Iron deficiency is a common and clinically relevant comorbidity in heart failure, associated with reduced functional capacity, higher symptom burden, and increased hospitalisation risk. Most evidence on iron deficiency in heart failure originates from hospital-based cohorts, whereas the epidemiology and clinical implications in primary care populations remain poorly described. This study aimed to determine the prevalence of iron deficiency among primary care patients with heart failure in southern Sweden and to examine its association with symptom severity.

This cross-sectional analysis used baseline data from the Heart Failure in Southern Sweden study, a prospective intervention project conducted at 20 primary health care centres. Adult patients with heart failure across all left ventricular ejection fraction categories were included. Iron deficiency was defined as transferrin saturation < 20%.

In total, 466 primary care patients with heart failure were included, of whom 124 (26.7%) had iron deficiency. Symptom severity was higher in patients with iron deficiency: 35.5% were classified as New York Heart Association (NYHA) class III-IV, compared with 18.7% among patients without iron deficiency. Similar findings were observed in the subgroup with left ventricular ejection fraction below 50%, where 25.2% had iron deficiency and 42.6% were classified as NYHA III-IV compared with 18.4% among patients without iron deficiency. In multivariable analysis adjusting for clinically relevant covariates, iron deficiency remained associated with NYHA class III-IV (OR 1.97, 95% CI 1.18-3.31, p = 0.010).

Iron deficiency is common among patients with heart failure managed in primary care and remained associated with higher symptom burden after adjustment for prespecified covariates. These findings highlight the potential clinical relevance of assessment of iron status in primary care.

ClinicalTrials.gov, NCT04129658. Registered on 15 October 2019.

Hemodynamic management after out-of-hospital cardiac arrest (OHCA) is critical, yet the impact of vasopressor-driven mean arterial pressure (MAP) targets on pulmonary circulation and right ventricular (RV) function remains unclear.

In this substudy of the randomized, double-blinded BOX trial, comatose OHCA survivors were allocated to low (63 mmHg) or high (77 mmHg) MAP targets. Pulmonary artery catheters (PAC) were used for serial hemodynamic assessment for 48 h after Intensive Care Unit admission. The primary endpoint was calculated pulmonary vascular resistance (PVR), secondary endpoints included pulmonary capillary wedge pressure (PCWP), pulmonary artery pulsatility index (PAPi), and RV cardiac power output (RV-CPO)-a measurement of RV pumping function.

Among 730 included patients (median time randomization to PAC insertion 1.3 h), mPAP was consistently higher in the high-MAP group (mean difference 1.11-1.71 mmHg, 95% CI range 0.12-2.59). Calculated PVR was transiently lower in the high-MAP group during the first 24 h (mean difference -0.16 to -0.30, 95% CI range -0.31 to 0.11), before converging between groups. RV-CPO was lower in the low-MAP group throughout the observation period (mean difference 0.01-0.04 W [95% range 0.00-0.07], with the largest difference at 48 h. PCWP decreased in both groups but was significantly lower in the low-MAP group during the first 12 h (mean difference 1.06-1.40 mmHg, 95% CI range 0.25-2.38).

In comatose OHCA survivors, targeting a higher MAP increased pulmonary artery pressures, PCWP, RV-CPO, heart rate, and cardiac output. The proportionally greater increase in cardiac output over pulmonary artery pressures resulted in a decreased calculated PVR.

ClinicalTrials.gov identifier: NCT03141099.

In this secondary analysis of a subgroup in the BOX out of hospital cardiac arrest treatment trial for oxygen level targets, blood pressure treatment target levels, higher or lower were analyzed, including central circulatory outcomes, using a pulmonary artery catheter. The higher blood pressure target group had accompanying higher pulmonary artery pressures and cardiac output, with initially a small reduction in calculated pulmonary vascular resistance.

