTR varies depending on the stage of the disease, the presence and type of TTR mutation and the patient's comorbidities. ATTR findings can be grouped into four major categories: clinical profile and cardiac phenotype, extra-cardiac findings, electrocardiogram and imaging findings, which cumulatively form the full phenomap of ATTR. Results from any diagnostic test for ATTR should be interpreted in light of the pre-test probability for the disease. Findings that suggest negative markers for ATTR can point towards other forms of amyloidosis (such as AL amyloidosis) or alternate causes of left ventricular hypertrophy, including hypertrophic cardiomyopathy or Fabry disease. The rising number of referrals for ATTR cardiomyopathy presents a challenge in daily clinical practice. To prevent an increase in false-positive diagnostic test results, an ATTR phenomap can serve as a valuable tool for guiding diagnostic assessments, interpreting test outcomes and prioritizing appropriate referrals for ATTR screening.

Aims: Obesity increases the risk of heart failure with preserved (HFpEF), but not reduced ejection fraction (HFrEF). The glucagon-like peptide-1 receptor agonist (GLP-1-RA) semaglutide improves outcome of patients with obesity with or without HFpEF, while GLP-1-RAs were associated with adverse outcome in patients with HFrEF. Here, we investigate the effect of in vivo treatment with semaglutide on excitation-contraction coupling in a rat model of obesity.

Methods and results: Rats received high-fat/high-fructose diet for 8 weeks and were then randomized to semaglutide (HFD/Sema) or vehicle (HFD/Veh) for another 8 weeks, during which they could choose between HFD and a low-fat/high-fructose diet (LFD). Control rats received either standard chow (CON), HFD or LFD only, without treatment. After 16 weeks, sarcomere shortening and cytosolic Ca²⁺ concentrations ([Ca²⁺]_c) were determined in isolated cardiomyocytes. Compared with CON, HFD/Veh increased the amplitude of [Ca²⁺]_c transients and systolic sarcomere shortening in absence or presence of β-adrenergic stimulation, which was reversed by HFD/Sema. Caffeine-induced sarcoplasmic reticulum (SR) Ca²⁺ release and L-type Ca²⁺ channel (LTCC) currents were reduced by HFD/Sema versus HFD/Veh, while SR Ca²⁺ ATPase activity remained unaffected. Compared with HFD, LFD increased [Ca²⁺]_c transients and sarcomere shortening further despite similar effects on body weight.

Conclusions: While HFD increased cardiomyocyte [Ca²⁺]_c transients and systolic sarcomere shortening, semaglutide normalized these alterations, mediated by reduced SR Ca²⁺ load and LTCC currents. Because increased LTCC currents were previously traced to cardiac hypertrophy, these effects may explain why GLP-1-RAs provide benefits for patients with obesity with or without HFpEF, but rather adverse outcome in HFrEF.

Aims: Immune checkpoint inhibitors (ICI) are the cornerstone of modern oncology; however, side effects such as ICI-related myocarditis (irM) can be fatal. Recently, Bonaca proposed criteria for irM; however, it is unknown if they correlate well with cardiovascular (CV) ICI-related adverse events. Additionally, whether incident irM portends worse long-term CV outcomes remains unclear. We aimed to determine the incidence of long-term CV comorbidities and CV mortality among irM patients.

Patients and methods: The ICI-related adverse event (irAE) registry was queried to identify irM patients by using Bonaca criteria. Random controls were selected after excluding patients with other concomitant irAEs. Patients' demographics, comorbidities and myocarditis presenting features were gathered. Outcomes included 2-year freedom from CV comorbidities (composite of atrial fibrillation, stroke, myocardial infarction and heart failure) and freedom from CV death. IrM was treated as a time-varying covariate.

Results: Seventy-six patients developed irM at a median of 167 days (mean age 69, 63.2% male, 47% lung cancer). Majority of patients had new wall motion abnormalities or EKG changes on presentation. Mean LVEF was 43%, median peak TnT was 0.81, and median NTproBNP was 2057 at irM onset. Two-year freedom from CV comorbidities (67% vs 86.8%, P < 0.001) and death (93.4% vs 99.3%, P = 0.003) was lower among irM patients. Incident irM was an independent predictor of CV death (HR 8.28, P = 0.048), but not CV comorbidities (HR 2.21, P = 0.080).

