Background: Frailty complicates anticoagulation management in older patients with atrial fibrillation (AF), particularly when long-term vitamin K antagonist (VKA) therapy is already established. Whether switching to a direct oral anticoagulant (DOAC) improves outcomes in this setting remains uncertain, and guideline recommendations are limited. We performed a systematic review and meta-analysis comparing outcomes of VKA-to-DOAC switching versus VKA continuation in frail elderly patients with AF. Methods: MEDLINE, Scopus, and the Cochrane Library were systematically searched from inception through 4 April 2026. Studies enrolling frail elderly patients with AF receiving VKA therapy and directly comparing switching to a DOAC versus continued VKA treatment were eligible. The primary outcome was a composite of stroke/systemic embolism, major bleeding, or all-cause mortality. Adjusted hazard ratios (HRs) were pooled using three-level random-effects models. Results: Four studies (five treatment comparisons) comprising 57,099 patients were included. Overall, switching from VKA to DOAC therapy was not associated with a significant difference in the composite outcome compared with continued VKA treatment (HR 1.18, 95% CI 0.84-1.67). No significant differences were observed for major bleeding (HR 1.13, 95% CI 0.80-1.60), thromboembolism (HR 1.03, 95% CI 0.63-1.68), or all-cause mortality (HR 0.95, 95% CI 0.77-1.16). In analyses restricted to randomized trials, results remained neutral across all outcomes. Conclusion: In frail elderly patients with AF receiving VKA therapy, switching to a DOAC was not associated with significant reductions in thromboembolism, major bleeding, mortality, or the composite outcome compared with continued VKA treatment.

Subvalvular aortic stenosis (SAS) is an important cause of fixed left ventricular outflow tract obstruction and the second most common form of aortic stenosis. Although traditionally considered a congenital lesion, increasing evidence suggests that SAS often behaves as a progressive condition influenced by anatomical and hemodynamic factors. The disease may lead to significant complications, including left ventricular hypertrophy and progressive aortic regurgitation.

A narrative review of the current literature was performed to summarize contemporary knowledge regarding the epidemiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of subvalvular aortic stenosis. Relevant studies were identified through searches of major medical databases and were critically analyzed to provide an overview of current concepts and clinical practice.

Subvalvular aortic stenosis demonstrates considerable anatomical and clinical heterogeneity, ranging from discrete subaortic membranes to fibromuscular tunnel-type obstruction. The condition often progresses over time, with increasing LVOT gradients and a high incidence of associated aortic regurgitation. Echocardiography remains the primary diagnostic modality, while advanced imaging techniques provide additional anatomical detail and assist in surgical planning. Surgical resection remains the cornerstone of treatment when significant obstruction or related complications develop.

Subvalvular aortic stenosis is a complex and progressive disease requiring careful imaging assessment and timely surgical management. Although surgical outcomes are generally excellent, recurrence and progressive aortic valve involvement remain important long-term considerations. Ongoing research aimed at improving risk stratification and optimizing surgical strategies may further enhance patient outcomes.

Cognitive impairment, particularly reduced information processing speed (IPS), is a clinically meaningful manifestation of multiple sclerosis (MS). The Symbol Digit Modalities Test (SDMT) is a sensitive, validated measure of IPS widely used in MS research. While vascular and hemodynamic factors are increasingly recognized as contributors to cognitive performance in MS, their relationship with IPS across distinct physiologic challenges remains unexplored.

This pilot study examined IPS and cardiovascular responses in ten people with MS (PwMS), all of whom had relapsing-remitting MS (RRMS), and ten age- and sex-matched healthy participants during four acute physiologic challenges: head-up tilt, head-down tilt, isometric handgrip, and aerobic cycling.

Beat-to-beat blood pressure and heart rate were continuously recorded; IPS was assessed using the oral SDMT.

