Heart failure (HF) remains associated with high mortality worldwide despite advances in guideline-directed therapy.

To characterise the patterns and causes of death among Thai patients with chronic HF enrolled in a nationwide registry and to identify predictors of mortality.

We performed a prospective cohort analysis of 2879 HF patients enrolled in the Thai Heart Failure Registry (THFR) which has enrolled patients since 2020. The present analysis included those enrolled between January 2021 and December 2023. Causes of death were ascertained via electronic health records and adjudicated as cardiovascular (CV), non-CV or undetermined. Mortality incidence rates were calculated per 100 person-years. Multivariable Cox proportional hazards models identified independent predictors of all-cause mortality.

Over a median follow-up of 23 months, 301 patients (10.5%) died (incidence rate 6.8 per 100 person-years). Of these, 149 (49.5%) were CV deaths, 116 (38.5%) were non-CV deaths, 36 deaths (12.0%) were undetermined. In HF with reduced ejection fraction/HF with mildly reduced ejection fraction patients, CV deaths predominated compared with non-CV mortality (5.3% vs 3.9%), whereas HF with preserved ejection fraction patients experienced higher non-CV mortality compared with CV mortality (5.5% vs 4.1%), particularly sepsis. Independent predictors of mortality included ischaemic aetiology (HR 1.34; 95% CI 1.06 to 1.69), atrial fibrillation (HR 1.57; 1.24-2.00), peripheral oedema at presentation (HR 2.11; 1.57-2.85), hyponatraemia (serum Na<135 mmol/L; HR 1.83; 1.39-2.39), hypokalaemia (serum K<3.5 mmol/L; HR 1.44; 1.06-1.95), elevated blood urea nitrogen (>25 mg/dL; HR 1.56; 1.23-1.98) and prior loop diuretic use (HR 1.61; 1.21-2.14). Good guideline-directed medical therapy adherence is associated with a lower mortality despite the adjustment of confounders.

Among Thai HF patients, mortality remains high, with distinct patterns of CV versus non-CV deaths across left ventricular ejection fraction phenotypes. Targeted strategies addressing ischaemic heart disease, rhythm management, fluid status and electrolyte disturbances may reduce mortality.

Amiodarone-induced thyrotoxicosis (AIT) is a potentially life-threatening complication of amiodarone therapy, particularly hazardous in patients with underlying structural heart disease. We report the case of a man in his mid-60s with severe cardiomyopathy and recurrent ventricular tachycardia who developed refractory thyrotoxicosis following amiodarone exposure. Overlapping features of type 1 and 2 AIT suggested mixed-type disease, posing a significant diagnostic challenge. Despite aggressive conventional therapy with high-dose thionamides and glucocorticoids, supplemented by adjunctive agents, including lithium and cholestyramine, thyrotoxicosis remained refractory and life-threatening arrhythmias persisted. Given the high cardiac risk and refractory disease course, total thyroidectomy was undertaken as definitive management; therapeutic plasma exchange was used as bridging therapy to achieve rapid biochemical improvement and minimise perioperative risk. This case highlights the complexity of managing severe, treatment-refractory AIT and underscores the value of multidisciplinary care and plasmapheresis as a bridging strategy prior to definitive surgical management.

Neurodevelopmental impairments and physical deconditioning are the most common long-term morbidities in congenital heart disease (CHD). Holistic interventions including combined neuro-cardiac training may improve physical and mental health in youth with CHD.

This is a European multicentre, two-arm randomised controlled study to test the efficacy of a home-based neuro-cardiac rehabilitation programme including physical activity and neuropsychological training versus the standard of care in children, adolescents and young adults with complex CHD. Patients aged 8-25 years who underwent infant surgical and/or catheter-based cardiac interventions will be randomly allocated to either an intervention group including a 12-week home-based cardiovascular rehabilitation and executive function training or to a control group. All participants will undergo a baseline assessment and a 12-month follow-up. The primary outcome is the difference in change in the Pediatric Quality of Life Inventory self-reported health-related quality of life score between baseline and final assessment for the intervention versus the control group. Secondary outcomes include standardised neuropsychological measures of executive function, social cognition and mental health. Cardiovascular secondary outcomes include cardiopulmonary fitness parameters such as maximum oxygen uptake, muscular strength and level of physical activity. Efficacy of the intervention will be evaluated by comparing within-subject group differences from baseline to 12-month follow-up, using an intention-to-treat analysis.