Conclusions: This is the largest case-control study on irM highlighting worse long-term CV outcomes. Future studies are needed to establish appropriate therapeutic strategies and efficient screening strategies for irM survivors.

Aims: Myocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown. We aimed at establishing a relevant role of cardiac inflammation in the impairment of mitochondrial energy production in advanced ischaemic and non-ischaemic HF.

Methods: We included 81 patients with stage D HF (ICM, n = 44; DCM, n = 37) undergoing left ventricular assist device implantation (n = 59) or heart transplantation (n = 22) and obtained left ventricular tissue samples during open heart surgery. We quantified mitochondrial oxidative capacity, citrate synthase activity (CSA) and fibrosis and lymphocytic infiltration. We considered infiltration of >14 CD3⁺ cells/mm² relevant inflammation.

Results: Patients with ICM or DCM did not differ regarding age (61.5 ± 5.7 vs. 56.5 ± 12.7 years, P = 0.164), sex (86% vs. 84% male, P = 0.725), type 2 diabetes mellitus (34% vs. 18%, P = 0.126) or chronic kidney disease (8% vs. 11%, P = 0.994). ICM exhibited oxidative capacity reduced by 23% compared to DCM (108.6 ± 41.4 vs. 141.9 ± 59.9 pmol/(s*mg), P = 0.006). Maximum production of reactive oxygen species was not significantly different between ICM and DCM (0.59 ± 0.28 vs. 0.69 ± 0.36 pmol/(s*ml), P = 0.196). Mitochondrial content, detected by CSA, was lower in ICM (359.6 ± 164.1 vs. 503.0 ± 198.5 nmol/min/mg protein, P = 0.002). Notably, relevant inflammation was more common in ICM (27% vs. 6%, P = 0.024), and the absolute number of infiltrating leucocytes correlated with lower oxidative capacity (r = -0.296, P = 0.019). Fibrosis was more prevalent in ICM (20.9 ± 21.2 vs. 7.2 ± 5.6% of area, P = 0.002), but not associated with oxidative capacity (r = -0.13, P = 0.327).

Conclusions: More than every fourth ICM patient with advanced HF displays myocardial inflammation in the range of inflammatory cardiomyopathy associated with reduced mitochondrial oxidative capacity. Future studies may evaluate inflammation in ICM at earlier stages in standardised fashion to explore the therapeutic potential of immunosuppression to influence trajectories of HF in ICM.

Background: Obesity is a known risk factor for cardiovascular disease (CVD), yet an 'obesity paradox' has been observed in various CVD contexts. The impact of obesity on heart failure (HF) patients treated with a wearable cardioverter-defibrillator (WCD) remains underexplored.

Methods: In a multicentre international registry, we retrospectively collected data from a consecutive series of 1003 patients. These patients were divided into three body mass index (BMI) groups: <25 kg/m² (n = 348), 25-30 kg/m² (n = 383), and >30 kg/m² (n = 272), with BMI > 30 kg/m² defined as the reference category. Demographics, indications, adherence, WCD shocks, arrhythmic events, rehospitalization due to cardiovascular causes, and mortality were analysed.

Results: At 3 month follow-up, patients with a BMI > 30 showed the greatest improvement in left ventricular ejection fraction (LVEF) at 51.4%, significantly higher than the 41.4% in those with a BMI < 25 (P = 0.017) and comparable with the 49.4% in the BMI 25-30 group (P = 0.635). WCD wearing time and adherence were similar across all BMI groups. The incidence of WCD shock was similar across BMI groups. Rates of ventricular tachycardia (VT), ventricular fibrillation and non-sustained VT (ns-VT) were comparable across BMI groups. The rate of implantable cardioverter-defibrillator (ICD) implantation was 40.3% across all patients, with a slightly lower rate in the BMI > 30 group (36.8%) compared with others, although not significantly. Rehospitalization due to cardiovascular causes was significantly lower in the BMI > 30 group (55.4%) compared with the BMI 25-30 group (70.9%; P = 0.048), but similar to the BMI < 25 group (54.9%; P = 0.957). At 2 year follow-up, mortality was lower in the BMI > 30 group (5.9%) compared with the BMI < 25 (7.5%; P = 0.029) and BMI 25-30 groups (7%; P = 0.681). In multivariable analysis, LVEF at long term was significantly associated with a reduction in mortality.

