Key result
Acute pulmonary edema was associated with a significantly greater decline in hemoglobin levels within 24 hours of admission compared to acute heart failure without pulmonary edema (adjusted mean difference -1.08 g/dl, P<0.001).
Why the study?
Does acute pulmonary edema presentation affect the acute change in hemoglobin levels at 24 hours compared to non-APE acute heart failure?
Observational (n=237)
No
Does acute pulmonary edema presentation affect the acute change in hemoglobin levels at 24 hours compared to non-APE acute heart failure?
Mean Difference: -1.08
Absolute Event Rate: -1.8% vs -0.5%
p-value: p=<0.001
Patients with acute pulmonary edema have higher admission hemoglobin levels and a more significant decline within 24 hours compared to other acute heart failure patients, suggesting mechanisms other than diuresis-induced hemoconcentration.
Acute pulmonary edema may warrant attentive hemoglobin monitoring in acute heart failure; leaves open non-diuresis mechanisms.
BACKGROUND: Acute pulmonary edema (APE) often occurs without remarkable fluid retention, and the benefits of diuretics are unclear in such patients. Although aggressive diuresis induces an increase in intravascular substances including hemoglobin (Hb), acute changes in Hb level remain to be investigated. METHODS AND RESULTS: We analyzed 237 consecutive acute heart failure patients (74±12 years; 60.8% men) without shock, hemodialysis, bleeding, or urgent coronary angiography. APE was defined as acute onset of dyspnea within the preceding 6h and radiographic alveolar edema requiring immediate airway intervention. At admission, Hb level was higher in APE (n=29) than non-APE patients (n=208; 13.4±2.2 vs 12.2±2.1g/dl, P<0.01). Although diuretic therapy was performed in 232 patients (97.9%), hemoconcentration (ie, any increase in Hb) was observed in only 64 patients (27.0%) at 24h after admission. Conversely, Hb level decreased in both groups and the difference was larger in APE patients (-1.8±1.1 in APE and -0.5±1.0g/dl in non-APE patients, P<0.001). APE was significantly related to a greater decrease in Hb after adjusting for baseline Hb (β=-1.08g/dl, SE=0.20, P<0.001, ANCOVA). CONCLUSIONS: APE patients had higher Hb level at admission and a more remarkable decline in 24h than did those without APE. Acute change in Hb might be caused by factors other than diuresis-induced hemoconcentration. The present findings may be useful in the selection of diuretic strategies.
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Konishi et al. (2014) conducted an observational in Acute heart failure syndrome (n=237). Acute pulmonary edema vs. Acute heart failure without acute pulmonary edema was evaluated on Change in hemoglobin level from admission to 24 hours (β=-1.08 g/dl, p=<0.001). Acute pulmonary edema was associated with a significantly greater decline in hemoglobin levels within 24 hours of admission compared to acute heart failure without pulmonary edema (adjusted mean difference -1.08 g/dl, P<0.001).
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