Sympathetic Hyperactivity and Aortic Sympathetic Nerve Sprouting in Patients with Thoracic Aortic Dissection

Hu, Zhipeng; Wang, Zhiwei; Yu, Lilei; Zhang, Hao; Wu, Hongbing; Ren, Zhigang; Hao, Chang‐Ning; Hu, Xiaoping

doi:10.1016/j.avsg.2013.11.016

Cited by 23 publications

(18 citation statements)

References 26 publications

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“…Second, aortic dissection is defined as the separation between the layers of the aortic wall, resulting in luminal stenosis and decreased blood supply to organs. The latter, and consequent sharp pain, further activate the sympathetic nervous and renin–angiotensin systems 20. All of these factors could cause increased blood pressure and strain on the left ventricular myocardium, leading to elevated secretion of NT-pro-BNP.…”

Section: Discussionmentioning

confidence: 99%

N-terminal pro-B-type natriuretic peptide and outcomes in type B aortic dissection in China: a retrospective multicentre study

et al. 2019

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ObjectivesN-terminal pro-B-type natriuretic peptide (NT-pro-BNP) is an unfavourable factor responsible for poor outcomes in the cardiovascular diseases. Nevertheless, the prognostic role of NT-pro-BNP in type B aortic dissection (TBAD) remains unclear. The aim of the current study was to investigate the relationship between NT-pro-BNP levels and in-hospital and long-term adverse prognosis in patients with TBAD.DesignA retrospective multicentre study.SettingLiutie Central Hospital, Nanfang Hospital and Huiyang Hospital in China.ParticipantsA total of 657 consecutive patients with TBAD were enrolled in the study. NT-pro-BNP was measured at admission and included patients were divided into three groups according to the tertiles of NT-pro-BNP (pg/mL): <95 (n=220), 95–312 (n=218) and >312 (n=219).Primary and secondary outcome measuresLong-term mortality and in-hospital major adverse clinical events.ResultsOverall, in-hospital death occurred in 27 patients (4.1%), which was significantly higher in upper tertiles of NT-pro-BNP (0.5% vs 4.1% vs 7.8%, p<0.001). The incident of in-hospital major adverse clinical events increased along with higher NT-pro-BNP (1.4% vs 11.5% vs 15.5%, p<0.001). NT-pro-BNP >210 pg/mL had 81.5% sensitivity and 58.6% specificity for predicting in-hospital death (area under the curve= 0.774, 95% CI 0.692 to 0.855; p<0.001). After a median of 3.1 years of follow-up, 97 (14.8%) patients died. The Kaplan-Meier analysis indicated that the long-term cumulative mortality was higher in patients with NT-pro-BNP >210 pg/mL compared with patients with NT-pro-BNP ≤210 pg/mL (log-rank=26.92, p<0.001). In multivariable Cox survival modelling, NT-pro-BNP >210 pg/mL was independently associated with long-term death (adjusted HR 2.47, 95% CI 1.45 to 4.22, p=0.001).ConclusionsNT-pro-BNP resulted as an independent predictor of adverse prognosis in patients with TBAD, thus could be used as a potential risk-stratification tool.

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Section: Discussionmentioning

confidence: 99%

N-terminal pro-B-type natriuretic peptide and outcomes in type B aortic dissection in China: a retrospective multicentre study

et al. 2019

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“…In the absence of enhanced protein catabolism, such as severe infection and burning, trauma, glucocorticoids therapy or high protein diet, urea levels in blood is determined by the GFR and tubular reabsorption. In the setting of AAD, hemodynamic disturbances lead to activation of the neurohormonal axis, resulting in increased sympathetic nervous system [10] and renin-angiotensin-aldosterone system activity [11]. Increased angiotensin and adrenergic stimulation decrease renal urea excretion via effects on vascular, glomerular, and tubular effects on the kidney.…”

Section: Discussionmentioning

confidence: 99%

Blood urea nitrogen in the prediction of in-hospital mortality of patients with acute aortic dissection

Sun

Wang

et al. 2018

Cardiol J.

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“…An Olympus BX53 fluorescent microscope (olympus corporation) was used to investigate and capture images. Sympathetic nerve densities were determined by image-Pro Plus 6.0 (Media cybernetics, inc.,) in tyrosine hydroxylase (TH) staining slides as previously described (3). nerve density was calculated as the nerve area divided by the total area examined (µm 2 /mm 2 ).…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have demonstrated that sympathetic activation and over-innervation promotes aortic dissection (3,4) and that norepinephrine (ne) released by sympathetic nerve endings can upregulate the expression of matrix metallopeptidase-2 (MMP2) and promote aortic remodeling (5). However, the signaling pathway involved in ne regulation of aortic remodeling is still unknown.…”

Section: Introductionmentioning

confidence: 99%

The sympathetic transmitter norepinephrine inhibits VSMC proliferation induced by TGFβ by suppressing the�expression of the TGFβ receptor ALK5 in aorta remodeling

Wang

et al. 2020

Mol Med Report

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The sympathetic system is involved in the arterial diseases, but its mechanism remains poorly understood. The present study aimed to explore the impact of the sympathetic neurotransmitter norepinephrine (ne) on transforming growth factor (TGF) β signaling and the role of ne in aortic remodeling. Guanethidine was used to induce a regional chemical sympathetic denervation (cSd) in angiotensin ii (angii) and β-aminopropionitrile (BaPn)-induced aortic aneurysm models. The diameter of the aorta was measured, and elastic fiber staining was performed. TGFβ type i receptor kinase (alK5) expression in rat aortic ne-treated vascular smooth muscle cells (VSMcs) was detected by reverse transcription-quantitative Pcr and western blotting. The effects of ne and alK5 overexpression on migration, proliferation, apoptosis and TGFβ signaling were also evaluated. Furthermore, adrenergic receptor blockers were used to determine which receptor was involved in the modulation on TGFβ signaling by ne. The results of the present study demonstrated that cSd protected rats from angii+BaPn-induced aortic remodeling and aneurysm formation. compared with the control group, ne inhibited VSMc proliferation and migration, but promoted apoptosis by suppressing alK5 expression, reversing the effects of TGFβ signaling through the suppression of the SMad-dependent canonical pathway and promotion of the non-canonical pathway. These effects were prevented by alK5 overexpression. The inhibition of α-or β-adrenergic receptors alleviated the ne-mediated suppression of alK5 expression. in conclusion, regional cSd protected rats from aortic aneurysm. ne inhibited SMad2/3-dependent TGFβ signaling by suppressing alK5 expression, which may serve an important role in VSMc biological functions. Both α-and β-adrenergic receptors were involved in the regulation of alK5 expression by ne. abnormal sympathetic innervation of the aorta may be used as a therapeutic target in aortic diseases.

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Sympathetic Hyperactivity and Aortic Sympathetic Nerve Sprouting in Patients with Thoracic Aortic Dissection

Cited by 23 publications

References 26 publications

N-terminal pro-B-type natriuretic peptide and outcomes in type B aortic dissection in China: a retrospective multicentre study

N-terminal pro-B-type natriuretic peptide and outcomes in type B aortic dissection in China: a retrospective multicentre study

Blood urea nitrogen in the prediction of in-hospital mortality of patients with acute aortic dissection

The sympathetic transmitter norepinephrine inhibits VSMC proliferation induced by TGFβ by suppressing the�expression of the TGFβ receptor ALK5 in aorta remodeling

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