Conclusions: Obese patients exhibited significantly greater improvement in LVEF, which was associated with reduced mortality. Adherence to WCD therapy was excellent across all BMI groups. ICD implantation occurred in 40.3% of patients, with similar WCD shock rates and arrhythmic events across BMI groups. An obesity paradox was observed, with obese patients demonstrating significantly lower rehospitalization rates due to cardiovascular causes and reduced mortality at follow-up.

Objective: This study aimed to evaluate the utility of left atrial volume and function in uraemic patients using four-dimensional automatic left atrial quantification (4D auto LAQ) technology.

Methods: Thirty-four undialysed uraemic patients (U-ND group), 60 dialysed uraemic patients (U-D group), and 32 healthy volunteers (N group) were enrolled in our current study. Conventional echocardiographic parameters were recorded, and left atrial volume and strain parameters were analysed to determine statistical differences among the three groups. The Pearson correlation coefficient was employed to assess the relationships between left atrial ejection fraction and left atrial strain parameters.

Results: Compared to the N group, uraemic patients often displayed left atrial enlargement and left ventricular hypertrophy. Significant increases were noted in left atrial diameter, interventricular septum thickness, left ventricular posterior wall thickness, E/e', diastolic blood pressure, systolic blood pressure, left atrial minimum volume, left atrial maximum volume, left atrial pre-atrial contraction volume, left atrial emptying volume and left atrial maximum volume index (P < 0.05). Conversely, the e', E/A ratio and left atrial reservoir longitudinal strain were significantly decreased (P < 0.05). However, no statistically significant differences were observed in the aforementioned parameters between the U-ND and U-D groups. The absolute values of left atrial conduit longitudinal strain and left atrial conduit circumferential strain, as well as left atrial passive ejection fraction, were notably lower in the U-D group compared to the N and U-ND groups, with statistically significant differences identified among the three groups (P < 0.05).

Conclusions: Uraemic patients exhibit marked left atrial enlargement and left ventricular hypertrophy, coupled with altered atrial function, particularly ductal dysfunction in the U-D group. The 4D auto LAQ technology proves advantageous in detecting these alterations, offering a promising tool for thorough cardiac assessment in this patient cohort.

Large clinical data underscore that heart failure is independently associated to an increased risk of negative cognitive outcome and dementia. Emerging evidence suggests that cerebral hypoperfusion, stemming from reduced cardiac output and vascular pathology, may contribute to the largely overlapping vascular dementia and Alzheimer's disease. Despite these insights, cognitive outcomes remain largely overlooked in heart failure management. This narrative review outlines the prevalence and risk of cognitive impairment in heart failure patients, exploring potential shared pathophysiological mechanisms and examining the impact of heart failure therapy on cognitive deficits. Additionally, it discusses clinical implications and suggests future treatment approaches targeting therapeutic outcomes. Cognitive impairment is prevalent among individuals with heart failure, with reported rates varying widely depending on assessment methods. Shared pathological pathways and risk factors, including atrial fibrillation (AF), hypertension, obesity and type 2 diabetes mellitus, suggest a causal link. Mechanisms such as poor perfusion, microembolic events, ischaemic syndromes and cerebral inflammation contribute to this relationship. Moreover, heart failure itself may exacerbate cognitive dysfunction. This emerging understanding posits that vascular dementia and Alzheimer's disease may represent a pathophysiological continuum, driven by both the accumulation of misfolded proteins and cerebrovascular pathology due to cardiovascular dysfunction. Understanding these links is crucial for developing effective treatment strategies. The complex interplay between heart failure and cognitive impairment underscores the necessity for a holistic patient care approach. Both conditions share analogous disease processes, influencing self-management and independence in patients. Prioritizing brain health in heart failure management is essential to enhance patient prognosis and general well-being.