N-Terminal Pro Brain, N-Terminal Pro Atrial Natriuretic Peptides, and Dynamic Cerebral Autoregulation.

N-Terminal Pro Brain, N-Terminal Pro Atrial Natriuretic Peptides, and Dynamic Cerebral Autoregulation.
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DOI:
10.1161/jaha.120.018203
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发表时间:
2020-10-20
影响因子:
5.4
通讯作者:
Sorond FA
Sorond FA
中科院分区:
医学2区
文献类型:
--
作者:
Mahinrad S;Sabayan B;Garner CR;Lloyd-Jones DM;Sorond FA

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升高的利钠肽(NP)与不良脑血管疾病相关,包括中风、脑小血管疾病和痴呆。然而,这些关联背后的机制仍不清楚。在这项研究中,我们研究了NT-proBNP(N-末端前脑NP)和NT-proANP(N-末端前心房NP)与脑血管功能的关系,通过脑自动调节测量。我们纳入了来自CARDIA(年轻人冠状动脉风险发展)队列的154名参与者(平均年龄56±4岁)。分别使用电化学发光免疫测定法和酶联免疫测定法测量25年检查的血液样本中的NT‐proBNP和NT‐proANP。在第30年检查时,通过经颅多普勒超声,使用自发血压和流速振荡的传递函数分析(相位和增益)评估动态脑自动调节(dCA),其中较低的相位和较高的增益反映脑自动调节效率较低。我们使用多变量线性回归模型,调整人口统计学,血管危险因素,肾脏和心脏疾病史。第25年时较高的NT‐proBNP水平与第30年时较低的相位(β [95% CI]=较低的相位程度[-10.05至-0.54])和较高的增益(β [95% CI]=每mmHg增益高0.06 cm/s [0.004-0.12])相关。同样,较高的NT-proANP水平与较低的相位相关(β [95%CI]=-9.08较低的相位度[-16.46至-1.70])。NT‐proBNP和NT‐proANP的循环水平较高与5年后dCA效率较低相关。这些发现将循环NP与脑自动调节联系起来,并且可能是将NP与不良脑血管结局联系起来的一种机制。
Elevated natriuretic peptides (NP) are associated with adverse cerebrovascular conditions including stroke, cerebral small vessel disease, and dementia. However, the mechanisms underlying these associations remain unclear. In this study, we examined the relationship of NT‐proBNP (N‐terminal pro brain NP) and NT‐proANP (N‐terminal pro atrial NP) with cerebrovascular function, measured by cerebral autoregulation. We included 154 participants (mean age 56±4 years old) from the CARDIA (Coronary Artery Risk Development in Young Adults) cohort. NT‐proBNP and NT‐proANP were measured in blood samples from the year 25 examination using electrochemiluminescence Immunoassay and enzyme‐linked immunoassay, respectively. Dynamic cerebral autoregulation (dCA) was assessed at the year 30 examination by transcranial Doppler ultrasound, using transfer function analysis (phase and gain) of spontaneous blood pressure and flow velocity oscillations, where lower phase and higher gain reflect less efficient cerebral autoregulation. We used multivariable linear regression models adjusted for demographics, vascular risk factors, and history of kidney and cardiac diseases. Higher NT‐proBNP levels at year 25 were associated with lower phase (β [95% CI]=−5.30 lower degrees of phase [−10.05 to −0.54]) and higher gain (β [95% CI]=0.06 higher cm/s per mm Hg of gain [0.004–0.12]) at year 30. Similarly, higher NT‐proANP levels were associated with lower phase (β [95% CI]=−9.08 lower degrees of phase [−16.46 to −1.70]). Higher circulating levels of NT‐proBNP and NT‐proANP are associated with less efficient dCA 5 years later. These findings link circulating NP to cerebral autoregulation and may be one mechanism tying NP to adverse cerebrovascular outcomes.