title: The synergistic combined effect of anemia with high plasma levels of B-type natriuretic peptide significantly predicts an enhanced risk for major adverse cardiac events.
abstract: The prevalence of anemia in patients with heart failure (HF) increases according to disease severity as a consequence of renal insufficiency, cytokine production, plasma volume expansion, and/or malnutrition. B-type natriuretic peptide (BNP) has been recognized as a biochemical marker of ventricular dysfunction. The aim of this study was to evaluate the clinical significance of anemia in HF patients and furthermore, to investigate whether a significant correlation exists between anemia, BNP, and poor clinical outcomes in HF patients. We studied 185 consecutive HF patients. We assessed the occurrence of major adverse cardiac events (MACE) post hospital discharge. Anemia was defined as Hb concentrations <12.9 g/dl in men and <11.3 g/dl in women, respectively. Kaplan-Meier analysis revealed that anemia and high BNP levels (>259 pg/ml) were significantly associated with the occurrence of MACE. Multiple logistic analysis revealed that the most predictive independent risk factor for the occurrence of MACE was high BNP levels, followed by anemia (relative risk [RR] = 2.803 and 2.241, respectively). We divided the patients with or without anemia and high or low BNP levels into four groups according to their respective Hb and BNP levels. The hazard ratio for MACE in the group with anemia and high BNP levels was 10.3 in comparison to the group without anemia and with low BNP levels (P = 0.0002). Both anemia and high plasma levels of BNP are significantly and independently associated with the occurrence of MACE in HF patients; furthermore, the synergistic effect of anemia combined with high BNP levels significantly predicts an enhanced risk for MACE.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Ueno
authors.forename: Masafumi
authors.initials: M
authors.lastname: Nakayama
authors.forename: Sunao
authors.initials: S
authors.lastname: Kojima
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kusuhara
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nagayoshi
authors.forename: Megumi
authors.initials: M
authors.lastname: Yamamuro
authors.forename: Tsunenori
authors.initials: T
authors.lastname: Nishijima
authors.forename: Hiroki
authors.initials: H
authors.lastname: Usuku
authors.forename: Kouichi
authors.initials: K
authors.lastname: Kaikita
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sumida
authors.forename: Hiroshige
authors.initials: H
authors.lastname: Yamabe
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000740:Anemia / Q000097:blood* / Q000150:complications / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology*; D018572:Disease-Free Survival; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000628:therapy; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D053208:Kaplan-Meier Estimate; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D006454:Hemoglobins; D020097:Natriuretic Peptide, Brain