BackgroundOlder adults presenting to emergency departments or acute wards are at increased risk of functional decline, delirium, falls, prolonged hospital stay, and early mortality. Early recognition of vulnerability is crucial for timely preventive interventions, yet specific geriatric assessment is often not performed at admission due to time limitations.AimTo provide a clinically focused synthesis of short geriatric screening tools and present a practical two-step model linking early screening with targeted clinical action.MethodsThis narrative review summarizes brief screening instruments that can be completed within minutes and are suitable for routine use. A targeted literature review identified tools used and evaluated available evidence on predictive accuracy, feasibility, and clinical integration.ResultsRapid tools such as ISAR, TRST, PRISMA-7, and APOP allow early identification of patients at risk of functional decline, readmission, or short-term mortality. Multidomain instruments, including HARP, SHERPA, and ISAR-HP, provide broader prognostic information, supporting discharge planning and targeted follow-up. Predictive accuracy is generally moderate, with the area under the curve (AUC) typically between 0.60 and 0.70. Clinical impact depends on embedding screening into routine workflows and linking results to actionable interventions such as early mobilization, cognitive assessment, medication review, or referral to geriatric specialists. Clinical integration seems to require a tiered, two-step approach: rapid screening upon admission, followed by a comprehensive multidomain assessment on the ward.ConclusionShort geriatric screening tools are essential in acute care. A two-step approach appears to be a practical and clinically reasonable strategy for optimizing early detection and linking screening to targeted interventions. However, further research is needed to validate its effectiveness and define the optimal implementation strategy.

Anti-amyloid therapy (AAT) with monoclonal antibodies (mAbs) modestly slow cognitive and functional decline in early Alzheimer's disease (AD). However, both the magnitude of clinical benefit and the risk of treatment-related complications vary substantially even among patients with similar biomarker profiles. Frailty, both brain and systemic, is highly prevalent in older adults with AD and affects a large proportion of those considered for AAT. Despite this, it has been largely absent from current decision frameworks. Brain frailty, defined by structural and microvascular damage (e.g., small-vessel disease, microbleeds, and atrophy), limits the clinical benefit of amyloid clearance and increases susceptibility to amyloid-related imaging abnormalities. In contrast, systemic frailty, reflecting reduced physiological reserve, mainly affects treatment tolerance and recovery from adverse events. In this narrative, conceptual review, we synthesize evidence that both forms of frailty act as biologically grounded modifiers of AAT efficacy and safety and may limit the clinical benefit while increasing susceptibility to complications and decompensation. Importantly, the precise empirical thresholds at which frailty begins to exert harmful effects remain unknown. We further outline how MRI-based markers of brain frailty, combined with brief systemic frailty measures, could support risk stratification, patient selection, monitoring intensity, and shared decision-making, including deferring treatment when the benefit-risk balance is unfavorable, while avoiding exclusion of patients who may still benefit. Taken together, we propose that future studies should incorporate frailty measures and perform precise assessments of both brain and systemic frailty, as this may improve patient stratification and better characterize the effects of AAT.

The use of intravenous thrombolysis (IVT) in acute ischemic stroke (AIS) patients with recent direct oral anticoagulant (DOAC) intake remains one of the most debated issues in contemporary stroke medicine. Current international guidelines generally discourage IVT within 48 h of DOAC ingestion, largely because of concerns regarding symptomatic intracranial hemorrhage (sICH) and the absence of randomized evidence. However, an increasing body of evidence from international registries and multicenter cohorts has not identified a clear increase in sICH among carefully selected patients with recent DOAC exposure who received IVT. Some observational studies have also reported an association with more favorable functional outcomes than those observed in otherwise eligible patients in whom reperfusion therapy was withheld, although these comparisons are susceptible to selection bias and confounding by indication. In this Perspective, we discuss recent advances that have challenged the traditional practice of broadly excluding patients with recent DOAC exposure from IVT. We review observational evidence concerning IVT in selected patients, examine biological hypotheses that could be relevant to the observed clinical findings, and discuss evolving roles of reversal agents and laboratory assessment of anticoagulant activity. We further highlight current implementation barriers and future research priorities, including prospective studies, improved point-of-care anticoagulant testing, and refinement of patient-selection strategies. We argue that contemporary evidence supports reconsideration of rigid time-based exclusion criteria in favor of more individualized, evidence-informed decision-making. Although important uncertainties remain, recent DOAC exposure may not necessarily preclude IVT in appropriately selected patients, particularly when anticoagulant activity can be reliably assessed.

[This corrects the article DOI: 10.3389/fmed.2026.1815638.].

