暂无摘要。

UNASSIGNED: Heart failure with preserved ejection fraction (HFpEF) often coexists with chronic kidney disease (CKD). Exercise intolerance is a major determinant of quality of life and morbidity in both scenarios. We aimed to evaluate the associations between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and carbohydrate antigen 125 (CA125) with maximal aerobic capacity (peak VO2) in ambulatory HFpEF and whether these associations were influenced by kidney function.
UNASSIGNED: This single-centre study prospectively enrolled 133 patients with HFpEF who performed maximal cardiopulmonary exercise testing. Patients were stratified across estimated glomerular filtration rate (eGFR) categories (<60 ml/min/1.73 m2 versus ≥60 ml/min/1.73 m2).
UNASSIGNED: The mean age of the sample was 73.2 ± 10.5 years and 56.4% were female. The median of peak VO2 was 11.0 ml/kg/min (interquartile range 9.0-13.0). A total of 67 (50.4%) patients had an eGFR <60 ml/min/1.73 m2. Those patients had higher levels of NT-proBNP and lower peak VO2, without differences in CA125. In the whole sample, NT-proBNP and CA125 were inversely correlated with peak VO2 (r = -0.43, P < .001 and r = -0.22, P = .010, respectively). After multivariate analysis, we found a differential association between NT-proBNP and peak VO2 across eGFR strata (P for interaction = .045). In patients with an eGFR ≥60 ml/min/1.73 m2, higher NT-proBNP identified patients with poorer maximal functional capacity. In individuals with eGFR <60 ml/min/1.73 m2, NT-proBNP was not significantly associated with peak VO2 [β = 0.02 (95% confidence interval -0.19-0.23), P = .834]. Higher CA125 was linear and significantly associated with worse functional capacity without evidence of heterogeneity across eGFR strata (P for interaction = .620).
UNASSIGNED: In patients with stable HFpEF, NT-proBNP was not associated with maximal functional capacity when CKD was present. CA125 emerged as a useful biomarker for estimating effort intolerance in HFpEF irrespective of the presence of CKD.

In rats with unilateral nephrectomy and cardiac dysfunction, renal function deteriorates at an accelerated rate, as evidenced by increased proteinuria. Whether myocardial infarct-induced heart failure (HF) exacerbates renal injury in hypertensive rats with mild renal injury has not been reported. Rats underwent either coronary ligation or sham surgery. Thirty spontaneously hypertensive rats (SHRs) aged 8 weeks were randomly divided into two groups. Group 1 was the sham group, in which the rats underwent thoracotomy without ligation of the coronary artery. Group 2 underwent coronary artery ligation. The rats in group 2 underwent coronary artery ligation on week 0. The experiment lasted 12 weeks. Urine was collected in metabolic cages over a 24-h period. Urine was collected from the rats 2 days before the end of the experiment, and the ratio of urinary protein to urinary creatinine was measured in the clinical laboratory. All rats were examined by echocardiogram one day before the end of the experiment. On the last day of the experiment, blood was collected and sent to the laboratory for analysis. Hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining were performed on heart and kidney sections. The ejection fraction in group 2 was lower than that in group 1 (P < 0.001). The urinary albumin to creatinine ratio in group 2 was greater than that in group 1 (P < 0.001). The urea and creatinine levels in group 1 were significantly lower than those in group 2 (P < 0.01). The levels of brain natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C were greater in the second group than in the first group (P < 0.05). The interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels in group 2 were significantly greater than those in group 1 (P < 0.001). The malondialdehyde (MDA) levels in Group 2 were greater than those in Group 1 (P < 0.01). The glutathione peroxidase (GSH-Px) levels in Group 2 were lower than those in Group 1 (P < 0.05). The level of angiotensin II (AT-II) in group 1 was lower than that in group 2 (P < 0.001). Cardiac dysfunction secondary to myocardial infarction could induce cardiorenal interactions in SHRs. It could be interpreted by the activation of oxidative stress, changes in inflammation and alteration of renin-angiotensin-aldosterone system.

While the existence of cardiorenal perturbations has been known for nearly 2 centuries, only in the past 2 decades has significant progress been made in classifying these alterations and characterizing the pathobiology and hemodynamic signature of cardiorenal syndrome (CRS). Empiric intravenous diuretic therapy with fluid and sodium restriction and selective use of vasoactive agents have remained cornerstones of managing acute heart failure with or without acute CRS; however, recent clinical data has exposed the shortcomings of this approach. The traditional view of CRS has long focused on low cardiac output with resultant renal arterial hypoperfusion as the central hemodynamic derangement but this too, has been challenged by new preclinical and clinical observations. Renal venous congestion/hypertension has since been identified as an important hemodynamic contributor to the development of CRS, resulting in diminished renal perfusion pressure, defined as the difference between arterial driving pressure and renal venous pressure. Novel circulatory renal assist devices for the treatment of acute (type I) CRS are in development and may be divided into 2 broad categories: \"pushers\" which aim to improve renal arterial perfusion (renal preload) and \"pullers\" which are designed to reduce renal venous congestion (renal afterload). Numerous devices have shown promise in early-stage clinical studies but none have been approved yet for commercial use in the United States. The value of CRS device therapies will ultimately rest on safety as well as the ability of these devices to effect predictable, meaningful, and durable improvements in renal function along with clinical and hemodynamic markers of congestion.

