Explore the vast range of titles available.

Aims: To establish a nomogram-scoring model for evaluating the risk of death in patients with critical cardiovascular disease after continuous renal replacement therapy (CRRT) in a coronary care unit (CCU). Methods: This retrospective cohort study included data collected on 172 patients, in whom CRRT was initiated in the CCU between January 2017 and June 2021. Predictors of mortality were selected using an adaptive least absolute shrinkage and selection operator logistic model and used to construct a nomogram. The nomogram was evaluated using the concordance index (C-index) and Hosmer–Lemeshow test. Results: The number of patients who died in-hospital after CRRT was 91 (52.9%). The results of the multivariate logistic regression analyses clarified that age, history of hypertension and/or coronary artery bypass grafting, a diagnosis of unstable angina pectoris or acute myocardial infarction, ejection fraction, systolic blood pressure, creatinine, neutrophil, and platelet counts before CRRT initiation were significant predictors of early mortality in patients treated with CRRT. The nomogram constructed on these predictors demonstrated significant discriminative power with an unadjusted C-index of 0.902 (95% CI: 0.858–0.945) and a bootstrap-corrected C-index of 0.875. Visual inspection showed a good agreement between actual and predicted probabilities (Hosmer–Lemeshow χ2 = 5.032, p-value = 0.754). Conclusions: Our nomogram based on nine readily available predictors is a reliable and convenient tool for identifying critical patients undergoing CRRT at risk of mortality in the CCU.

Soluble urokinase plasminogen activation receptor (suPAR) is an emerging new biomarker, which has been shown to not only correlate with traditional biomarkers but also outperform CRP at prognosticating CVD. More clinical trials on suPAR is in the future research agenda.

Ectopia cordis (EC) is a rare congenital condition characterized by a partial or complete defect of the anterior chest wall. It is associated with ventricular and atrial septal defects (ASD), Ebstein's anomaly, truncus arteriosus, transposition of the great vessels, tetralogy of Fallot, and hypoplastic left heart syndrome. This study aimed to explore the cardiac manifestations of EC complicated by coronavirus disease 2019 (COVID‐19). A 23‐year‐old male, born with EC, was admitted to the hospital for acute cough and fever. The patient was diagnosed with EC and ASD by computed tomography and COVID‐19 via a polymerase chain reaction swab test. Patients with ECs rarely survive till adulthood. However, due to the rarity of this syndrome, upon literature review, we did not find a case of EC with concurrent COVID‐19 infection. The patient underwent the required investigations and conventional treatment such as fluid resuscitation, antibiotics administration, and full code cardiopulmonary resuscitation. The interventions performed were unsuccessful, and the patient died. This case demonstrates a patient who lived with EC and its associated cardiac anomalies but died of COVID‐19 and its complications despite full resuscitation attempts. Our findings suggest that patients with EC may survive to adulthood if they have an incomplete EC, fewer intracardiac defects except for ASD, and an absence of an omphalocele. Ectopia cordis (EC) is a rare anomaly of unknown etiology rarely surviving to adulthood. We described EC who died of COVID‐19 and its complications despite full resuscitation. Patients with EC may survive to adulthood if they have an incomplete EC, fewer intracardiac, and an absence of an omphalocele.

In this randomized, placebo-controlled trial involving patients with giant-cell arteritis, the oral Janus kinase inhibitor upadacitinib (15 mg) significantly improved remission of disease, with less glucocorticoid use.

Prior studies have demonstrated that the cardiac intensive care unit (CICU) patient population has evolved over time. We sought to describe the temporal changes in comorbidities, illness severity, diagnoses, procedures and adjusted mortality within our CICU practice in recent years. We retrospectively reviewed unique CICU admissions at the Mayo Clinic from January 2007 to April 2018. Comorbidities, severity of illness scores, discharge diagnosis codes and CICU procedures and therapies were recorded, and temporal trends were assessed using linear regression and Cochran-Armitage trend tests. Trends in adjusted hospital mortality over time were assessed using multivariable logistic regression. We included 12,418 patients with a mean age of 67.6 years (including 37.7% females). Temporal trends in the prevalence of several comorbidities and discharge diagnoses were observed, reflecting an increase in the prevalence of non-coronary cardiovascular diseases, critical care diagnoses, and organ failure (all P ≪ .05). The use of several CICU therapies and procedures increased over time, including mechanical ventilation, invasive lines and vasoactive drugs (all P ≪ .05). A temporal decrease in adjusted hospital mortality was observed among the subgroup of patients with (adjusted OR per year 0.97, 95% CI 0.94–0.99, P = .023) and without (adjusted OR per year 0.91, 95% CI 0.85–0.96, P = .002) a critical care discharge diagnosis. We observed an increasing prevalence of critical care and organ failure diagnoses as well as increased utilization of critical care therapies in this CICU cohort, associated with a decrease in risk-adjusted hospital mortality over time.