Baseline SDMT scores were lower in PwMS than in healthy participants (p < 0.05). A between-group effect was observed for cycling-related SDMT change (r = 0.49, 95% CI 0.05-0.76; p = 0.03). Despite comparable training impulse (TRIMP)-standardized workloads, systolic blood pressure during cycling was higher in PwMS (p < 0.05), and the cycling-related systolic blood pressure response showed a between-group effect of r = 0.46 (95% CI 0.02-0.75; p = 0.04). In healthy participants, baseline SDMT performance was correlated with resting heart rate and blood pressure, and cycling-related SDMT change was inversely correlated with the blood pressure response.

These exploratory findings suggest possible differences in the relationship between cardiovascular measures and IPS during acute physiologic challenges, particularly aerobic exercise. However, the small sample size and wide confidence intervals preclude firm conclusions regarding an exercise-specific effect or differences in cardiovascular-cognitive coupling.

Mitral valve repair failure encompasses heterogeneous anatomical patterns requiring redo surgery, yet the factors determining why repaired valves fail through different mechanisms remain poorly understood. We investigated the association of patient characteristics and index repair features with the anatomical mechanisms of failure among patients requiring redo surgery after degenerative mitral valve repair.

We retrospectively reviewed all consecutive patients undergoing redo mitral valve surgery after previous degenerative mitral valve repair between January 2010 and June 2026. To minimize misclassification bias, only patients with complete operative documentation of the index repair and detailed intraoperative information regarding the mechanism of repair failure were included. Operative reports were reviewed to identify the reconstructive techniques used during the initial repair and the anatomical mechanism of failure at reoperation. To account for mutually exclusive clinical outcomes (prolapse recurrence and mitral stenosis), a competing-risks framework was employed.

A total of 121 patients constituted the study cohort. Recurrent leaflet prolapse was the most frequent mechanism of repair failure (71.6%) among patients with mitral regurgitation; mitral stenosis was present in 27.3% overall. Leaflet preservation versus resection, implantation of expanded polytetrafluoroethylene (ePTFE) neochordae, edge-to-edge repair, and annuloplasty ring size were not significantly associated with the anatomical mechanism of repair failure. In multivariable analysis, older age at the index operation was independently associated with recurrent prolapse, whereas younger age and female sex independently predicted the development of mitral stenosis. Within this redo cohort, no statistically significant association was observed between the recorded index repair features and the predominant anatomical mechanisms of failure after adjustment for patient characteristics.

Among patients requiring redo surgery after degenerative mitral valve repair, the anatomical mechanisms of failure were associated with selected patient characteristics, whereas no significant association was observed with the recorded index repair features. These findings should be interpreted within the context of a selected redo population and do not support conclusions regarding the comparative durability of different repair strategies.

Hypertension remains one of the leading causes of global morbidity and mortality and is the leading modifiable risk factor for cardiovascular disease worldwide. The inability of conventional risk factors alone to fully explain the global prevalence of hypertension, together with accumulating evidence implicating endocrine-disrupting chemicals (EDCs) in the pathogenesis of hypertension, has led to growing scientific interest in this field over recent years. EDCs are exogenous environmental chemicals capable of disrupting hormone synthesis, transport, metabolism, and signaling pathways, thereby adversely affecting vascular and metabolic homeostasis. In particular, per- and polyfluoroalkyl substances (PFASs), bisphenol A, phthalates, PCBs, heavy metals, and pesticides have been associated with hypertension and may influence blood pressure regulation through multiple interconnected mechanisms, including oxidative stress, endothelial dysfunction, inflammation, epigenetic modifications, and activation of the renin-angiotensin-aldosterone system. Moreover, prenatal exposure to EDCs has been associated with hypertensive disorders of pregnancy, including gestational hypertension and preeclampsia, with potential implications for long-term maternal cardiovascular health. This review provides a comprehensive overview of the experimental and epidemiological evidence linking endocrine-disrupting chemicals to hypertension, with particular emphasis on the underlying molecular mechanisms, emerging clinical evidence, and future research directions.