The trial protocol was first approved by the sponsor's drawn National Ethics Committee (CPP Paris-III, number 2023-A00038-37) and registered on Clinicaltrial.gov (number NCT05670132). It was also approved by Ethics Committees in Germany (Technische Universitat Munchen, number 2023-276-S-KH) and Belgium (UCLouvain, number B4032025000116).

NCT05670132.

Palliative reasoning aims to support the integration of palliative care (PC) into heart failure (HF) management and includes multidimensional monitoring of symptoms, wishes, and needs.

This study aimed to establish expert agreement on palliative reasoning and the content of a PC monitoring instrument within the European context.

A two-round modified Delphi study complemented by expert panel meetings after each round. Experts in HF and PC from nine European countries rated the relevance and wording of 57 items. Agreement was pre-defined as Individual item Content Validity Index (I-CVI) ≥0.80 on a 5-point Likert scale (score ≥4), with items between I-CVI 0.75-0.80 agreement reformulated by the panel and re-assessed in round two. Items with I-CVI<0.75 on relevance were removed.

Round one included 155 participants and round two 121 participants (78.1% retention). Agreement was reached in the first Delphi round on all steps of palliative reasoning (I-CVI range across steps: 0.82-0.95). Across the two Delphi rounds, 25 of the 33 symptoms (76%) achieved agreement on both relevance and formulation (I-CVI range for relevance: 0.81-0.99). Nineteen of the 20 items (95%) addressing wishes and needs reached agreement on both relevance and formulation (I-CVI range for relevance: 0.84-0.97).

This Delphi study established expert agreement on the steps of palliative reasoning and the content of a multidimensional monitoring instrument. These findings provide a shared foundation for earlier, more person-centred and coordinated PC, while allowing national adaptations.

Human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) have revolutionized cardiac research and medicine by offering patient-specific platforms for disease modeling, drug discovery, and regenerative therapies. The ability of iPSC-CMs to replicate key aspects of human cardiac physiology makes them invaluable for studying genetic disorders, evaluating cardiotoxicity, and guiding therapeutic interventions. However, a persistent challenge limiting their clinical and translational utility is their structural and functional immaturity, as iPSC-CMs often retain fetal-like characteristics rather than adult cardiomyocyte properties. This review examines the diverse applications of iPSC-CMs in both preclinical and clinical research, emphasizing their role in modeling inherited cardiac diseases, screening drugs for cardiotoxicity, and advancing personalized medicine. It also explores current maturation strategies including biochemical, biophysical, and bioengineering approaches designed to enhance electrophysiological function, contractile performance, and metabolic maturation. The review further proposes a framework for standardized iPSC-CMs maturity assessment that integrates transcriptomic, structural, electrophysiological, metabolic, and functional parameters against adult cardiomyocyte reference standards. In addition, the review addresses critical considerations such as scalability, standardization, and regulatory frameworks, which are essential for the successful translation of iPSC-CMs from the bench to the bedside. By overcoming these limitations, iPSC-CMs hold the potential to transform cardiovascular research, enabling the development of more effective regenerative therapies and accelerating the progress of precision medicine.

Ginsenosides represent a fascinating class of natural products with diverse biological activities and therapeutic potential. While it is debatable whether modulating energy metabolism is the most prominent function of ginsenosides, it is nevertheless a pivotal function shared by most of these compounds. This review aims to provide an overview of the beneficial effects of ginsenosides on energy metabolism and to elucidate their underlying molecular mechanisms. We tease out the versatile roles of ginsenosides in regulating energy metabolism by integrating evidence from studies on the cardiovascular, hepatic, skeletal muscle, and central nervous systems, as well as systemic metabolic disorders and cancer. A key finding is that ginsenosides not only exert common regulatory effects on mitochondrial energetics, substrate utilization, and oxidative stress, but also tailor their actions to meet the distinct energetic demands and metabolic characteristics of different organs. In addition, most ginsenosides do not specifically target a single organ; instead, they enhance the metabolic adaptability of multiple organs across various pathophysiological conditions, particularly through the restoration of energy homeostasis. This highlights that ginsenosides function not merely as energy boosters, as previously thought, but more likely serve as harmonizers of energy balance. Furthermore, this review illuminates future research directions for ginsenosides, paving the way for advanced applications in disease treatment and health promotion.

Fructose consumption has been associated with cardiometabolic disease, including type 2 diabetes and cardiovascular disease. The formation of the fructose-specific glycation product glucoselysine (GL) may underlie the development of these complications. A previous study showed that endogenously produced fructose contributes to GL formation.

