CLINICAL RESEARCH: HEART FAILURE
Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy
Marc Vanderheyden, MD*,*,
Marc Goethals, MD*,
Sofie Verstreken, MD*,
Bernard De Bruyne, MD*,
Kristin Muller, RN ,
Eddy Van Schuerbeeck, RN* and
Jozef Bartunek, MD*
* Cardiovascular Center, Onze Lieve Vrouw Ziekenhuis, Aalst, Belgium
Cardiovascular Center, Imelda Ziekenhuis, Bonheiden, Belgium
Manuscript received May 11, 2004;
accepted September 13, 2004.
* Reprint requests and correspondence: Dr. Marc Vanderheyden, Cardiovascular Center, Onze Lieve Vrouwziekenhuis, Moorselbaan 164, 9400 Aalst, Belgium (Email: Marc.Vanderheyden{at}olvz-aalst.be).
OBJECTIVES: 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.
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Abbreviations and Acronyms
| | AS = aortic stenosis | | BNP = B-type natriuretic peptide | | LV = left ventricle/ventricular | | PCWP = pulmonary capillary wedge pressure |
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