BackgroundPostoperative bleeding in patients with intracranial aneurysms remains a serious complication associated with high mortality. The platelet-to-albumin ratio, reflecting thrombotic potential and endothelial health, has demonstrated prognostic value in various clinical settings. However, its association with postoperative bleeding following endovascular treatment of intracranial aneurysms has not yet been investigated.MethodsThis retrospective cohort study (January 2021 to January 2025) included 219 participants undergoing endovascular treatment. Multivariable logistic regression, smooth curve fitting, and piecewise linear regression were used to assess the association between the platelet-to-albumin ratio and bleeding risk, adjusting for potential confounders. Predictive performance was evaluated using receiver operating characteristic curves and decision curve analysis.ResultsBleeding occurred in 58 participants (26.5%). A significant nonlinear inverse L-shaped relationship was observed between the platelet-to-albumin ratio and bleeding risk (nonlinearity p = 0.010), with an inflection point at the platelet-to-albumin ratio of 5.05. Below this threshold, a higher ratio was associated with reduced risk (odds ratio: 0.607, 95% confidence interval: 0.445-0.829, p = 0.0017); whereas above this value, the association was neutral. The incidence of bleeding decreased significantly across increasing platelet-to-albumin ratio quartiles (Q1: 45.5% vs. Q4: 14.3%, p < 0.001). Multivariable analysis confirmed platelet-to-albumin ratio as an independent predictor (continuous: odds ratio: 0.73, 95% confidence interval: 0.59-0.90, p = 0.004; Q4 vs. Q1: odds ratio: 0.05, 95% confidence interval: 0.01-0.21, p < 0.001). The platelet-to-albumin ratio demonstrated superior discriminative capacity (area under the curve, 0.670) compared with platelet count (area under the curve, 0.624) or albumin alone (area under the curve, 0.607). Decision curve analysis confirmed clinical application.ConclusionThe platelet-to-albumin ratio independently predicts postoperative bleeding with a nonlinear relationship. It should be considered an adjunctive marker within a multimodal framework to help balance bleeding and ischemic risks.

Post-cardiac arrest (CA) prognostication primarily focuses on predicting poor outcome, whereas early markers of good prognosis remain less explored. We aimed to identify early predictors of favorable outcome at 3 months in comatose CA survivors.

We prospectively enrolled adult patients with post-anoxic coma admitted to the Intensive Care Unit of a secondary-care hospital (2020-2025). Demographic, CA-related, clinical, electroencephalographic (EEG), neuron-specific enolase (NSE) and neuroimaging data were collected. Good outcome was defined as Cerebral Performance Category (CPC) 1-2 at 3 months. Logistic regression analyses identified independent predictors of good outcome. Model performance was internally validated with bootstrap resampling.

Among 121 included patients (median age = 66; 72% male), outcome was available for 118, of whom 42.3% achieved good outcome. Patients with CPC 1-2 were younger, had predominant shockable initial rhythms and cardiac etiology of CA, higher Glasgow Coma Scale scores, lower NSE levels, and decreasing NSE trend. Peak NSE ≤ 36 ng/mL was the optimal cut-off for favorable prognosis. Early benign EEG (continuous/nearly continuous background with preserved reactivity ≤72 h) was associated with neurological recovery. In multivariable analysis, independent predictors of favorable outcome were younger age (OR 0.92, 95% CI 0.86-0.99), shockable initial rhythm (OR 28.0, 95% CI 3.87-202.1), early benign EEG (OR 10.76, 95% CI 1.95-59.4) and peak NSE ≤ 36 ng/mL (OR 43.17, 95% CI 6.01-309.9). The model showed excellent discrimination (apparent AUC 0.97, optimism-corrected AUC 0.96).

In comatose post-CA patients, a model combining age, initial rhythm, early benign EEG and peak NSE independently predicted good outcome at 3 months.

Ambient air pollution is a leading modifiable environmental determinant of cardiovascular morbidity and mortality worldwide. Long-term and short-term exposure to fine particulate matter and traffic-related pollutants is consistently associated with an increased risk of ischemic heart disease, stroke, heart failure, arrhythmia and cardiovascular death. Mechanistic studies demonstrate that inhaled pollutants induce pulmonary and systemic oxidative stress, inflammation, endothelial dysfunction, autonomic imbalance and prothrombotic changes, providing biological plausibility for these associations. Air pollution rarely acts in isolation but clusters with other environmental stressors, such as transportation noise, heat and limited access to green space and disproportionately affects socioeconomically disadvantaged and medically vulnerable groups. This review summarizes the current evidence on the cardiovascular effects of air pollution, highlights high-risk populations and discusses clinical, public health and policy strategies to reduce exposure and vulnerability. We argue that contemporary cardiovascular prevention must adopt an exposome-oriented perspective and engage with transport, energy, housing and urban planning policies to effectively protect vulnerable patients and communities.