Chronic total coronary occlusion (CTO) occurs within advanced coronary artery disease (CAD), but its association with left ventricular (LV) deformation and pressure-strain-loop-derived myocardial work beyond global LV ejection fraction (LVEF) is uncertain. We performed a retrospective cross-sectional analysis of 148 unique patients with multivessel or left-main CAD, including 70 with and 78 without CTO. Absolute global longitudinal strain (GLS) was the principal endpoint; global work index (GWI), constructive work (GCW), wasted work (GWW), and work efficiency (GWE) were secondary endpoints. Sequential CTO coefficients were estimated using HC3 heteroscedasticity-consistent linear models in a pool of patients with complete global mechanics and LVEF data. A history of myocardial infarction was more frequent with CTO (42.9% vs. 23.1%), with lower LVEF and larger LV volumes. In crude distributional comparisons among 136 patients with global mechanics data, median GLS was 14.0% versus 15.5% (p = 0.021), while median GCW was 1723 versus 1997 mmHg% (p = 0.026). In the multivariable regression analysis, the CTO-minus-non-CTO GLS coefficient was -1.40 percentage points (95% CI, -2.80 to 0.00) unadjusted, -1.10 (95% CI, -2.58 to 0.38) after clinical adjustment, and -0.16 (95% CI, -1.24 to 0.92) after adding LVEF. CTO status marked a modest adverse global LV mechanical phenotype, but clinically adjusted estimates were imprecise and markedly attenuated after accounting for LVEF. Prospective studies integrating ischemia, scar, viability, and longitudinal follow-up are needed.

The detrimental effect of cigarette smoking has become undeniable, based on decades of research. Twenty years ago, the electronic cigarette was introduced to the market and has since then been presented as the alleged healthy alternative. Clever marketing by the industry has led to a global rise in the number of users, especially adolescents and young adults. Clinicians and scholars have praised the electronic cigarette as a tool for tobacco smoke cessation, hoping for a reduction in burden on healthcare systems. Yet accumulating evidence suggests otherwise. Over the years, several in vitro and in vivo studies in animal models and humans have shown electronic cigarettes to be associated with pulmonary, cancerous and cardiovascular diseases. This review revisits the so-far available clinical evidence concerning cardiovascular diseases and discusses research gaps that still need to be addressed, specifically focusing on patients undergoing cardiac surgery.

Hypertension remains the leading modifiable cause of cardiovascular death, yet fewer than one in four treated adults achieves guideline-recommended blood pressure targets. Catheter-based renal denervation interrupts efferent and afferent renal sympathetic signalling and lowers blood pressure continuously and independently of medication adherence. After a decade of controversy following the neutral SYMPLICITY HTN-3 trial, a coherent body of second-generation sham-controlled randomised evidence, generated with radiofrequency, endovascular ultrasound, and perivascular alcohol platforms, has established a reproducible, modest, and durable antihypertensive effect with a favourable safety profile. Between 2024 and 2026, the field crossed three thresholds simultaneously: guideline endorsement on both sides of the Atlantic, including the first United States recommendation in the 2025 AHA/ACC guideline; a national coverage determination with coverage with evidence development; and the maturation of randomised and real-world follow-up to three years in cohorts exceeding 3000 patients. This state-of-the-art review synthesises the contemporary evidence base; quantifies the expected treatment effect and its heterogeneity; appraises safety across renal and vascular domains; examines emerging data in chronic kidney disease, diabetes, heart failure, and atrial fibrillation; and details the practical requirements for delivering renal denervation responsibly. We conclude by defining the research agenda that must now be addressed: the identification of responders, the development of an intraprocedural endpoint, a direct comparison with newly approved pharmacotherapy, and evidence of cardiovascular event reduction.

This study aimed to investigate the predictive value of the multi-parameter combined application of cadmium-zinc-telluride single-photon emission computed tomography (CZT-SPECT) and coronary computed tomography angiography (CCTA) for short-term myocardial ischemic events in patients with chronic coronary syndromes (CCS).

