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Low hemoglobin levels are a predictor of increased risk of death in heart failure
Aug 18, 2005, 02:05, Reviewed by: Dr.
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"It is important to pursue hemoglobin's role in the risk of death and complications in heart failure patients"
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By American Heart Association,
Low hemoglobin levels are a predictor of increased risk of death and complications among heart failure patients, according to a report in Circulation: Journal of the American Heart Association.
Hemoglobin (Hgb) is the major substance in red blood cells, and its level indicates the blood's ability to carry oxygen throughout the body. Studies have shown that low hemoglobin, which may result in anemia, is more common among patients with heart failure than it is among people in the general population. As many as 25 percent to 60 percent of heart failure patients have anemia, defined as hemoglobin less than 12 grams/deciliter in women and 13g/dL in men. "Studies have shown that if you have anemia and heart failure, your risk of death and complications are increased appreciably -- with as much as 30 percent to 60 percent additional risk of death and hospitalization from heart failure," said Inder S. Anand, M.D., FRCP, D. Phil. (Oxon.), the study's lead author, and professor of medicine at University of Minnesota Medical School and director of the Heart Failure Program, VA Medical Center, Minneapolis, Minn.
To study the association between anemia and mortality risk, the researchers used a database on 5,002 patients enrolled in the Valsartan Heart Failure Trial, a study evaluating the high blood pressure drug valsartan.
At the beginning of the study, researchers took a complete blood cell count, and repeated these measurements at regular intervals up to 24 months. Of the patients enrolled in the heart failure study, 23 percent were anemic. Anemic patients tended to be older, have diabetes and to have worse heart failure.
The researchers found that the quartile of patients with the largest average decreases in Hgb over 12 months (defined as an average decrease of 1.6 g/dL, from 14.2 to 12.6 g/dL) experienced 47 percent more hospitalizations and 60 percent more deaths, compared to those in the quartile that exhibited an insignificant (0.10 g/dL) change in hemoglobin during 12 months.
The researchers report that an increase in Hgb was associated with a 22 percent lower death rate in patients with anemia, compared to 21 percent without anemia, at the start of the study.
Patients who had anemia at the start of the study or whose Hgb decreased during the study had worse heart failure and an associated elevation of several other risk factors for heart disease, including neurohormones and C-reactive protein.
"If you are a heart failure patient and your hemoglobin drops, then you are at a greater risk of having problems. What remains unclear, however, is the ideal level of hemoglobin to be achieved in patients with heart failure," he said.
Researchers said one of the causes of anemia may be related to iron deficiency in heart failure patients because of malabsorption, nutritional deficiencies and impaired metabolism. Hemodilution (excess fluid retention) may also contribute to anemia in heart failure patients.
Researchers don't know if anemia worsens heart failure or if it is a marker of heart failure severity, or what effect raising hemoglobin will have on the heart's function.
"It is important to pursue hemoglobin's role in the risk of death and complications in heart failure patients," Anand said.
"The lifetime risk for developing heart failure for men and women at age 40 is one in five. If 30 percent to 60 percent of these people are at higher risk for death and complications because of low hemoglobin, we might have an opportunity to treat these patients," he said. "Treatment for anemia is relatively simple, with iron supplements, multivitamins or drugs. However, we do not yet know if treatment is the best strategy and what the goals of treatment should be." 
- Circulation: Journal of the American Heart Association.
American Heart Association
Co-authors are Michael A. Kuskowski, Ph.D.; Thomas S. Rector, Ph.D.; Viorel G. Florea, M.D.; Robert D. Glazer, M.D.; Allen Hester, Ph.D.; Yann Tong Chiang, Ph.D.; Nora Aknay; Aldo P. Maggioni, M.D.; Cristina Opasich, M.D.; Roberto Latini, M.D.; and Jay N. Cohn, M.D.
The study was funded by a grant from Novartis Pharmaceuticals AG, Basel, Switzerland. Drs. Glazer and Chiang, and Nora Aknay are employees of Novartis Pharmaceuticals Corporation.
Statements and conclusions of study authors that are published in the American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect association policy or position. The American Heart Association makes no representation or warranty as to their accuracy or reliability.
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