Impairments in peripheral glucose metabolism and reduced brain insulin sensitivity are linked to an increased risk of both metabolic and neurodegenerative diseases. Brain insulin resistance represents a shared pathological mechanism underlying these disorders. Notably, hippocampal insulin responsiveness declines with age and differs between men and women. This study aimed to identify clinically relevant metabolic predictors of hippocampal insulin sensitivity in the context of age and sex.

In 260 non-diabetic participants (165 women, mean BMI 29.7 ± 6.2 kg/m², mean age 44.2 ± 16.6 years), functional MRI was performed before and after intranasal insulin administration to assess hippocampal insulin response. Metabolic phenotyping comprised laboratory assessments including oral glucose tolerance tests, whole-body MRI and ¹H-MRS. In addition, participants were assigned to high- and low-risk prediabetes clusters using the Tübingen risk cluster tool. Prediabetes was defined as impaired fasting glucose and/or impaired glucose tolerance and/or elevated HbA₁c. We used linear regression models to select the most relevant predictors, including interactions with sex and age.

Fasting plasma glucose levels predicted lower hippocampal insulin response with age independently of sex (estimate 0.533, p=0.016). Significant interactions were present between age, sex and body fat distribution (waist-to-hip ratio [WHR]: estimate 0.233, p=0.010; visceral adipose tissue [VAT]: estimate 0.007, p=0.013; intrahepatic lipid content [IHL]: estimate 0.003, p=0.010). In women, higher WHR, VAT and IHL were predictors of lower hippocampal insulin responsiveness with increasing age. These effects remained significant after adjusting for BMI. Postmenopausal women showed lower hippocampal insulin responsiveness with higher WHR and IHL (p<0.05), and women in high-risk Tübingen prediabetes clusters also showed lower hippocampal insulin responsiveness than men (sex × cluster type: estimate 0.39, p=0.02). The hippocampal insulin response did not correlate with hippocampal volume (p>0.05).

Unhealthy body fat distribution was a sex-dependent predictor for decreased hippocampal insulin sensitivity with increasing age. Older women with high abdominal fat and/or those assigned to high-risk clusters were most vulnerable to impaired insulin responsiveness in the hippocampus. These findings may contribute to explaining sex differences in the development of type 2 diabetes and neurodegenerative diseases.

Durable left ventricular assist devices (LVADs) have transformed the management of advanced heart failure, but early post-operative management remains a time of heightened vulnerability with disproportionate impact on short-term and long-term outcomes. This article provides a practical, physiology-driven framework for intensive care unit (ICU) management following LVAD implantation, emphasizing early hemostasis and anticoagulation strategies, systematic hemodynamic assessment, and optimization of right ventricular function. Additional sections address respiratory management, dysrhythmia control, nutrition, and early mobilization as essential components of recovery. By synthesizing contemporary evidence with bedside decision-making, this guide aims to support multidisciplinary ICU teams in standardizing care.

Right ventricular (RV) failure is a clinically distinct entity with significant prognostic implications across multiple cardiovascular conditions. Its diagnosis is challenging due to overlapping features with left ventricular failure, often leading to delayed recognition. This article reviews the unique pathophysiology, clinical presentation, and diagnostic strategies for RV failure, emphasizing hemodynamic assessment. A structured approach to medical management is presented, focusing on optimization of preload, afterload, contractility, and rhythm control. Disease-specific considerations and timely escalation to mechanical circulatory support are discussed to improve outcomes in patients with RV-related cardiogenic shock.

Studies have examined the association between excess body weight and risk of cardiovascular (CV) outcomes in the general population. However, the impact of the follow-up period of excess body weight on the association between excess weight and CV outcomes is less investigated. We sought to investigate this using the UK Biobank data.

Population-based prospective cohort study.

The UK.

