title: Ventricular expression of brain natriuretic peptide in hypertrophic cardiomyopathy.
abstract: BACKGROUND
  Brain natriuretic peptide (BNP), as a cardiac hormone, is expressed together with atrial natriuretic peptide (ANP) in the ventricles in congestive heart failure. However, the ventricular expression of BNP in hypertrophic cardiomyopathy (HCM) with normal systolic function is still unclear.
  
  
  RESULTS
  The study population consisted of 39 HCM patients with asymmetric septal hypertrophy and 10 control subjects without any specific cardiac disease. Eleven cases of HCM were obstructive (HOCM), and the other 28 cases were nonobstructive (HNCM). All of these patients had a normal ejection fraction. Immunohistochemical analysis of endomyocardial biopsy specimens with specific monoclonal antibodies showed BNP immunoreactivity in the HOCM group (5/10, 50%) but not in the HNCM group (0/22) or in control subjects (0/5). In HOCM, left ventricular end-diastolic pressure was significantly higher in the BNP-positive patients than the BNP-negative patients. Histological changes such as myocardial fiber disarray, hypertrophy of myocytes, and fibrosis were greater in BNP-positive patients than BNP-negative patients in HCM. However, the expression had no significant relation with other clinical parameters. The elevation of the BNP plasma level versus control subjects was marked in both HOCM (85-fold) and HNCM (23-fold). By contrast, the elevation of the ANP plasma level versus control subjects was mild in HOCM (5.7-fold) and HNCM (4.2-fold). The ratio of BNP level to ANP level was higher in HOCM (4.16) than in HNCM (1.46) and control subjects (0.28), and it was higher than the ratio previously reported for severe congestive heart failure (1.72).
  
  
  CONCLUSIONS
  These findings suggest that BNP is expressed in the ventricular myocytes of HCM with normal systolic function. In HOCM, ventricular expression of BNP may be augmented in response to both obstruction and diastolic dysfunction.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hasegawa
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
authors.forename: K
authors.initials: K
authors.lastname: Doyama
authors.forename: M
authors.initials: M
authors.lastname: Miyamae
authors.forename: T
authors.initials: T
authors.lastname: Fujiwara
authors.forename: S
authors.initials: S
authors.lastname: Suga
authors.forename: M
authors.initials: M
authors.lastname: Mukoyama
authors.forename: K
authors.initials: K
authors.lastname: Nakao
authors.forename: H
authors.initials: H
authors.lastname: Imura
authors.forename: S
authors.initials: S
authors.lastname: Sasayama
mesh_terms: D000328:Adult; D000368:Aged; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood / Q000378:metabolism*; D005260:Female; D006352:Heart Ventricles; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000097:blood / Q000378:metabolism*; D011863:Radioimmunoassay
chemical_list: D009419:Nerve Tissue Proteins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor