Future cardiology最新文献

Transthyretin amyloid cardiomyopathy (ATTR-CM) has long been considered a rare and inexorably fatal condition. However, advances in noninvasive diagnosis, disease awareness, and available treatments have enabled diagnosis in asymptomatic stages, before development of clinical heart failure (HF). The emerging entity of asymptomatic ATTR-CM presents both challenges and new opportunities for improving patient care. Data remain limited, as asymptomatic patients have been excluded from clinical trials, and their management currently relies on empirical judgment. Understanding the natural history of asymptomatic ATTR-CM is essential for guiding individualized clinical decisions at the patient level and for designing future clinical trials in this population. While these patients do not exhibit overt HF, recent evidence suggests that a subset may experience disease progression and develop significant morbidity and mortality within a relatively short time. This review explores the rapidly evolving landscape of asymptomatic ATTR-CM with regard to diagnostic pathways, phenotypic variability, natural history, and prognostic stratification. It also discusses current barriers encountered in clinical practice for timely diagnosis, the clinical role of imaging and biomarkers, and potential indications for early therapeutic interventions in this under-recognized population, which is projected to exponentially increase in the coming years.

The Superior cavopulmonary connection (SCPC) is typically the second stage of the single ventricle palliation. There are modifiable factors that have a complex interplay in determining outcomes such as mortality or hospital length of stay. There is no clear consensus on the timing of SCPC as this involves a critical balance between the timing of operation and the length of the high-risk interstage period. Younger age has not been associated with reduced transplant-free survival but has been associated with longer hospital length of stay. Another critical decision is for children with viral respiratory infections; a patient with a symptomatic viral respiratory infection may need to be delayed for weeks but this extends time in the interstage. While age is an important consideration, weight-for-age-Z-score and rate of weight gain are also critical factors in reduced transplant-free survival with those poor weight gain. Atrioventricular valve regurgitation, pulmonary artery obstruction and arch obstruction can all impact outcomes of SCPC. A systematic approach to pre-operative evaluation can identify these residual lesions to individualize the approach and optimize outcomes of single ventricle palliation.

Background: Heart failure (HF) and ST-elevation myocardial infarction (STEMI) are the major causes of morbidity and mortality worldwide. Recent evidence indicates that long noncoding RNAs (lncRNAs) participate in cardiac fibrosis, which develops to varying degrees in these conditions.

Patients and methods: This retrospective study analyzed the plasma expression levels of lncRNA Wisper using RT-qPCR in 28 patients with HF (NYHA class III - IV, reduced ejection fraction), 37 patients with STEMI, and 15 healthy controls. Diagnostic accuracy was assessed using receiver operating characteristic (ROC) curve analysis, and correlations with clinical parameters were evaluated.

Results and conclusions: Patients with HF and STEMI showed significantly higher plasma Wisper expression than that of controls (p = 0.021 and p = 0.03, respectively), with no significant difference between the HF and STEMI groups (p = 1.0). In patients with HF, Wisper expression negatively correlated with age (rho = -0.452, p = 0.016). ROC analysis demonstrated good discriminatory power of Wisper in distinguishing HF (AUC = 0.783, 95% CI: 0.648-0.919, p = 0.002) and STEMI (AUC = 0.780, 95% CI: 0.658-0.903, p = 0.002) from controls. The elevated plasma expression of Wisper in patients with HF and STEMI suggests its potential role as a circulating biomarker of cardiac fibrosis.

Atrial cardiomyopathy (ACM) is an underrecognized cardiac entity marked by structural, contractile, or electrophysiological changes in the atria, yet it lacks established clinical diagnostic criteria and management guidelines. These alterations - driven by molecular, mechanical, and genetic factors - lead to atrial remodeling and contribute to arrhythmogenesis, thromboembolic complications, and the progression of heart failure. Despite recent advances in imaging, biomarkers, and histopathological classifications, the pathophysiology of ACM remains complex and multifactorial, involving processes such as inflammation, oxidative stress, and genetic predisposition. This review synthesizes current knowledge on ACM, including its classification, pathophysiologic mechanisms, and clinical relevance in atrial fibrillation, ischemic stroke, and heart failure with preserved ejection fraction (HFpEF). We also explore emerging diagnostic tools and biomarkers that may aid in risk stratification and therapeutic decision-making. Ultimately, we aim to underscore the clinical significance of ACM and advocate for the development of standardized diagnostic frameworks and personalized treatment strategies to improve patient outcomes.