Chronic obstructive pulmonary disease (COPD) represents a major health and economic challenge in Belgium, affecting approximately 800,000 individuals, half of whom remain undiagnosed. Beyond respiratory morbidity, COPD patients face substantial cardiopulmonary (CP) risk-encompassing severe exacerbations and cardiovascular (CV) events-that is often under-recognized and insufficiently addressed due to limited clinical awareness, fragmented care, and the absence of national guidance. A multidisciplinary Belgian taskforce (general practitioners, pulmonologists, cardiologists, pharmacists, epidemiologists) convened through structured workshops and iterative consensus-building to develop a pragmatic, evidence-informed care pathway. The recommendations focus on COPD patients with at least one moderate or severe exacerbation, who are at heightened CP risk. This consensus introduces an integrated, stepwise framework that positions CP risk as a central component of COPD management after exacerbation and operationalizes it across primary care, hospitalization, and post-exacerbation follow-up. Core elements include systematic and proactive CP risk identification in primary care, standardized diagnostic workups during hospitalization, and multidisciplinary discharge planning. Pharmacological strategies combine eosinophil-guided inhaler therapy with guideline-directed CV treatment, while non-pharmacological measures reinforce smoking cessation, vaccination, physical activity, and pulmonary rehabilitation. Clear referral thresholds between primary care, pulmonology, and cardiology are defined, supported by patient education and digital monitoring tools. This Belgian consensus complements international guidelines by consolidating fragmented recommendations into coherent, actionable algorithms that bridge gaps in routine practice. Its contribution lies in translating emerging evidence into structured, real-world pathways that integrate respiratory and cardiac care. Adoption of this framework may help reduce exacerbations, improve CV outcomes, and support multidisciplinary COPD care in Belgium.

Purpose of ReviewCoronavirus disease 2019 (COVID-19) has been the cause of significant global morbidity and mortality. Here, we review the literature to date of the short-term and long-term consequences of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection on the heart.Recent FindingsEarly case reports described a spectrum of cardiovascular manifestations of COVID-19, including myocarditis, stress cardiomyopathy, myocardial infarction, and arrhythmia. However, in most cases, myocardial injury in COVID-19 appears to be predominantly mediated by the severity of critical illness rather than direct injury to myocardium from viral particles. While cardiac magnetic resonance imaging remains a powerful tool for diagnosing acute myocarditis, it should be used judiciously in light of low baseline prevalence of myocarditis. Guiding an athletic patient through return to play (RTP) after COVID-19 infection is a challenging process. More recent data show RTP has been a safe endeavor using a screening protocol. “Long COVID” or post-acute sequelae of SARS-CoV-2 infection has also been described. The reported symptoms span a large breadth of cardiopulmonary and neurologic complaints including fatigue, palpitations, chest pain, breathlessness, brain fog, and dysautonomia including postural tachycardia syndrome (POTS). Management of POTS/dysautonomia primarily centers on education, exercise, and salt and fluid repletion.SummaryOur understanding of the impact of COVID-19 on the cardiovascular system is constantly evolving. As we enter a new age of survivorship, additional research is needed to catalogue the burden of persistent cardiopulmonary symptoms. Research is also needed to learn how acute management may alter the likelihood and prevalence of this chronic syndrome.

Many patients with chronic obstructive pulmonary disease (COPD) have an accelerated loss of lung function. It is unclear whether drug treatment can modify this in patients with moderately severe disease. In a prespecified analysis of the key secondary outcome in SUMMIT (Study to Understand Mortality and Morbidity), we investigated whether the inhaled corticosteroid fluticasone furoate (FF; 100 μg), the long-acting β-agonist vilanterol (VI; 25 μg), or their combination (FF/VI) modified the rate of decline in FEV compared with placebo. We also investigated how baseline covariates affected this decline. Spirometry was measured every 12 weeks in this event-driven, randomized, placebo-controlled trial of 16,485 patients with moderate COPD and heightened cardiovascular risk. An average of seven spirometric assessments per subject among the 15,457 patients with at least one on-treatment measurement were used in the analysis of rate of FEV decline. All statistical comparisons are considered nominal. The adjusted rates of FEV decline were -46 ml/yr (-3.0% of baseline) with placebo, -47 ml/yr (-3.1%) with VI, -38 ml/yr (-2.5%) with FF, and -38 ml/yr (-2.3%) with FF/VI. FF-containing regimens had lower rates of decline than placebo (P < 0.03), and FF/VI had a lower rate of decline than VI alone (P < 0.005). The FEV decline was faster in current smokers, those with a lower body mass index, males, and patients with established cardiovascular disease. In patients with moderate COPD and heightened cardiovascular risk, FF alone or in combination with VI appears to reduce the rate of FEV decline. Clinical trial registered with www.clinicaltrials.gov (NCT01313676).

