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      The Role of Macrophages in Aortic Dissection


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          Aortic dissection (AD) is a fatal disease that accounts for a large proportion of aortic-related deaths and has an incidence of about 3–4 per 100,000 individuals every year. Recent studies have found that inflammation plays an important role in the development of AD, and that macrophages are the hub of inflammation in the aortic wall. Aortic samples from AD patients reveal a large amount of macrophage infiltration. The sites of macrophage infiltration and activity vary throughout the different stages of AD, with involvement even in the tissue repair phase of AD. Angiotensin II has been shown to be an important factor in the stimulation of macrophage activity. Stimulated macrophages can secrete metalloproteinases, inflammatory factors and other substances to cause matrix destruction, smooth muscle cell apoptosis, neovascularization and more, all of which destroy the aortic wall structure. At the same time, there are a number of factors that regulate macrophages to reduce the formation of AD and induce the repair of torn aortic tissues. The aim of this review is to take a close look at the roles of macrophages throughout the course of AD disease.

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          Most cited references65

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          The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease.

          Acute aortic dissection is a life-threatening medical emergency associated with high rates of morbidity and mortality. Data are limited regarding the effect of recent imaging and therapeutic advances on patient care and outcomes in this setting. To assess the presentation, management, and outcomes of acute aortic dissection. Case series with patients enrolled between January 1996 and December 1998. Data were collected at presentation and by physician review of hospital records. The International Registry of Acute Aortic Dissection, consisting of 12 international referral centers. A total of 464 patients (mean age, 63 years; 65.3% male), 62.3% of whom had type A dissection. Presenting history, physical findings, management, and mortality, as assessed by history and physician review of hospital records. While sudden onset of severe sharp pain was the single most common presenting complaint, the clinical presentation was diverse. Classic physical findings such as aortic regurgitation and pulse deficit were noted in only 31.6% and 15.1% of patients, respectively, and initial chest radiograph and electrocardiogram were frequently not helpful (no abnormalities were noted in 12.4% and 31.3% of patients, respectively). Computed tomography was the initial imaging modality used in 61.1%. Overall in-hospital mortality was 27.4%. Mortality of patients with type A dissection managed surgically was 26%; among those not receiving surgery (typically because of advanced age and comorbidity), mortality was 58%. Mortality of patients with type B dissection treated medically was 10.7%. Surgery was performed in 20% of patients with type B dissection; mortality in this group was 31.4%. Acute aortic dissection presents with a wide range of manifestations, and classic findings are often absent. A high clinical index of suspicion is necessary. Despite recent advances, in-hospital mortality rates remain high. Our data support the need for continued improvement in prevention, diagnosis, and management of acute aortic dissection.
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            2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine.

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              Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice.

              Increased plasma concentrations of angiotension II (Ang II) have been implicated in atherogenesis. To examine this relationship directly, we infused Ang II or vehicle for 1 month via osmotic minipumps into mature apoE(-/-) mice. These doses of Ang II did not alter arterial blood pressure, body weight, serum cholesterol concentrations, or distribution of lipoprotein cholesterol. However, Ang II infusions promoted an increased severity of aortic atherosclerotic lesions. These Ang II-induced lesions were predominantly lipid-laden macrophages and lymphocytes; moreover, Ang II promoted a marked increase in the number of macrophages present in the adventitial tissue underlying lesions. Unexpectedly, pronounced abdominal aortic aneurysms were present in apoE(-/-) mice infused with Ang II. Sequential sectioning of aneurysmal abdominal aorta revealed two major characteristics: an intact artery that is surrounded by a large remodeled adventitia, and a medial break with pronounced dilation and more modestly remodeled adventitial tissue. Although no atherosclerotic lesions were visible at the medial break point, the presence of hyperlipidemia was required because infusions of Ang II into apoE(+/+) mice failed to generate aneurysms. These results demonstrate that increased plasma concentrations of Ang II have profound and rapid effects on vascular pathology when combined with hyperlipidemia, in the absence of hemodynamic influences.

                Author and article information

                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                05 February 2020
                : 11
                : 54
                [1] 1Department of Vascular and Endovascular Surgery, The First Medical Center of Chinese PLA General Hospital , Beijing, China
                [2] 2Department of General Surgery , PLA No. 983 Hospital, Tianjin, China
                [3] 3Department of Obstetrics, Zibo Central Hospital , Zibo, China
                Author notes

                Edited by: Yi Zhu, Tianjin Medical University, China

                Reviewed by: Suowen Xu, University of Rochester, United States; Sivareddy Kotla, The University of Texas MD Anderson Cancer Center, United States

                *Correspondence: Wei Guo, guoweiplagh@ 123456sina.com

                This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology

                Copyright © 2020 Wang, Zhang, Cao, He, Ma and Guo.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 30 August 2019
                : 21 January 2020
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 73, Pages: 8, Words: 0
                Mini Review

                Anatomy & Physiology
                aortic dissection,macrophage,inflammation,ang ii,aortic wall
                Anatomy & Physiology
                aortic dissection, macrophage, inflammation, ang ii, aortic wall


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