Explore the vast range of titles available.

Abstract Aims Chronic kidney disease (CKD) increases the risk of morbidity and mortality in patients with heart failure (HF). Guidelines recommend assessing CKD using the urinary albumin-to-creatinine ratio (UACR), as albuminuria is strongly associated with the risk of incident HF and outcomes in chronic HF; however, its prognostic role in acute HF (AHF) remains unclear. We evaluated if albuminuria was associated with adverse outcomes in individuals hospitalized with AHF in Renal Optimization Strategies Evaluation-Acute Heart Failure (ROSE-AHF). Methods There were 339 participants with baseline UACR, 248 with UACR at Day 7 and 237 with both measurements for assessing change in UACR. Associations of baseline, Day 7 and change in UACR with all-cause mortality at 6 months and the composite of first HF hospitalization or cardiovascular mortality at 2 months were assessed with Cox proportional hazards models. We assessed for effect modification by treatment arm and diabetes status. Results The mean age was 70 years, 73.2% were male, 55.8% had diabetes mellitus, the mean estimated glomerular filtration rate was 45 mL/min/1.73 m2 and mean UACR was 208 mg/g. There were 65 deaths and 82 HF hospitalizations or cardiovascular deaths. Baseline UACR was not associated with either outcome; however, there was a significant interaction by diabetes status for all-cause mortality (P = 0.022) such that baseline UACR was associated with the risk of death in non-diabetics [hazard ratio (HR) 2.58, 95% CI 1.00, 6.66, P = 0.050 third tertile versus first tertile], but not diabetics. Neither Day 7 UACR nor the change in UACR were associated with outcomes. Conclusions Albuminuria is largely not associated with the risk of death, cardiovascular death, or HF hospitalization in AHF, except admission UACR is associated with the risk of death in non-diabetics.

•Prompt initiation of diuretic therapy was not correlated with faster decongestion in acute heart failure.•The timing of decongestion but not diuretics was associated with better biomarker trajectories.•Residual congestion rather than the timing of decongestion or diuretics predicted prognosis. Prompt treatment may mitigate the adverse effects of congestion in the early phase of heart failure (HF) hospitalization, which may lead to improved outcomes. We analyzed 814 acute HF patients for the relationships between time to first intravenous loop diuretics, changes in biomarkers of congestion and multiorgan dysfunction, and 1-year composite end point of death or HF hospitalization. B-type natriuretic peptide (BNP), high sensitivity cardiac troponin I (hscTnI), urine and serum neutrophil gelatinase–associated lipocalin, and galectin 3 were measured at hospital admission, hospital day 1, 2, 3 and discharge. Time to diuretics was not correlated with the timing of decongestion defined as BNP decrease ≥ 30% compared with admission. Earlier BNP decreases but not time to diuretics were associated with earlier and greater decreases in hscTnI and urine neutrophil gelatinase–associated lipocalin, and lower incidence of the composite end point. After adjustment for confounders, only no BNP decrease at discharge was significantly associated with mortality but not the composite end point (p = 0.006 and p = 0.062, respectively). In conclusion, earlier time to decongestion but not the time to diuretics was associated with better biomarker trajectories. Residual congestion at discharge rather than the timing of decongestion predicted a worse prognosis.

Aims Kidney function changes dynamically during AHF treatment, but risk factors for and consequences of worsening renal function (WRF) at hospital admission are uncertain. We aimed to determine the significance of WRF at admission for acute heart failure (AHF). Methods and results We evaluated a subgroup of 406 patients from The Acute Kidney Injury Neutrophil gelatinase–associated lipocalin Evaluation of Symptomatic heart failure Study (AKINESIS) who had serum creatinine measurements available within 3 months before and at the time of admission. Admission WRF was primarily defined as a 0.3 mg/dL or 50% creatinine increase from preadmission. Alternative definitions evaluated were a ≥0.5 mg/dL creatinine increase, ≥25% glomerular filtration rate decrease, and an overall change in creatinine. Predictors of admission WRF were evaluated. Outcomes evaluated were length of hospitalization, a composite of adverse in‐hospital events, and the composite of death or HF readmission at 30, 90, and 365 days. Biomarkers' prognostic ability for these outcomes were evaluated in patients with admission WRF. One‐hundred six patients (26%) had admission WRF. These patients had features of more severe AHF with lower blood pressure, higher BUN, and lower serum sodium concentrations at admission. Higher BNP (odds ratio [OR] per doubling 1.16–1.28, 95% confidence interval [CI] 1.00–1.55) and lower diastolic blood pressure (OR 0.97–0.98, 95% CI 0.96–0.99) were associated with a higher odds for the three definitions of admission WRF. The primary WRF definition was not associated with a longer hospitalization, but alternative WRF definitions were (1.3 to 1.6 days longer, 95% CI 1.0–2.2). WRF across definitions was not associated with a higher odds of adverse in‐hospital events or a higher risk of death or HF readmission. In the subset of patients with WRF, biomarkers were not prognostic for any outcome. Conclusions Admission WRF is common in AHF patients and is associated with an increased length of hospitalization, but not adverse in‐hospital events, death, or HF readmission. Among those with admission WRF, biomarkers did not risk stratify for adverse events.