Introduction:The 2019 ESC/EAS guidelines introduced stricter low-density lipoprotein cholesterol (LDL-C) targets, particularly for patients at high and very high cardiovascular (CV) risk. However, data on the implementation of these targets in real-world clinical practice-especially in countries with high/very high CV risk-remain limited. The DISCOVERY study aimed to assess LDL-C management, lipid-lowering therapy (LLT) use, and guideline adherence across multiple countries in Central and Eastern Europe and Central Asia. Methods:This prospective, observational, multicenter study enrolled adult patients with hypercholesterolemia (HCL) from 10 countries grouped into three regions. Data was collected at baseline and after 12 weeks of follow-up. LLT patterns, LDL-C levels, target attainment (both investigator-defined and 2019 ESC/EAS-recommended), and physician adherence to guidelines were analyzed. Results:A total of 6,447 patients were included; 53.2% were female, and the mean age was 60.5 ± 11.9 years. Most patients (66%) were in secondary prevention. At baseline, 36.8% had been treated with LLT. After the first visit, treatment was changed in 78% of patients, but only 42.4% received high-intensity statins and 9.3% received statin-ezetimibe combinations at follow-up. LDL-C target achievement was poor: only 5.6% of patients met the guideline-recommended LDL-C goals, compared to 45.5% who met physician-defined targets. Among patients with ASCVD, only 3.3% achieved guideline LDL-C targets. The most significant gap was observed between guideline recommendations and physician-set LDL-C goals. No significant difference in LDL-C target attainment was observed between specialists and general practitioners. Discussion:The DISCOVERY study reveals suboptimal LDL-C control and low adherence to the 2019 ESC/EAS guidelines in routine practice across countries with high/very high CV risk. These findings highlight the urgent need for strategies to improve physician awareness, promote intensive LLT use, and close the gap between guidelines and clinical practice. A paradigm shift toward proactive LDL-C management is essential to reduce residual CV risk in these populations.

INTRODUCTION:People on a ketogenic diet may develop an increase in low-density lipoprotein cholesterol (LDL-C), known as the lean mass hyper-responder (LMHR) phenotype. However, this increase does not necessarily correspond to a heightened cardiovascular (CV) risk, and optimal treatment strategies for high-risk individuals within this group remain uncertain. CASE PRESENTATION:A 61-year-old man with type 1 diabetes developed the LMHR phenotype after adopting a ketogenic diet. An atherosclerotic plaque was discovered in the bulb of his left common carotid artery, reclassifying him into the secondary prevention category of CV disease. After the introduction of rosuvastatin 20 mg daily, his LDL-C subfraction profile changed from a more atherogenic type B phenotype to a less atherogenic type A phenotype without significantly decreasing overall LDL-C levels. This suggests that rosuvastatin provided a beneficial effect, complementing the metabolic improvements associated with the ketogenic diet, including better blood glucose and insulin control, potential prior reductions in small dense LDL-C and triglycerides, and an increase in high-density lipoprotein cholesterol (HDL-C).In this case, no trend toward a lower threshold was observed for the development of diabetic ketoacidosis. CONCLUSION:Assessing LDL-C subfractions before and after the initiation of lipid-lowering therapy is essential in individuals who develop the lean mass hyper-responder (LMHR) phenotype, particularly in the presence of confirmed atherosclerosis. Given the markedly elevated LDL-C levels often observed in this population, it may be difficult to accurately evaluate the burden of atherogenic cholesterol and the extent of its reduction without subfraction analysis. In such cases, statin therapy appears to be a reasonable and potentially beneficial intervention, even among LMHR individuals.

Background/Objectives: People with type 1 diabetes have an unmet need for cardiovascular protection due to the lack of new recommended antidiabetic therapies with cardiovascular benefits. We examined whether the addition of an empagliflozin/metformin combination, and each drug alone, can complement insulin to improve glucometabolic parameters in overweight people with type 1 diabetes at high cardiovascular risk. Methods: This pilot, single-center double-blind randomized controlled trial included 40 people with type 1 diabetes. In addition to insulin, they received empagliflozin (25 mg daily), metformin (2000 mg daily), an empagliflozin/metformin combination, or a placebo. The intervention period was 12 weeks. Glycemic parameters, insulin requirements, and blood and urine samples were analyzed. Indices for liver fibrosis were calculated. Due to potential safety concerns, participants regularly measured blood ketone values. Results: The empagliflozin/metformin combination decreased HbA1c (−0.6%, p < 0.05) and weight (−6.1 kg, p < 0.05). Empagliflozin decreased the urinary albumin-to-creatinine ratio (−31.4 ± 4.9%, p = 0.002). The empagliflozin/metformin combination and empagliflozin decreased the estimated daily proteinuria (−34.6 ± 5.0%, p = 0.006 and −35.9 ± 6.2%, p = 0.03, respectively), the calculated FIB-4 (up to −17.8 ± 5.2%, p = 0.04 and −10.7 ± 3.7%, p = 0.02, respectively), and other liver fibrosis indices and uric acid values. No significant side effects occurred during the study. Conclusions: The empagliflozin/metformin combination improved glycemic control, reduced weight and insulin requirements, and produced several additional beneficial metabolic effects in overweight people with type 1 diabetes with increased cardiovascular risk.

