Cardiac Failure Review最新文献

Water and salt retention, in other words congestion, are fundamental to the pathophysiology of heart failure and are important therapeutic targets. Echocardiography is the key tool with which to assess cardiac structure and function in the initial diagnostic workup of patients with suspected heart failure and is essential for guiding treatment and stratifying risk. Ultrasound can also be used to identify and quantify congestion in the great veins, kidneys and lungs. More advanced imaging methods might further clarify the aetiology of heart failure and its consequences for the heart and periphery, thereby improving the efficiency and quality of care tailored with greater precision to individual patient need.

In patients with AF, the presence of left atrial/left atrial appendage (LA/LAA) thrombus is related to an increased risk of thromboembolic events. Anticoagulation therapy, either with vitamin K antagonists or novel oral anticoagulants (NOACs) is therefore mandatory in AF with LA/LAA thrombus in order to lower the risk of stroke or other systemic embolic events. Despite the efficacy of these treatments, some patients will have persistent LAA thrombus remaining or may have contraindications to oral anticoagulation. Currently, little is known about the occurrence, risk factors and resolution rate of LA/LAA thrombus in patients who are already under optimal chronic oral anticoagulation, including vitamin K antagonists or NOACs. The common action in clinical practice in this scenario is switching from one to another anticoagulant drug exhibiting a different mechanism of action. Repeated cardiac imaging is then advised within several weeks to visually verify thrombus dissolution. Finally, there is a substantial scarcity of data on the role and optimal use of NOACs after LAA occlusion. The aim of this review is to critically evaluate data and provide up-to-date information on the best antithrombotic strategies in this challenging clinical scenario.

Background: This study aims to evaluate the cardiopulmonary effects of sacubitril/valsartan therapy in patients with heart failure with reduced ejection fraction (HFrEF), investigating a possible correlation with the degree of myocardial fibrosis, as assessed by cardiac magnetic resonance. Methods: A total of 134 outpatients with HFrEF were enrolled. Results: After a mean follow-up of 13.3 ± 6.6 months, an improvement in ejection fraction and a reduction in E/A ratio, inferior vena cava size and N-terminal pro-B-type natriuretic peptide levels were observed. At follow-up, we observed an increase in VO₂ peak of 16% (p<0.0001) and in O₂ pulse of 13% (p=0.0002) as well as an improvement in ventilatory response associated with a 7% reduction in the VE/VCO₂ slope (p=0.0001). An 8% increase in the ΔVO₂/Δ work ratio and an 18% increase in exercise tolerance were also observed. Multivariate logistic regression analysis showed that the main predictors of events during follow-up were VE/VCO₂ slope >34 (OR 3.98; 95% CI [1.59-10.54]; p=0.0028); ventilatory oscillatory pattern (OR 4.65; 95% CI [1.55-16.13]; p=0.0052); and haemoglobin level (OR 0.35; 95% CI [0.21-0.55]; p<0.0001). In patients who had cardiac magnetic resonance, when delayed enhancement >4.6% was detected, a lower response after sacubitril/valsartan therapy was observed as expressed by improvement in ΔVO₂ peak, O₂ pulse, LVEF and N-terminal pro-B-type natriuretic peptide. No significant differences were observed in ΔVO₂/Δ work and VE/VCO₂ slope. Conclusion:Sacubitril/valsartan improves cardiopulmonary functional capacity in HFrEF patients. The presence of myocardial fibrosis on cardiac magnetic resonance is a predictor of response to therapy.

Heart failure with preserved ejection fraction (HFpEF) is increasingly recognised to be strongly associated with obesity and abnormalities in fat distribution. Epicardial fat has been associated with abnormal haemodynamics in HFpEF, with potential for direct mechanical effects on the heart causing constriction-like physiology and local myocardial remodelling effects from secretion of inflammatory and profibrotic mediators. However, patients with epicardial fat generally have more systemic and visceral adipose tissue making determination of causality between epicardial fat and HFpEF complex. In this review, we will summarise the evidence for epicardial fat being either directly causal in HFpEF pathogenesis or merely being a correlate of worse systemic inflammatory and generalised adiposity. We will also discuss therapies that directly target epicardial fat and may have potential for treating HFpEF and elucidating the independent role of epicardial fat in its pathogenesis.