Despite advancements in treatment, cancer and cardiovascular disease remain the leading causes of morbidity and mortality in developed nations. Cancer therapies have led to improved cancer-specific outcomes at the potential risk of cardiotoxicity. Additionally, basic and translational research have demonstrated a common shared pathophysiology of cancer and cardiovascular disease. Recent clinical research has suggested a potential role of repurposing cancer and cardiovascular medications for the treatment of each other. This narrative review aims to review and examine current literature of repurposing cancer and cardiovascular drugs via exploitation of off-target effects to benefit each condition. A better understanding of underlying pathophysiologic effects of these off-target mechanisms of action may aid in identifying novel therapeutics for both cancer and cardiovascular disease.

Introduction: Wilson's disease (WD) is a rare autosomal recessive disorder caused by ATP7B gene mutations, leading to systemic copper accumulation. This systematic review examines the cardiac manifestations of WD and aims to summarize key diagnostic and therapeutic findings from available studies.

Methods: We conducted a systematic review of 21 studies using databases such as PubMed and Scopus. Studies were selected based on relevance to WD and cardiac involvement. Data extraction focused on diagnostic methods, outcomes, and treatments. Risk of bias and methodological quality were assessed qualitatively.

Results: A total of 21 studies were included. Cardiac complications included arrhythmias, myocardial fibrosis, and diastolic dysfunction. Oxidative stress and mitochondrial dysfunction were identified as key pathological mechanisms. Cardiac MRI was highlighted as a valuable diagnostic tool. While chelation remains the cornerstone therapy, gene therapy and liver transplantation are considered for advanced cases.

Conclusions: This review underscores the importance of early cardiac assessment in WD patients. New diagnostic tools and emerging therapies show promise, though evidence remains limited by small sample sizes. Further longitudinal studies are needed to inform clinical guidelines.

Protocol registration: www.crd.york.ac.uk/prospero identifier is CRD420251107174.

Background: Data on outcomes of surgical pulmonary valve replacement or repair (SPVR/SPVr) in patients with heart failure (HF) are limited. We aimed to assess the safety and complications of SPVR/SPVr in this population.

Methods: Adults (≥18 years) who underwent SPVR/SPVr between 2018-2021 were identified from the National Inpatient Sample. Patients were stratified by HF status. In-hospital outcomes included mortality, cardiac arrest, cardiogenic shock, mechanical ventilation (MV), vasopressor use, heart block, permanent pacemaker (PPM), ECMO, bleeding, and acute kidney injury (AKI). Propensity score matching was performed to adjust for comorbidities, hospital factors, income, and elective status. Logistic regression was used to assess associations between HF and outcomes.

Results: There were 4595 SPVR/SPVr; the median age was 35 (26-52). Patients with heart failure had an increased risk of mortality, odds ratio (OR) 3.42 (95% confidence interval [CI] 1.19-6.12); p-value < 0.0001, heart block 1.75 (1.45-2.13); < 0.0001, bleeding 1.31 (1.12-1.52); 0.0005, AKI 1.35 (1.12-1.61); 0.001, vasopressor use 1.33 (1.08-1.65); 0.007, cardiogenic shock 2.34 (1.87-2.93); < 0.0001, MV 1.45 (1.09-1.94); 0.01, in-hospital cardiac arrest 2.29 (1.35-3.91); 0.002, ECMO 2.23 (1.43-3.45); 0.0003. No significant difference in PPM 1.51 (0.85-2.67); 0.1.

Conclusion: Heart failure is associated with worse in-hospital outcomes following surgical pulmonic valve replacement or repair. Preoperative optimization and considering earlier surgical intervention may improve outcomes in this high-risk population.