Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy
Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy
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DOI：
10.1016/j.jacc.2004.09.038
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发表时间：
2004-12-21
影响因子：
24
通讯作者：
Bartunek, J
中科院分区：
文献类型：
--
作者：
Vanderheyden, M;Goethals, M;Bartunek, J
目的我们推测舒张期和收缩期负荷均可调节人压力超负荷肥厚/衰竭时B型利钠肽(BNP)的产生。背景：在分离的心肌细胞中，舒张期牵张诱导BNP信使核糖核酸的表达。方法对40例有症状的主动脉狭窄(AS)、左心室(LV)表现、收缩和舒张期室壁应力进行超声心动图检查。结果血浆脑钠素水平与肺毛细血管楔压(p<；0.001)、收缩分数(p=0.001)和主动脉瓣面积(p=0.006)显著相关。此外，BNP与LV质量指数(p=0.005)以及与舒张期负荷的标志物如LV舒张末应力(p=0.011)、指数LV舒张末容量(p<；0.001)和等容松弛时间(p=0.02)之间也存在显著的相关性。强直性脊柱炎患者术前BNP水平明显高于非AS患者。前负荷储备受损的AS患者血浆BNP水平明显高于前负荷储备正常的AS患者(P=0.017)和瓣膜置换术后临床恶化的AS患者(399±/-82pg/ml vs.124+/-41pg/ml；P=0.011)。这支持了这样一种假设，即在人类压力超负荷肥大/衰竭时，心肌牵张调节BNP的产生。(C)2004年，由美国心脏病学会基金会提供。
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. (C) 2004 by the American College of Cardiology Foundation.