Cardiorenal Medicine最新文献

Background: Accumulating evidence has challenged the traditional model of the liver-kidney connection in hepatorenal syndrome. Cirrhosis can significantly impact cardiac function, leading to cirrhotic cardiomyopathy. Recent understanding reveals how cardiac dysfunction plays a pivotal role in the development of renal dysfunction in this setting, suggesting that disturbances traditionally categorized under hepatorenal syndrome may actually represent a hepatic form of cardiorenal syndrome - hepatocardiorenal syndrome - where the liver affects the kidney through cardiorenal pathways.

Summary: Effective management of hepatocardiorenal syndrome and acute kidney injury in cirrhosis relies on accurately assessing a patient's hemodynamic and volume status. Point-of-care ultrasound, including lung and focused cardiac ultrasound, is a valuable diagnostic tool that provides crucial data on fluid tolerance, subclinical pulmonary congestion, and left ventricular filling pressures. This objective, bedside approach offers a comprehensive assessment that directly influences patient management and therapeutic decisions.

Key messages: Point-of-care ultrasound plays an essential role in evaluating and managing hepatocardiorenal syndrome, providing insights into the underlying pathophysiology. By assessing hemodynamic parameters, it helps guide therapy and monitor patient responses, ensuring more accurate and effective treatment of patients with cirrhosis and acute kidney injury.

Introduction: The objective of this study was to evaluate the effects of renal denervation (RDN) on cardiac remodeling, cardiac function, and cardiovascular (CV) neurohormones in heart failure patients with reduced ejection fraction (HFrEF).

Methods: We searched PubMed, Embase, Web of Science, and China National Knowledge Infrastructure (CNKI), identifying 6 randomized controlled trials (RCTs) and 9 single-arm studies, totaling 352 participants. Meta-analyses for RCTs and single-arm studies were conducted using STATA 17 software and the metafor package in R, respectively.

Results: In RCTs, RDN significantly reduced left ventricular end-diastolic diameter (LVEDD) (weighted mean difference [WMD] = -3.55 mm, 95% CI [-5.51, -1.59], p < 0.01), left ventricular end-systolic diameter (LVESD) (WMD = -4.13 mm, 95% CI [-6.08, -2.18], p < 0.01), and significantly increased left ventricular ejection fraction (LVEF) (WMD = 6.30%, 95% CI [4.64, 7.96], p < 0.01) and 6-min walk test (6MWT) distance (WMD = 51.25 m, 95% CI [8.30, 94.20], p < 0.05). Brain natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were significantly reduced (standardized mean difference = -1.24, 95% CI [-1.57, -0.90], p < 0.01). In single-arm studies, RDN significantly reduced LVEDD (MC = -2.41 mm, 95% CI [-3.74, -1.09], p < 0.01), LVESD (MC = -1.72 mm, 95% CI [-2.77, -0.67], p < 0.01), left atrial diameter (MC = -1.62 mm, 95% CI [-3.16, -0.08], p < 0.01), and interventricular septal thickness (IVST) (MC = -0.76 mm, 95% CI [-1.05, -0.47], p < 0.01). RDN significantly increased LVEF (MC = 29.52%, 95% CI [12.74, 46.31], p < 0.01) and 6MWT distance (MC = 100.49 m, 95% CI [49.12, 151.86], p < 0.05). RDN significantly reduced BNP or NT-proBNP levels (SMC = -0.57, 95% CI [-0.83, -0.31], p < 0.01). Our study also found that RDN had varying degrees of reduction on renin, angiotensin II, aldosterone, and norepinephrine in HFrEF patients. Additionally, we found that RDN had no significant effect on SBP/DBP in HFrEF patients but reduced heart rate (WMD = -7.22 bpm, 95% CI [-9.84, -4.60], p < 0.01).

Conclusion: Our meta-analysis demonstrates that RDN can improve cardiac remodeling, enhance cardiac function, reduce CV neurohormones and has no significant effect on blood pressure in patients with HFrEF.

Introduction: Approximately 70% of patients with heart failure (HF) also have kidney disease. Mortality is increased both by cardiorenal syndrome (CRS) and by the exacerbation of other comorbidities. The purpose of this study is to evaluate the clinical performance of patients with CRS who are followed up by the Cardiorenal Unit (CRU).