Adults aged between 40 and 69 years were recruited between 2006 and 2010. The study included 469 162 participants; the median (IQR) age was 57 (50-63) years, and 56.3% of the participants were female.

Body mass index, age, gender, ethnicity, education, smoking status (never, previous and current), alcohol status (never, previous and current), systolic blood pressure, sleep duration, walking pace, overall health rating (excellent, good, fair and poor), dietary patterns (such as red and processed meat consumption, and intake of fish, fruit, poultry and vegetables) and self-reported medical history (such as diabetes, chest pain/discomfort and falls).

CV outcomes, including CV events such as cerebrovascular disease, ischaemic heart disease, heart failure and CV death.

Of the 469 162 participants without CV disease at baseline, 56.3% were female. The mean age was 57 (SD: 9.6) years. During the median follow-up of 13.7 (IQR: 12.9-14.4) years, 27 305 participants developed a CV outcome, including 6698 who had a CV death. Overall, the strength of association between obesity and CV outcomes increased gradually as the follow-up period increased compared with normal weight. A significant association between obesity and the first CV event was observed after 4 years follow-up period (HR (95% CI) 1.14 (1.02 to 1.26)). The association of obesity with CV death was found after 10 years of follow-up, and there was an increasing strength of the association between 10 years (1.11 (1.01 to 1.22)) and 15 years (1.21 (1.13 to 1.29)) follow-up periods. No association was found between being overweight and CV death at any follow-up. Both overweight and obesity in men were associated with CV death observed before 8 years, while obese women were found to be associated with CV events and CV death after 8 years follow-up period.

This large observation study shows that obesity could lead to CV death as early as 10 years follow-up period, while individuals who were obese were more likely to have their first CV event after 4 years follow-up. No association between being overweight and CV death was observed in any follow-up time. Further studies are needed to evaluate the impact of the follow-up period on associations between overweight/obesity and CV outcomes. Screening or early intervention for obesity can be highly valuable for preventing and managing CV outcomes in a primary care setting.

Evidence on how different antithrombotic therapies influence microsurgical evacuation efficacy in spontaneous intracerebral hemorrhage (ICH) is limited. Antithrombotic agents may increase hematoma volume and impact postoperative outcomes, complicating surgical management. As growing evidence supports surgical ICH evacuation, understanding the role of antithrombotics and emergency reversal strategies is critical. The aim of this study was a comparative overview on how common types of antithrombotic therapy influence radiographic and clinical outcomes in surgically treated ICH.

In this retrospective study, we included consecutive patients who underwent microsurgical hematoma evacuation for supratentorial ICH between 2008 and 2022. Patient characteristics, antithrombotic therapy, reversal strategies, neuroimaging, and 12-month functional outcome (modified Rankin Scale) were reviewed. Preoperative antiplatelet therapy (APT), vitamin K antagonists, direct oral anticoagulants, and combined antiplatelet/anticoagulant therapy (Comb) was compared with no antithrombotic medication. Multivariable regression models were used to analyze the association between antithrombotic therapy, radiographic, and clinical outcomes.

Overall, we included 232 patients with supratentorial ICH (APT: 53, vitamin K antagonists: 29, direct oral anticoagulant: 13, Comb: 17). Patients with any type of antithrombotic therapy presented with larger absolute preoperative hematoma volumes than patients without prior antithrombotic medication. Combined antiplatelet/anticoagulant therapy affected preoperative ICH volume to the greatest extent (volume difference: 14.9 mL; 95% CI: 0.9, 29.0). APT was associated with a 1.4-fold increase in relative postoperative ICH volume (95% CI: 0.9, 2.1), while combined therapy was associated with a 2.1-fold increase (95% CI: 1.1, 4.0). Unfavorable outcome (modified Rankin Scale ≥4) affected 73.5% of patients and was linked to larger preoperative hematomas (63 mL vs 49 mL) and higher relative postoperative hematoma volume (13.7% vs 7.5%).

Despite preoperative emergency reversal, antithrombotics contributed to higher hematoma volumes, poorer microsurgical evacuation efficacy and worse functional outcome. Particularly for patients receiving APT, the findings underline the importance of optimizing antithrombotic reversal strategies.