暂无摘要。

Congestion is the most common manifestation of acute decompensated heart failure (ADHF). Residual congestion despite initial medical therapy is common and is recognized to be associated with worse outcomes; however, there are currently no standardized definition regarding decongestion end point. In the second part of this 2-part review, we provide a critical appraisal of decongestion definitions previously used in ADHF studies, review alternative metrics to define severity of volume overload, and propose a more granular 4-class congestion grading scheme and decongestion end point definitions that could potentially be included in future ADHF trials and consensus definitions.

Despite recent advances in the treatment of patients with chronic heart failure, acute decompensated heart failure remains associated with significant mortality and morbidity because many novel therapies have failed to demonstrate meaningful benefit. Persistent congestion in the setting of escalating diuretic therapy has been repeatedly shown to be a marker of poor prognosis and is currently being targeted by various emerging device-based therapies. Because these therapies inherently carry procedural risk, patient selection is key in the future trial design. However, it remains unclear which patients are at a higher risk of residual congestion or adverse outcomes despite maximally tolerated decongestive therapy. In the first part of this 2-part review, we aimed to outline patient risk factors and summarize current evidence for early recognition of high-risk profile for residual congestion and adverse outcomes. These factors are classified as relating to the following: (1) previous clinical course, (2) severity of congestion, (3) diuretic response, and (4) degree of renal impairment. We also aimed to provide an overview of key inclusion criteria in recent acute decompensated heart failure trials and investigational device studies and propose potential criteria for selection of high-risk patients in future trials.

暂无摘要。

UNASSIGNED: Traditionally, low cardiac output has been considered the primary hemodynamic driver of renal function and injury. Adult data suggest that central venous pressure (CVP) is a more important factor.
UNASSIGNED: The authors hypothesized that in children with cardiovascular disease, higher CVP predicts lower estimated glomerular filtration rate (eGFR) and worsening renal function (WRF).
UNASSIGNED: We performed a single-center cohort study of patients aged 3 months to 21 years with biventricular circulation undergoing cardiac catheterization. Pearson\'s correlation and linear and Cox regression analyses were performed to determine associations with eGFR at the time of catheterization and WFR within 180 days after catheterization.
UNASSIGNED: 312 patients had median age 7.9 years (IQR: 2.3 to 14.5 years), median eGFR 97 mL/min/1.73 m2 (IQR: 81-118 mL/min/1.73 m2), median CVP 7 mm Hg (IQR: 5-9 mm Hg), and median cardiac index 3.7 mL/min/m2 (IQR: 2.9-4.6 mL/min/m2). Nearly half (48%) were transplant recipients. In multivariable analysis, CVP was independently associated with eGFR (β = -2.65; 95% CI: -4.02, -1.28; P < 0.001), as was being a transplant recipient (β = -10.20; 95% CI: -17.74, -2.65; P = 0.008), while cardiac index was not. Fifty-one patients (16%) developed WRF. In a proportional hazards model adjusting for cardiac index, only higher CVP (HR: 1.10; 95% CI: 1.04-1.17; P = 0.002) and greater contrast volume by weight (HR: 1.05; 95% CI: 1.01-1.10; P = 0.021) predicted WRF. CVP ≥7 mm Hg likewise predicted WRF (HR: 2.57; 95% CI: 1.29-5.12; P = 0.007).
UNASSIGNED: Among children with a spectrum of cardiovascular disease, higher CVP is associated with lower eGFR and development of WRF, independent of cardiac index.

The term \"Cardiorenal Syndrome\" (CRS) refers to the complex interplay between heart and kidney dysfunction. First described by Robert Bright in 1836, CRS was brought to its modern view by Ronco et al. in 2008, who defined it as one organ\'s primary dysfunction leading to secondary dysfunction in the other, a view that led to the distinction of five different types depending on the organ of primary dysfunction and the temporal pattern (acute vs. chronic). Their pathophysiology is intricate, involving various hemodynamic, neurohormonal, and inflammatory processes that result in damage to both organs. While traditional biomarkers have been utilized for diagnosing and prognosticating CRS, they are inadequate for the early detection of acute renal damage. Hence, there is a pressing need to discover new biomarkers to enhance clinical outcomes and treatment approaches.