Andexanet alfa is a specific reversal agent for factor Xa inhibitors with immediate reversal of their anticoagulant effect. Andexanet alfa is currently approved for use in patients treated with rivaroxaban and apixaban who have life-threatening or uncontrolled bleeding. New data from both controlled clinical trials and real-world experience are continuously being published, providing greater insight into the clinical characteristics of the drug, such as efficacy and safety. It is worth considering that andexanet alfa could be of benefit in a variety of different clinical scenarios where patients receiving treatment with apixaban and rivaroxaban (and endoxaban) have life-threatening conditions. These different clinical scenarios, which range from pre-treatment of urgent surgery, especially neurosurgical interventions, and concomitant use of andexanet alfa and prothrombin complex concentrate to onset of bleeding more than 6 h prior to admission, should be clarified as well as the issue of "low/high" dose of andexanet alfa and the need for baseline anti-Xa inhibitor levels measured by point-of-care testing. Finally, management of patients at high risk of thrombosis or recent arterial/venous thrombotic events needs to be further explored. In this current opinion, we address these urgent questions in the light of recent literature and clinical trial data.

Idarucizumab is an antibody fragment specific for the immediate reversal of dabigatran anticoagulation effects. The use of idarucizumab is approved for dabigatran-treated patients suffering from life-threatening or uncontrolled bleeding and those in need of urgent surgery or invasive procedures. Data from randomized controlled clinical trials and real-world experience provide reassuring evidence about the efficacy and safety of idarucizmab use in patients with acute stroke. In this narrative review, we summarize the available real-world evidence and discuss the relevance and importance of idarucizumab treatment in acute stroke patients in everyday clinical practice. In addition, we also discuss special issues like prothrombin complex concentrate application as an alternative to idarucizumab, its application before endovascular therapy, sensitivity of thrombi to lysis, and necessary laboratory examinations.

Objective: The 2023 ESH guidelines strongly emphasize the lack of data on women, both in randomized clinical trials and in real-world data. It is not known whether the considerable efforts to equalize the treatment of women and men have led to changes in routine practice, which was the main aim of our study. Design and method: The DISCOVERY study is a large real-world prospective observational study investigating the treatment of patients with hypertension and/or hypercholesterolemia in primary or secondary care in 10 countries in 2021 and 2022. Patients of both sexes over 18 years were included. Investigators (301 GPs, 127 internists, 271 cardiologists) treated the patients according to their usual routine. They collected data on admission and up to 12 weeks after admission so that treatment characteristics could be analyzed. The physicians were not informed about the aim (comparison of women vs. men) of the study to avoid information bias. Results: The study included 11,287 patients, 93.6% of whom had hypertension at baseline that was either newly diagnosed (N=2247) or previously treated (N=8280; 86.6% inadequately treated). Patients were recruited in consecutive order. Slightly more women (53.2%, mean age 62.2±11.3 years, 94% with hypertension) than men (46.8%, mean age 58.6±12.3 years, 93.2% with hypertension) were included. There were no significant differences in mean blood pressure (women 156/92mmHg, men 157/93mmHg) and in antihypertensive treatment (mainly monotherapy). There were several gender-specific differences such as age, body mass index, physical activity, smoking status and comorbidities that did not affect the results. At the second observation, blood pressure had decreased significantly (p<0.001) and consistently. Mean pressure in women was 130/80mmHg and in men 131/81mmHg. The blood pressure target < 140/90mmHg was achieved by 73.2% of women and 72.1% of men. The prescribed antihypertensive medications did not differ between women and men, being mainly single-pill combinations (71.6% for women, 71.5% for men). Conclusions: The study showed no differences in the treatment of hypertension between women and men under real-world conditions. The effectiveness was quite good, mainly achieved by single-pill combinations, although the treatment can still be improved.

Hypothyroidism and hyperthyroidism, both overt and subclinical, are associated with increased risk of cardiovascular morbidity and mortality. The association between thyroid-stimulating hormone levels and cardiovascular risk has been demonstrated in large epidemiological studies and meta-analyses and is now considered a U-shaped curve. Several pathophysiological mechanisms linking thyroid and cardiovascular disease are known; however, specific clinical complications of peripheral arterial disease as endpoints of clinical trials have not been adequately investigated. The potential mechanisms linking hypothyroidism and peripheral arterial disease are endothelial dysfunction, blood pressure changes, dyslipidemia, and low-grade systemic inflammation. The potential mechanisms linking hyperthyroidism and peripheral arterial disease are hyperdynamic circulation, elevated systolic blood pressure, hypercoagulability, and possibly increased arterial inflammation.