Heart failure (HF) is a rapidly growing public health issue with an estimated prevalence of 64 million people globally. Although the incidence of HF has stabilised worldwide and seems to be declining in developed countries, the prevalence is increasing due to the ageing of the population, improved survival after MI and improved treatment and survival of patients with HF. Yet, HF remains associated with high mortality and morbidity, poor quality of life and functional capacity, and confers a substantial burden to the healthcare system. The prevalence, incidence, mortality and morbidity rates reported show geographical variations, depending on the different aetiologies and clinical characteristics observed among patients with HF. In this review, we provide an overview of the global epidemiology of HF with updated data on prevalence, incidence, mortality and morbidity worldwide.

Cardiovascular involvement is common in Fabry's disease and is the leading cause of morbidity and mortality. The research is focused on identifying diagnostic clues suggestive of cardiovascular involvement in the preclinical stage of the disease through clinical and imaging markers. Different pathophysiologically driven therapies are currently or will soon be available for the treatment of Fabry's disease, with the most significant benefit observed in the early stages of the disease. Thus, early diagnosis and risk stratification for adverse outcomes are crucial to determine when to start an aetiological treatment. This review describes the cardiovascular involvement in Fabry's disease, focusing on the advances in diagnostic strategies, outcome prediction and disease management.

Cardiovascular disease (CVD) represents a significant threat to women's health. Heart failure (HF) is one CVD that still has an increasing incidence and about half of all cases involve women. HF is characterised by strong sex-specific features in aetiology, clinical manifestation and outcomes. Women are more likely to have hypertensive heart disease and HF with preserved ejection fraction, they experience worse quality of life but have a better overall survival rate. Women's hearts also have unique morphological characteristics that should be considered during cardiovascular assessment. It is important to understand and highlight these sex-specific features to be able to provide a tailored diagnostic approach and therapeutic management. The aim of this article is to review these aspects together with the challenges and the unique characteristics of different imaging modalities used for the diagnosis and follow-up of women with HF.

Heart failure with preserved ejection fraction (HFpEF) currently accounts for approximately half of all new heart failure cases in the community. HFpEF is closely associated with chronic lifestyle-related diseases, such as obesity and type 2 diabetes, and clinical outcomes are worse in those with than without comorbidities. HFpEF is pathophysiologically distinct from heart failure with reduced ejection fraction, which may explain, in part, the disparity of treatment options available between the two heart failure phenotypes. The mechanisms underlying HFpEF are complex, with coronary microvascular dysfunction (MVD) being proposed as a potential key driver in its pathophysiology. In this review, the authors highlight the evidence implicating MVD in HFpEF pathophysiology, the diagnostic approaches for identifying MVD (both invasive and non-invasive) and the prevalence and prognostic significance of MVD.

Implementation of guideline-directed medical therapy for patients with heart failure is suboptimal. The use of guideline-directed medical therapy improves minimally after heart failure hospitalisation, despite this event clearly indicating increased risk of further hospitalisation and death. In-hospital initiation and titration of guideline-directed medical therapies is one potential strategy to fill these gaps in care, both in the acute vulnerable period after hospital discharge and in the long term. The purpose of this article is to review the knowledge gaps in best practices of in-hospital initiation and up-titration of guideline-directed medical therapies, the benefits and risks of in-hospital initiation and post-discharge focused titration of guideline-directed medical therapies, the recent literature evaluating these practices, and propose strategies to apply these principles to the care of patients with heart failure with reduced ejection fraction.

Telemonitoring through multiple variables measured on cardiac devices has the potential to improve the follow-up of patients with heart failure. The HeartLogic algorithm (Boston Scientific), implemented in some implantable cardiac defibrillators and cardiac resynchronisation therapy, allows monitoring of the nocturnal heart rate, respiratory movements, thoracic impedance, physical activity and the intensity of heart tones, with the aim of predicting major clinical events. Although HeartLogic has demonstrated high sensitivity for the detection of heart failure decompensations, its effects on hospitalisation and mortality in randomised clinical trials has not yet been corroborated. This review details how the HeartLogic algorithm works, compiles available evidence from clinical studies, and discusses its application in daily clinical practice.