Methods: We conducted a retrospective observational study of patients referred to the CRU from April 1, 2022, to April 30, 2023. Demographics, laboratory and ultrasonographic tests, and outcomes were evaluated.

Results: Fifty-four patients were seen in the CRU. A total of 45 (83%) and 16 (30%) patients completed follow-up in the CRU at 6 and 12 months, respectively. The mean age was 70 years ± 1.6, and 65% were men. Almost 50% of patients had ischemic heart disease-related HF. The mean cardiac ejection fraction (EF) was 40% ± 1.6, and 61% of patients had HF with reduced EF (HFrEF). NYHA functional classes II and III were the most frequent (60% and 35%, respectively). At 6 months after follow-up, treatment was optimized with sacubitril-valsartan in 33% vs. 49% (p = 0.02) and SGLT2 inhibitors in 48% vs. 72% (p = 0.008), without significant deterioration in renal function (creatinine: p = 0.61; eGFR: p = 0.19). There was also a reduction of more than 50% in the number of hospital admissions (p = 0.002). A total of 22% required peritoneal dialysis, and 20% required hemodialysis. Ten (19%) patients died, five of them due to cardiovascular (CV) events.

Conclusions: The CRU is vital for the management of complex patients as it ensures the implementation of medications that reduce CV mortality and decrease the number of hospital admissions in HF.

Background: Acute Kidney Injury (AKI) is a common and critical condition associated with significant morbidity and mortality across various patient populations. The recovery process following AKI is complex and involves a multitude of biological, clinical, and environmental factors. Despite considerable research, there remains substantial debate regarding the exact role and significance of these factors, as well as how they interact with one another.

Summary: This systematic review aims to examine the currently available evidence on the key factors influencing AKI recovery. We hope to offer a clearer understanding of the complex dynamics in AKI recovery, including where current evidence remains inconclusive or contradictory.

Key messages: This review will provide valuable insights for clinicians and researchers aiming to improve treatment strategies and patient outcomes in AKI recovery.

Background: Pulse pressure (PP), the difference between systolic (SBP) and diastolic blood pressure (DBP), is an essential marker of cardiovascular (CV) health and arterial stiffness. Elevated PP is linked to a higher risk of CV events, a major cause of global mortality. This study examines its association with key electrolytes - sodium, potassium, calcium, magnesium, phosphate, and vitamin D - in blood-pressure regulation and vascular function.

Methods: We analysed data from 3,316 LURIC participants who underwent coronary angiography and had a median follow-up of 9.9 years. Fasting blood samples were collected at baseline. Associations between PP and electrolyte levels were assessed using Spearman correlation. Logistic regression models were used to calculate odds ratios (ORs) per standard deviation (SD) of PP and electrolyte concentrations for four clinical outcomes: all-cause mortality, CV mortality, reduced estimate the glomerular filtration rate (eGFR), and type 2 diabetes mellitus.

Results: The cohort's average age was 62.7 years, with 70% of participants being male. Higher PP was significantly associated with older age, increased body mass index, and the prevalence of coronary artery disease (CAD), carotid stenosis, and peripheral arterial disease. Potassium, phosphate, renin, 25-OH, and 1,25-OH vitamin D concentrations decreased significantly as PP increased, while sodium remained unchanged. Sodium-potassium ratio and aldosterone-renin ratio increased with higher PP. Women had a higher risk of CV mortality per SD of PP (OR 1.57; 95% confidence interval [CI]: 1.33-1.86), while men showed a greater risk of reduced eGFR (OR 1.59; 95% CI: 1.40-1.80).

Conclusion: Specific electrolyte imbalances are closely linked to increased PP and arterial stiffness. Our findings highlight sex-specific CV risk and support further research into nutrient-based and hormonal interventions targeting PP modulation.

Introduction: The effects of glucagon-like peptide 1 receptor agonists (GLP-1 RA) in patients with diabetes and established chronic kidney disease (CKD) remain unclear.

Methods: We systematically searched PubMed, Embase, and Cochrane Library from inception to May 2024 for randomized controlled trials (RCTs) and respective post hoc studies comparing GLP-1 RAs versus placebo in patients with type 2 diabetes mellitus (T2DM) and established CKD (as per study definition or otherwise defined as having an estimated glomerular filtration rate less than 60 mL/min/1.73 m2 and/or urine albumin-to-creatinine ratio more than 30 mg/g). We applied a random-effects model to pool risk ratios (RRs), hazard ratios (HRs), and 95% confidence intervals (CIs).

