Vanderbilt Translational and Clinical Cardiovascular Research Center, University Medical Center, Nashville, TN (H.F.-T., J.F.F., K.N.B., D.K.G).
Department of Medicine (N.P.), University of Alabama-Birmingham, Birmingham, AL.
Circ Heart Fail. 2020 Jul;13(7):e006570. doi: 10.1161/CIRCHEARTFAILURE.119.006570. Epub 2020 Jun 8.
NPs (natriuretic peptides) are cardiac-derived hormones that promote natriuresis, diuresis, and vasodilation. Preclinical evidence suggests that nonhemodynamic triggers for NP release exist, with a few studies implicating inflammatory stimuli. We examined the association between inflammation and NP levels in humans.
The associations between inflammation and NP levels were examined in 3 independent studies. First, in 5481 MESA (Multi-Ethnic Study of Atherosclerosis) participants, the cross-sectional (exam 1) and longitudinal (exams 1 to 3) associations between circulating IL6 (interleukin-6) and NT-proBNP (N terminal pro B-type natriuretic peptide) levels were examined in multivariable-adjusted models. Second, in a prospective study of 115 healthy individuals, changes in NP levels were quantified following exposure to lipopolysaccharide as an inflammatory stimulus. Third, in 13 435 hospitalized patients, the association between acute inflammatory conditions and circulating NP levels was assessed using multivariable-adjusted models.
At the baseline MESA exam, each 1-unit higher natural log IL6 was associated with 16% higher NT-proBNP level ([95% CI, 10%-22%]; =0.002). Each 1-unit higher baseline natural log IL6 level also associated with 6% higher NT-proBNP level ([95% CI, 1%-11%]; =0.02) at 4-year follow-up. In the lipopolysaccharide study, median NT-proBNP levels rose from 21 pg/mL pre-lipopolysaccharide to 54 pg/mL post-lipopolysaccharide, <0.001. In the hospitalized patient study, acute inflammatory conditions were associated with 36% higher NP levels ([95% CI, 17%-60%]; <0.001).
Inflammation appears to be associated with NP release. Interpretation of NP levels should therefore take into account inflammatory conditions.
NP(利钠肽)是心脏衍生的激素,可促进利钠、利尿和血管舒张。临床前证据表明,NP 释放存在非血流动力学触发因素,一些研究提示炎症刺激。我们研究了炎症与人类 NP 水平之间的关系。
在 3 项独立研究中,我们研究了炎症与 NP 水平之间的关系。首先,在 5481 名 MESA(动脉粥样硬化多民族研究)参与者中,在多变量调整模型中,研究了循环白细胞介素 6(IL6)和 N 末端 pro B 型利钠肽(NT-proBNP)水平在横断面(第 1 次检查)和纵向(第 1 次至第 3 次检查)之间的关联。其次,在一项 115 名健康个体的前瞻性研究中,量化了在脂多糖作为炎症刺激物暴露后 NP 水平的变化。第三,在 13435 名住院患者中,使用多变量调整模型评估急性炎症状况与循环 NP 水平之间的关系。
在基线 MESA 检查时,IL6 的自然对数每增加 1 个单位,NT-proBNP 水平就会升高 16%([95%CI,10%-22%];=0.002)。基线 IL6 的自然对数每增加 1 个单位,也与 4 年随访时 NT-proBNP 水平升高 6%([95%CI,1%-11%];=0.02)相关。在脂多糖研究中,中位数 NT-proBNP 水平从脂多糖前的 21pg/mL 升高到脂多糖后的 54pg/mL,<0.001。在住院患者研究中,急性炎症状况与 NP 水平升高 36%相关([95%CI,17%-60%];<0.001)。
炎症似乎与 NP 释放有关。因此,解释 NP 水平时应考虑炎症状况。