Here, we aimed to investigate the effects of exogenous fructose on the formation of GL. Methods We first developed and validated an ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) stable isotope dilution method for the quantification of total GL in human serum samples. GL levels were subsequently measured in serum samples obtained from: 1) a case-control study, comparing patients with hereditary fructose intolerance (HFI) (n=15) on a fructose restricted diet with age-, sex- and BMI-matched healthy controls; and 2) a double-blind randomized control trial to study effects of dietary fructose restriction in adults with overweight and hepatic steatosis (n=35).

We successfully developed a UPLC-MS/MS method for the detection of total GL in serum, with inter- and intra-assay variability ranging from 1.1% to 6.0%. Serum GL concentrations were significantly lower in HFI patients compared to healthy controls (35.1 compared with 45.8 nmol/L, difference: -11.5; 95%CI: -14.3, -8.8). Similarly, dietary fructose restriction resulted in significantly lower serum GL levels in individuals with overweight and hepatic steatosis (38.8 pre- compared with 31.2 nmol/L post-intervention, change from baseline: -8.0; 95%CI: -12.0, -4.5).

Total serum GL can be analyzed accurately and precisely using UPLC-MS/MS. Our findings from two clinical studies demonstrate that GL formation is significantly influenced by dietary fructose intake. The observation that GL levels were not completely reduced after dietary fructose restriction suggests that additional factors such as an endogenous fructose pool contribute to GL formation. Further research is needed to elucidate the role of GL formation in fructose-induced cardiometabolic complications.

The FRUITLESS study was registered at https://clinicaltrials.gov/study/NCT03067428, identifier: NCT03067428.

Tricuspid valve disease encompasses a spectrum of conditions, among which tricuspid regurgitation is the most prevalent and clinically significant. Affected patients are typically elderly and present with systemic congestion, impaired renal and hepatic function, and reduced quality of life. Echocardiography enables mechanistic classification, severity grading, and assessment of right ventricular function. While medical therapy remains foundational, transcatheter interventions - including edge-to-edge repair and valve replacement - have emerged as options for high-risk patients. Randomized trials demonstrate improvements in symptoms and quality of life, with emerging evidence for reductions in heart failure hospitalizations. This article provides a practice-oriented overview of diagnosis, management, and referral pathways for tricuspid valve disease, including rarer entities such as tricuspid stenosis, endocarditis, and carcinoid heart disease.

Mitral valve disease ranks among the most frequent valvular conditions and carries significant morbidity and mortality if left untreated. This review addresses anatomy, the Carpentier classification, and echocardiographic severity grading, as well as current management of primary and secondary mitral regurgitation (MR) and mitral stenosis. Transcatheter therapies, including edge-to-edge repair and transcatheter mitral valve replacement, receive particular attention and are discussed in the context of four clinical cases from a specialized valve center.

Tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 have transformed chronic myeloid leukemia (CML) into a chronic condition with near-normal life expectancy, but peripheral artery disease (PAD) has emerged as a major source of morbidity, particularly with nilotinib and ponatinib. Current cardiovascular management relies on general population risk scores and ankle-brachial index (ABI) measurement, tools not designed to capture TKI-specific vascular biology or detect subclinical arterial damage.

We appraise cardiovascular risk stratification tools and vascular imaging modalities in the context of TKI-treated CML, and propose an integrated algorithm combining dual risk scoring, ABI, and targeted femoral duplex ultrasound (DUS).

Vascular outcome reporting in TKI trials is hampered by terminological inconsistency: Major Adverse Limb Events (MALE), the standard limb-specific endpoint in contemporary cardiovascular trials, has never been adopted in any TKI/CML publication. Existing risk scores (SCORE2, HFA-ICOS) neither capture TKI-accelerated atherosclerosis nor discriminate limb-specific risk. ABI detects only established stenosis and is further limited by TKI-induced medial arterial calcification. The femoral artery is both the earliest site of subclinical atherosclerosis and the preferential anatomical target of TKI-induced vascular damage; thus, femoral plaque detection may serve as a risk reclassification instrument. Because vascular risk differs by line of therapy and imaging resources are finite, screening should be targeted to patients in whom the result would change agent selection and preventive strategies.

Integrating femoral DUS into cardiovascular risk stratification shifts the objective from diagnosing established disease to preventing it. Whether this translates into fewer events remains to be demonstrated.