Background Stress hyperglycemia ratio (SHR) has emerged as a potential prognostic marker in critical illness, but its association with mortality in cardiovascular disease remains incompletely characterized. This study investigated the relationship between SHR and all-cause mortality in critically ill patients with cardiovascular disease, adjusting for a variety of confounding factors using propensity score matching (PSM). Methods A cohort of 3,352 critically ill patients with cardiovascular disease was stratified by SHR quartiles (Q1–Q4). Baseline characteristics, comorbidities (e.g., heart failure, diabetes), and severity scores (OASIS, APSIII, SOFA) were extracted from a large database containing de-identified health data patients admitted to the intensive care units (ICUs) of Beth Israel Deaconess Medical Center. PSM (670 matched pairs) balanced covariates between high (SHR > 1.355) and low SHR groups. The associations between SHR and mortality risk (in-hospital, 28-day, 90-day, 365-day) were evaluated using Cox models, restricted cubic spline (RCS) analysis, and Kaplan-Meier survival curves. Cox proportional hazards models were implemented with three sequential adjustment levels: Model 1 (unadjusted); Model 2 (adjusted for demographic factors and comorbidities); and Model 3 (fully adjusted). Predictive performance of SHR combined with severity scores was assessed via area under the curve (AUC) improvement. Results Higher SHR quartiles exhibited greater comorbidity burden (e.g., acute kidney injury: 84.6% in Q4 vs. 79.7% in Q1, P  < 0.001) and severity scores ( P  < 0.001). Unadjusted analysis showed a significant association between SHR and mortality, with Q4 having the highest in-hospital (Q4: 16.3% vs. Q1–Q3: 5.1–6.4%, P  < 0.001) and 365-day mortality (Q4: 29.2% vs. Q1–Q3: 15.7–16.9%, P  < 0.001). The RCS analysis revealed a U-shaped mortality risk, with average optimal SHR cutoffs of 1.355. After PSM, cox proportional hazard models confirmed that high SHR (Q4) remained associated with early mortality (in-hospital HR = 2.117, [95% CI: 1.223–3.665], P  = 0.007; 28-day HR = 1.859, [95% CI: 1.100-3.141], P  = 0.020) but not long-term outcomes (90-day mortality, P  = 0.127; 365-day mortality, P  = 0.123) in the Model 1. Similar trends were obtained after adjusting for demographic factors and comorbidities (Model 2) and in the fully adjusted model (Model 3). Adding SHR improved short-term mortality prediction performance (e.g., OASIS AUC: +0.034 for in-hospital, P  < 0.001), though benefits diminished post-PSM (e.g., OASIS: +0.012 for in-hospital, P  = 0.009). However, incorporating SHR did not enhance the predictive performance of OASIS and SAPSII for 90-day and 365-day mortality prediction after PSM. Conclusion Elevated SHR contributes to early mortality in patients with cardiovascular disease, even after rigorous confounder adjustment. The incremental predictive value of SHR support its utility for risk stratification, particularly for short-term outcomes, but its prognostic value fades for long-term mortalities. These findings highlight SHR as a favorable biomarker for clinical decision-making in acute cardiovascular care. Graphical abstract

Stress-induced hyperglycemia (SIH) is a physiological response to acute or chronic stress characterized by elevated blood glucose levels. It is prevalent in both patients with and without diabetes, particularly those with acute or critical illnesses. The development of SIH is characterized by complex interactions among catecholamines, cortisol, and inflammatory mediators such as cytokines, resulting in increased hepatic glucose production and insulin resistance. While mild to moderate SIH may provide a protective mechanism during stress, prolonged or excessive hyperglycemia can exacerbate inflammation and oxidative stress, contributing to adverse outcomes in conditions such as acute myocardial infarction, heart failure, and cerebrovascular diseases. The stress-hyperglycemia ratio (SHR), defined as the ratio of admission glucose to estimated mean glucose (derived from glycated hemoglobin [HbA1c]), has emerged as a valuable tool for quantifying stress hyperglycemia. Unlike absolute glucose levels, the SHR accounts for background hyperglycemia and provides a more accurate indicator of the relative glucose elevation associated with critical illness. Extensive research has demonstrated a U-shaped or J-shaped relationship of the SHR with disease outcomes, indicating that both low and high SHRs are associated with increased mortality and morbidity. The SHR has shown significant predictive value in cardiovascular diseases (e.g., acute coronary syndrome, heart failure), cerebrovascular diseases (e.g., acute ischemic stroke, intracerebral hemorrhage), and infectious diseases (e.g., sepsis, pneumonia). It also plays a role in other conditions, such as acute pancreatitis and certain cancers. The ease of calculating the SHR from widely available admission glucose and HbA1c tests makes it a practical and valuable prognostic marker in clinical settings. This review examines the relationship between the SHR and critical illnesses, highlighting its mechanisms and predictive value across various diseases. Graphical abstract Predictive value of SHR in cardiovascular, cerebrovascular, infectious, and other diseases.