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Diversity of Molecular Forms of Plasma Brain Natriuretic Peptide in Heart failure –Different proBNP-108 to BNP-32 Ratios in Atrial and Ventricular Overload–
  1. Toshio Nishikimi1,*,
  2. Naoto Minamino2,
  3. Ikeda Masashi3,
  4. Yosuke Takeda1,
  5. Kazuyoshi Tadokoro1,
  6. Ikuko Shibasaki4,
  7. Hirotugu Fukuda4,
  8. Yuji Horiuchi5,
  9. Shinji Oikawa5,
  10. Tamio Ieiri, Professor5,
  11. Masako Matsubara2,
  12. Toshihiko Ishimitsu1
  1. 1 Department of Hypertension and Cardiorenal Medicine,Dokkyo Medical University, Japan;
  2. 2 Department of Pharmacology, Research Institute National Cardiovascular Center, Japan;
  3. 3 Institute of International Education and Research, Dokkyo Medical University, Japan;
  4. 4 Department of Cardiovascular Surgery,Dokkyo Medical University, Japan;
  5. 5 Department of Clinical Laboratory, Dokkyo Medical University, Japan
  1. Correspondence to: Toshio Nishikimi, Hypertension and Cardiorenal Medicine, Dokkyo University School of Medicine, Department of Internal Medicine, Dokkyo University School of Medicine, Mibu, Tochigi, 321-0293, Japan; nishikim{at}dokkyomed.ac.jp

Abstract

Objective: Recent studies have shown that plasma levels of brain natriuretic peptide (BNP)-32 and proBNP-108 are increased in heart failure (HF) and that BNP-32 assay kit crossreacts proBNP-108. We investigated why proBNP is increased without processing in HF.

Design, setting, and patients: We measured plasma BNP-32 and proBNP-108 in normal subjects (n=10) and patients with atrial fibrillation (AF) (n=18) and HF (n=132). We also measured BNP-32 and proBNP-108 in ventricular and atrial tissue and in pericardial fluid by specific fluorescent enzyme immunoassay following Sep-Pak C18 cartridge extraction and gel-filtration.

Main outcome measures: Both BNP-32 and proBNP-108 were higher in HF than in control or AF (both P<0.01), and there was a significant correlation between the levels of these peptides (r=0.94, P<0.001). The proBNP-108/total BNP (BNP-32+proBNP-108) ratio was widely distributed and lower in HF (0.33±0.17) than in control (0.41±0.06, P<0.05) and AF (0.45±0.04: P<0.002). HF with ventricular overload had higher proBNP-108/ total BNP ratio (45±10%) than HF with atrial overload (20±11%, P<0.001). Consistent with this finding, proBNP-108 was the major molecular form in ventricular tissue (n=6, 67±4%), and BNP-32 was the major molecular form in atrial tissue (n=7, 76±5%, P<0.0001). In addition, proBNP-108 was the major molecular form of BNP in pericardial fluid (n=8, 82±5%). The proBNP-108/total BNP ratio increased with deterioration of HF and decreased with improvement of HF.

Conclusion: These results suggest that not only BNP-32, but also proBNP-108 is increased in HF and that proBNP/total BNP ratio increases in association with pathophysiological conditions such as ventricular overload.

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