Measurement of cardiac biomarkers has become routine for the care of patients with heart failure (HF). While troponin and natriuretic peptides are well-entrenched in the guidelines, soluble ST2 (sST2) is a novel biomarker that has shown consistent performance and is ready for clinical use. Multiple studies support the use of sST2 in both acute and chronic HF for prognostication. We suggest a novel scheme to guide HF management based on ambulatory sST2 levels.

Markers of glomerular disease, estimated glomerular filtration rate (eGFR) and albuminuria, are associated with cardiac structural abnormalities and incident cardiovascular disease (CVD). We aimed to determine whether biomarkers of kidney tubule injury, function, and systemic inflammation are associated with cardiac structural abnormalities. Among 393 Multi-Ethnic Study of Atherosclerosis participants without diabetes, CVD, or chronic kidney disease, we assessed the association of 12 biomarkers of kidney tubule injury, function, and systemic inflammation with the left ventricular mass/volume ratio (LVmvr) and left ventricular ejection fraction (LVEF) on cardiac magnetic resonance imaging using linear regression. The average age was 60 ± 10 years; 48% were men; mean eGFR was 96±16 ml/min/1.73 m2; mean LVmvr was 0.93±0.18 g/ml, and mean LVEF was 62±6%. Each twofold greater concentration of plasma soluble urokinase plasminogen activator receptor was associated with a 0.04 g/ml (95% confidence interval [CI] 0.01 to 0.08 g/ml) higher LVmvr and 2.1% (95% CI 0.6 to 3.5%) lower LVEF, independent of risk factors for CVD, eGFR, and albuminuria. Each twofold greater plasma monocyte chemoattractant protein 1 was associated with higher LVmvr with a similar coefficient to that of plasma soluble urokinase plasminogen activator receptor. Each twofold greater concentration of plasma chitinase-3-like protein 1 and urine alpha-1-microglobulin was associated with a 1.1% (95% CI 0.4 to 1.7%) and 1.2% (95% CI 0.2 to 2.2%) lower LVEF, respectively. In conclusion, abnormal kidney tubule health may lead to cardiac dysfunction above and beyond eGFR and albuminuria.

Hemoconcentration during the treatment of acute decompensated heart failure is a surrogate for plasma volume reduction and is associated with improved survival, but most definitions only allow for hemoconcentration to be determined retrospectively. An increase in serum creatinine can also be a marker of aggressive decongestion, but in isolation is not specific. Our objective was to determine if combined hemoconcentration and worsening creatinine could better identify patients that were aggressively treated and, as such, may have improved postdischarge outcomes. A total of 4,181 patients hospitalized with acute decompensated heart failure were evaluated. Those who experienced both hemoconcentration and worsening creatinine at any point had a profile consistent with aggressive in-hospital treatment and longer length of stay (p <0.01), higher loop diuretic doses (p <0.001), greater weight (p = 0.001), and net fluid loss (p <0.001) compared with the remainder of the cohort. In isolation, neither worsening creatinine (p = 0.11) nor hemoconcentration (p = 0.36) at any time were associated with improved survival. However, patients who experienced both (21%) had significantly better survival (hazard ratio 0.80, 95% confidence interval 0.69 to 0.94, pinteraction = 0.005). In conclusion, this combination of hemoconcentration and worsening creatinine, which can be determined prospectively during patient care, was associated with in-hospital parameters consistent with aggressive diuresis and improved postdischarge survival.

