title: Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy.
abstract: OBJECTIVE
  We postulated that both diastolic and systolic load modulate B-type natriuretic peptide (BNP) production in human pressure overload hypertrophy/failure.
  
  
  BACKGROUND
  In isolated myocytes, diastolic stretch induces BNP messenger ribonucleic acid expression. However, the mechanism of the BNP release in human hypertrophy remains controversial.
  
  
  METHODS
  In 40 patients with symptomatic aortic stenosis (AS), left ventricular (LV) performance and systolic and diastolic wall stress were calculated from combined invasive and echocardiographic data. Plasma BNP was determined by the rapid point-of-care bedside analyzer (Biosite Triage, Biosite Diagnostics Inc., San Diego, California).
  
  
  RESULTS
  A significant relationship was observed between plasma BNP and pulmonary capillary wedge pressure (p < 0.001), fractional shortening (p = 0.001), and aortic valve area (p = 0.006). Furthermore, a significant correlation was noted between BNP and LV mass index (p = 0.005) as well as between BNP and markers of diastolic load such as LV end-diastolic wall stress (p = 0.011), indexed LV end-diastolic volume (p < 0.001), and isovolumic relaxation time (p = 0.02). Preoperative BNP levels were elevated in patients with AS compared with patients without AS. Plasma BNP was higher in AS patients with impaired versus normal preload reserve (297 +/- 56 pg/ml vs. 168 +/- 44 pg/ml; p = 0.017) and in AS patients with clinical deterioration after valve replacement compared with those without (399 +/- 82 pg/ml vs. 124 +/- 41 pg/ml; p = 0.011).
  
  
  CONCLUSIONS
  In patients with AS, BNP appears to be regulated not only by systolic but also by diastolic load. This supports the hypothesis that myocardial stretch modulates BNP production in human pressure overload hypertrophy/failure.
authors.affiliation: Cardiovascular Center, Onze Lieve Vrouw Ziekenhuis, Moorselbaan 164, 9400 Aalst, Belgium. Marc.Vanderheyden@olvz-aalst.be
authors.forename: Marc
authors.initials: M
authors.lastname: Vanderheyden
authors.forename: Marc
authors.initials: M
authors.lastname: Goethals
authors.forename: Sofie
authors.initials: S
authors.lastname: Verstreken
authors.forename: Bernard
authors.initials: B
authors.lastname: De Bruyne
authors.forename: Kristin
authors.initials: K
authors.lastname: Muller
authors.forename: Eddy
authors.initials: E
authors.lastname: Van Schuerbeeck
authors.forename: Jozef
authors.initials: J
authors.lastname: Bartunek
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001024:Aortic Valve Stenosis / Q000150:complications*; D001794:Blood Pressure; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology*; D016022:Case-Control Studies; D003971:Diastole; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000209:etiology; D007297:Inpatients; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D020097:Natriuretic Peptide, Brain / Q000096:biosynthesis* / Q000097:blood; D011669:Pulmonary Wedge Pressure; D013314:Stress, Mechanical; D013318:Stroke Volume; D013599:Systole; D016277:Ventricular Function, Left
chemical_list: D020097:Natriuretic Peptide, Brain