The Predictive Value of Short-Term Changes in Hemoglobin Concentration in Patients Presenting With Acute Decompensated Heart Failure

Meer, Peter van der; Postmus, Douwe; Ponikowski, Piotr; Cleland, John G.F.; O’Connor, Christopher M.; Cotter, Gad; Metra, Marco; Davison, Beth A.; Givertz, Michael M.; Mansoor, George A.; Teerlink, John R.; Massie, Barry M.; Hillege, Hans L.; Voors, Adriaan A.

doi:10.1016/j.jacc.2012.12.050

Cited by 163 publications

(101 citation statements)

References 24 publications

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“…Most studies do not measure creatinine routinely, so in those that did, there was probably a reason, which perhaps means that these patients were more likely to have worsening of symptoms or nonresponse to diuretics [34][35][36] related to clinical outcomes. This theory of measurement bias is supported by a recent study composed of 599 patients who had their serum creatinine levels routinely measured.…”

Section: Discussionmentioning

confidence: 99%

Nesiritide, Renal Function, and Associated Outcomes During Hospitalization for Acute Decompensated Heart Failure

et al. 2014

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Editorial see p 936 Clinical Perspective on p 965The Acute Study of Clinical Effectiveness of Nesiritide and Decompensated Heart Failure (ASCEND-HF) was conducted to re-evaluate the efficacy and safety of nesiritide, compared with placebo, added to standard of care in 7141 acute Background-Contradictory results have been reported on the effects of nesiritide on renal function in patients with acute decompensated heart failure. We studied the effects of nesiritide on renal function during hospitalization for acute decompensated heart failure and associated outcomes. Methods and Results-A total of 7141 patients were randomized to receive either nesiritide or placebo and creatinine was recorded in 5702 patients at baseline, after infusion, discharge, peak/nadir levels until day 30. Worsening renal function was defined as an increase of serum creatinine >0.3 mg/dL and a change of ≥25%. Median (25 th -75 th percentile) baseline creatinine was 1.2 (1.0-1.6) mg/dL and median baseline blood urea nitrogen was 25 (18-39) mmol/L. Changes in both serum creatinine and blood urea nitrogen were similar in nesiritide-treated and placebo-treated patients (P=0.20 and P=0.41) from baseline to discharge. In a multivariable model, independent predictors of change from randomization to hospital discharge in serum creatinine were a lower baseline blood urea nitrogen, higher systolic blood pressure, lower diastolic blood pressure, previous weight gain, and lower baseline potassium (all P<0.0001). The frequency of worsening renal function during hospitalization was similar in the nesiritide and placebo group (14.1% and 12.8%, respectively; odds ratio with nesiritide 1.12; confidence interval, 0.95-1.32; P=0.19) and was not associated with death alone and death or rehospitalization at 30 days. However, baseline, discharge, and change in creatinine were associated with death alone and death or rehospitalization for heart failure (all tests, P<0.0001). Conclusions-Nesiritide did not affect renal function in patients with acute decompensated heart failure. Baseline, discharge, and change in renal function were associated with 30-day mortality or rehospitalization for heart failure. decompensated heart failure (ADHF) patients. Overall, compared with placebo, nesiritide did not improve (or worsen) clinical outcomes and nesiritide did not increase the risk of worsening renal function (predefined as >25% decrease in estimated glomerular filtration rate).

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Section: Discussionmentioning

confidence: 99%

Nesiritide, Renal Function, and Associated Outcomes During Hospitalization for Acute Decompensated Heart Failure

et al. 2014

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“…However, a primary pathophysiologic derangement of HF is the expansion of the PV and, therefore, it becomes difficult to accurately differentiate true anemia from dilution-related anemia or even the presence of excess RBCM (polycythemia) based on peripheral hemoglobin or hematocrit measurements alone. [22][23][24] Although the importance of a low hemoglobin and its causes in chronic HF should not be underestimated in terms of outcome implications, 25 the concept of pseudoanemia secondary to PV excess and even with RBCM polycythemia has been underrecognized. As a result, in the clinical setting of volume overload chronic HF, the complex of true anemia, pseudoanemia, and RBCM polycythemia with PV expansion and the relation to peripheral venous hemoglobin values has gone, with a few exceptions, 12,26 largely unreported and with it the implications for volume management.…”

Section: Millermentioning

confidence: 99%

“…The majority of indirect methods in use are based on the dilution of a known amount of an intrinsic marker such as plasma albumin, red blood cells, or an appropriate test substance introduced into the circulatory system. Although peripheral venous hemoglobin concentration and hematocrit and changes in these parameters have been used to estimate changes in intravascular volume status 25,36 with prognostic benefit, the absolute values show poor correlation with measured total BV in patients with chronic HF. 19 Recognizing the transcapillary fluid shifts that occur between interstitial and intravascular compartments with chronic HF makes this discrepancy not unexpected.…”

Section: Assessment Of Congestion and Extracellular Fluid Volume Overmentioning

confidence: 99%

Fluid Volume Overload and Congestion in Heart Failure

Miller

2016

Circ: Heart Failure

210

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Abstract-Volume regulation, assessment, and management remain basic issues in patients with heart failure. The discussion presented here is directed at opening a reassessment of the pathophysiology of congestion in congestive heart failure and the methods by which we determine volume overload status. Peer-reviewed historical and contemporary literatures are reviewed. Volume overload and fluid congestion remain primary issues for patients with chronic heart failure. The pathophysiology is complex, and the simple concept of intravascular fluid accumulation is not adequate. The dynamics of interstitial and intravascular fluid compartment interactions and fluid redistribution from venous splanchnic beds to central pulmonary circulation need to be taken into account in strategies of volume management. Clinical bedside evaluations and right heart hemodynamic assessments can alert clinicians of changes in volume status, but only the quantitative measurement of total blood volume can help identify the heterogeneity in plasma volume and red blood cell mass that are features of volume overload in patients with chronic heart failure and help guide individualized, appropriate therapy-not all volume overload is the same. (Circ Heart Fail. 2016;9:e002922.

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“…8,9) In patients with ADHF, the incidence of low Hb level is even higher; 68% in men and 52% in women. 10) Although anemia is a known indicator of an unfavourable clinical profile related to inferior survival in both ACS and heart failure (HF) patients, [5][6][7]11) this correlation is complex.…”

Section: Discussionmentioning

confidence: 99%

Predictors of Long-Term Mortality in Patients Hospitalized in an Intensive Cardiac Care Unit

et al. 2016

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SummaryPatients admitted to an intensive cardiac care unit (ICCU) are a heterogeneous population with a high mortality rate. The aim of our study was to investigate which clinical, biochemical, and echocardiographic parameters routinely assessed may affect long-term mortality in a non-selected ICCU population.A total of 392 patients hospitalized between 2008-2011 (mean age, 70 ± 13.8 years, 43% women) were consecutively and prospectively assessed with the following admission diagnoses: 168 with acute coronary syndromes (ACS), 122 with acute decompensated heart failure (ADHF), and 102 with other acute cardiac disorders. Patients were treated according to the current European Society of Cardiology (ESC) guidelines.During a mean 29.3 (± 18.9) months of observation, 152 (38.8%) patients died and 7.9% of the patients needed a red blood cell transfusion (RBC Tx). Patients who died were significantly older and had lower baseline levels of hemoglobin (Hb), serum iron concentration (SIC), total iron binding capacity (TIBC), cholesterol, and left ventricular ejection fraction (LVEF), as well as lower eGFR values, and higher white blood cell (WBC) counts and C-reactive protein (CRP) levels (P < 0.05). Predictors of death in multivariate regression analysis were age, Hb, LVEF, WBC, and CRP. The most powerful factor was hospitalization for non-ACS. The risk of long-term mortality increased with decreasing levels of Hb (P < 0.001), SIC (P = 0.001), TIBC (P = 0.009), and the need for RBC Tx (P < 0.001), as well as the diagnosis of ADHF (P < 0.001) and the absence of ACS (P = 0.007).In ICCU patients, age, Hb, parameters of iron status, and LVEF are strong predictors of long-term mortality. Among the ICCU population, patients with ACS diagnosis have better survival. (Int Heart J 2016; 57: 67-72)

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The Predictive Value of Short-Term Changes in Hemoglobin Concentration in Patients Presenting With Acute Decompensated Heart Failure

Abstract: Patients with AHF and preserved renal function are decongested better, as shown by an increase in hemoglobin. A rapid increase in hemoglobin during the first week is independently associated with a favorable outcome, despite a slight decrease in renal function.

Cited by 163 publications

References 24 publications

Nesiritide, Renal Function, and Associated Outcomes During Hospitalization for Acute Decompensated Heart Failure

Nesiritide, Renal Function, and Associated Outcomes During Hospitalization for Acute Decompensated Heart Failure

Fluid Volume Overload and Congestion in Heart Failure

Predictors of Long-Term Mortality in Patients Hospitalized in an Intensive Cardiac Care Unit

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