Abstract Introduction Greater sodium avidity in acute heart failure (AHF) is associated with worse outcomes, but whether kidney tubule injury is associated with sodium avidity and impaired diuretic responsiveness remains underexplored. Methods We evaluated 339 participants from the ROSE-AHF trial, which enrolled patients hospitalized for AHF with kidney dysfunction and randomized them to the dopamine, nesiritide, or placebo group. Urinary kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and neutrophil gelatinase-associated lipocalin (NGAL) were measured at enrolment. Associations between these biomarkers and urinary sodium (uNa) concentration at baseline, fractional excretion of sodium (FeNa), as well as total uNa output and urine output over 72-h were assessed using multivariable regression models. Results Higher KIM-1 and NAG values at baseline were associated with lower uNa concentration at baseline [−6.1% (−8.5%, −3.7%), P < 0.001 and −5.9% (−9.2%, −2.6%), P & .001, respectively, per two-fold increase in each biomarker]. Higher baseline KIM-1 and NAG were also associated with lower FeNa [−6.1% (−8.5%, −3.6%), P < .001 and −5.2% (−8.6%, −3.6%), P = 0 .001, respectively, per two-fold increase in each biomarker]. Higher baseline KIM-1 was associated with lower total uNa excretion over 72-h [−3.6% (−6.8%, −0.2%), P = 0.037 per two-fold increase]. None of the biomarkers were associated with urine output over 72-h. Conclusion Kidney tubular injury, as assessed by urine KIM-1 and NAG, is associated with greater sodium avidity and higher KIM-1 is associated with impaired diuretic responsiveness in AHF. Graphical Abstract Graphical Abstract Associations between urinary kidney tubular injury biomarkers and measures of diuretic responsiveness and renal sodium avidity (spot urine sodium, spot fractional excretion of sodium, total urine sodium, and 72-h urine output) were assessed in ROSE-AHF. Higher levels of KIM-1 and NAG were associated with reduced urinary sodium excretion, whereas NGAL was not associated with any sodium measures. None of the biomarkers were associated with urine output. FeNa, fractional excretion of sodium; KIM-1, kidney injury molecule-1; NAG, N-acetyl-β-D-glucosaminidase; NGAL, neutrophil gelatinase-associated lipocalin; ROSE-AHF, Renal Optimization Strategies Evaluation Acute Heart Failure; uNa, urine sodium. For image description, please refer to the figure legend and surrounding text.

Cardiovascular disease is a leading cause of death. Proneurotensin is a biomarker associated with the development of cardiovascular disease, cardiovascular mortality, and all-cause mortality. We assessed the association of fasting proneurotensin with mortal events by gender and race (black–white) in a US population. Using a case-cohort subpopulation of the Reasons for Geographic and Racial Differences in Stroke study, fasting proneurotensin was measured on a 1,046-person subcohort and in 651 participants with incident coronary heart disease. Higher proneurotensin was associated with all-cause mortality (hazard ratio [HR] 1.6 per interquartile range, 95% confidence interval [CI] 1.3 to 1.9) and cardiovascular mortality (HR 1.8, 95% CI 1.2 to 2.6). For all-cause and cardiovascular mortality, association was stronger in women (HR 1.9, 95% CI 1.4 to 2.6 and HR 2.5, 95% CI 1.4 to 4.7, respectively) than men (HR 1.4, 95% CI 1.0 to 1.8 and HR 1.4, 95% CI 0.9 to 2.3, respectively), although this difference was not significant. Proneurotensin predicted all-cause mortality in both races and was not predictive of cardiovascular mortality in whites but was in blacks. Proneurotensin was not associated with incident coronary heart disease events. Elevated proneurotensin levels predicted all-cause and cardiovascular mortality in both genders, with a trend toward stronger association in women. Associations were similar in blacks and whites. In conclusion, proneurotensin may be a useful biomarker for all-cause and cardiovascular mortality regardless of race, and it is potentially specific in women.

Purpose of Review To discuss the current status of the stethoscope as a vector for infection and possible interventions to promote stethoscope disinfection. Recent Findings Anywhere from 70 to 100% of stethoscopes are contaminated after a physical examination with bacterial counts of stethoscopes comparable to those of the physician’s dominant hand. Disinfection with alcohol agents can reduce the number of pathogens and risk of transmission, which is recommended by guidelines. However, only 0–11% of healthcare providers disinfected their stethoscope before patient contact and 0–24% disinfected after the contact. The effectiveness of educational programs with visual reminders and supplying disinfectants is uncertain. Summary Stethoscopes commonly harbor bacteria and can serve as a vector for transmission of infectious diseases. Only a minority of healthcare providers actually disinfect their stethoscope. There is a clear need for strategies to alter physicians’ recognition and behavior for stethoscope disinfection.