A total of 205 CCS patients who underwent both CZT-SPECT and concurrent CCTA were retrospectively enrolled. A reversible ischemia indicator (summed difference score, SDS) from CZT-SPECT and an inflammatory marker (fat attenuation index, FAI) from CCTA were obtained. Short-term myocardial ischemic major adverse cardiovascular events (MACEs) were recorded. Cox regression assessed independent predictive value, while net reclassification improvement (NRI), integrated discrimination improvement (IDI), and Kaplan-Meier curves evaluated incremental predictive and risk stratification ability.

19 myocardial ischemic MACEs occurred. SDS was an independent predictor (HR: 1.386; 95%CI: 1.032-1.861; p = 0.030). Adding FAI to the combination of clinical factors and SDS significantly improved prediction (NRI = 0.215, p = 0.037; IDI = 0.043, p = 0.017). The high-SDS plus high-FAI group had the highest event rates (20.0%, all p < 0.05).

SDS appears to be an independent predictor of short-term ischemic MACE. FAI may further stratify risk among patients with high SDS, with those exhibiting both high SDS and high FAI having the highest event rates. These findings should be considered hypothesis-generating and warrant confirmation in larger prospective cohorts.

Background: Left ventricular thrombus (LVT) is a serious complication associated with cardiomyopathy and impaired left ventricular (LV) systolic function. Patients with a resolved LVT remain at risk for recurrence and subsequent thromboembolism. However, the factors influencing the recurrence of LVT are not yet fully understood. The aim of this study was to identify the risk factors and clinical outcomes related to LVT recurrence and to improve follow-up strategies and treatment options. Methods and results: We retrospectively investigated patients confirmed to have a resolved LVT by transthoracic echocardiography from January 2018 to April 2021 at Zhongshan Hospital Fudan University. All patients received anticoagulant therapy for more than 6 months and underwent at least two follow-up transthoracic echocardiograms. No statistically significant differences were observed in baseline characteristics between the LVT recurrence and non-recurrence groups, including gender, age, diabetes, hyperlipidemia, renal function, previous stroke history, other underlying medical conditions, ejection fraction, or left ventricular diameter. Patients in the recurrence group exhibited a higher prevalence of previous myocardial infarction and percutaneous coronary intervention compared to the non-recurrence group (84.6% vs. 61.1%, p = 0.03; 76.9% vs. 52.8%, p = 0.03). Additionally, patients in the recurrence group tended to have more ventricular aneurysms (50.0% vs. 22.2%, p = 0.008) and larger previous thrombus sizes (27.7 ± 12.6 vs. 21.4 ± 9.1 mm, p = 0.008) compared to those in the non-recurrence group. Multivariate logistic regression analysis indicated that the longitudinal diameter of the LVT was an independent risk factor for LVT recurrence (OR 1.058, 95% CI 1.003-1.115, p = 0.04). ROC curve analysis revealed an area under the curve of 0.647 for the longitudinal diameter of the LVT, with an optimal cut-off value of 23.5 mm, a sensitivity of 62%, and a specificity of 64%. After a follow-up duration of 3.0 ± 2.5 years, the incidence of non-fatal myocardial infarction and major adverse cardiovascular events (MACEs) in the recurrence group was significantly higher than that in the non-recurrence group [non-fatal myocardial infarction: 3 (11.5%) vs. 1 (1.4%), p = 0.02; MACE: 7 (26.9%) vs. 7 (9.7%), p = 0.01]. No statistically significant differences were found in bleeding events, systemic embolism, or all-cause death between the two groups. Conclusions: Our study indicates that a history of myocardial infarction, the presence of ventricular aneurysm, and a larger thrombus diameter are significant factors influencing LVT recurrence. Furthermore, the longitudinal diameter of the thrombus is identified as an independent risk factor for recurrence following resolution. The threshold for LVT diameter requiring extended anticoagulation and the required duration of anticoagulation need to be confirmed in future studies.