Results: We included 10 RCTs and post hoc analyses comprising 18,042 patients, of whom 9,164 (50.8%) were treated with GLP-1 RAs. There were significantly lower rates of major adverse kidney events (RR 0.82; 95% CI: 0.74-0.90; p < 0.001; high certainty) and a slightly lower incidence of all-cause mortality (HR 0.84; 95% CI: 0.71-1.00; p = 0.046; moderate certainty) with the use of GLP-1 RAs relative to placebo. This kidney protection remained consistent in patients with stage 3b CKD (RR 0.78; 95% CI: 0.65-0.94; p = 0.009; high certainty). No significant differences were observed in major adverse cardiovascular events (HR 0.89; 95% CI: 0.78-1.02; p = 0.090; low certainty) or cardiovascular mortality (HR 0.80; 95% CI: 0.60-1.09; p = 0.155; very low certainty), possibly due to a lack of statistical power.

Conclusion: GLP-1 RAs were tied to a lower incidence of all-cause mortality and major adverse kidney events in patients with T2DM and established CKD.

Introduction: The objective of this research was to explore the possible link between markers of liver fibrosis and survival rates in a group of adults who have been diagnosed with both chronic kidney disease (CKD) and coronary artery disease (CAD).

Methods: The National Health and Nutrition Examination Survey (NHANES) data (1999-2018) for participants with both CAD and CKD were analyzed. The fibrosis-4 index (FIB-4), Nonalcoholic Fatty Liver Score (NFS), Forns index, and aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio were identified as crucial biomarkers. All-cause and cardiovascular disease (CVD) mortality were primary outcomes, assessed using Cox models, Kaplan-Meier curves, and receiver operating characteristic (ROC) analysis.

Results: A total of 1,192 CKD and CAD patients were included. The Cox regression analysis revealed substantial correlations between elevated FIB-4, NFS, Forns index, and AST/ALT levels and a heightened risk of all-cause (hazard ratio [HR]: 1.188, 95% confidence interval [CI]: 1.108-1.274; HR: 1.145, 95% CI: 1.069-1.227; HR: 1.142, 95% CI: 1.081-1.201; HR: 1.316, 95% CI: 1.056-1.639, respectively) and CVD mortality (HR: 1.133, 95% CI: 1.007-1.275; HR: 1.155, 95% CI: 1.024-1.303; HR: 1.208, 95% CI: 1.109-1.316 and HR: 1.636, 95% CI: 1.203-2.224, respectively). The ROC analysis indicated comparable predictive accuracy for all three biomarkers, with AST/ALT showing slightly superior performance.

Conclusion: Liver fibrosis markers, including AST/ALT, NFS, Forns index and FIB-4, are significant mortality predictors in CAD-CKD patients. The AST/ALT ratio, being easily measurable, may serve as an effective predictive tool for risk stratification in this population.

Background: The American Heart Association has recently updated the Cardiovascular-Kidney-Metabolic (CKM) Health Advisory, proposing a new framework for defining, staging, and predicting CKM risk. However, the prevalence and adverse effects of the CKM stages remain insufficiently characterized.

Methods: We analyzed data from the National Health and Nutrition Examination Survey (NHANES) (1999-2018), including 18,350 US adults aged 20-79 years. CKM syndrome encompasses subclinical or clinical cardiovascular disease (CVD), chronic kidney disease (CKD), and metabolic risk factors. The participants were categorized into 4 CKM stages based on their clinical severity. We assessed associations of CKM stages with mortality risk and life expectancy.

Results: Only 12.9% of participants were classified as having CKM stage 0. The prevalence of CKM stages 1, 2, 3, and 4 was 23.1%, 53.6%, 3.6%, and 6.7%, respectively. Compared with CKM stage 0, individuals in stage 4 had a markedly higher risk of all-cause mortality (HR: 4.30, 95% CI: 2.95-6.26) and lost 15.5 (12.5-19.8) years of life at age 50 years. Sex and racial/ethnic disparities were also observed.

Conclusions: A higher CKM stage was strongly associated with increased mortality and reduced life expectancy. Our findings underscore the urgent need for enhanced CKM health management, social support, and policy intervention.