Cerebral Aneurysms: Formation, Progression, and Developmental Chronology

Etminan, Nima; Buchholz, Bruce A.; Dreier, Rita; Brückner, Peter; Torner, James C.; Steiger, Hans‐Jakob; Hänggi, Daniel; Macdonald, R. Loch

doi:10.1007/s12975-013-0294-x

Cited by 56 publications

(28 citation statements)

References 66 publications

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“…Cerebral arteries have a well‐developed IEL but lack the EEL (Figure A). Moreover, the low amount of connective tissue within subarachnoid space together with the thin media and adventitia of cerebral arteries make them more susceptible to hemodynamic forces and at risk to develop aneurysms . Histologically, the aneurysmal wall composition and organization are quite different from the ones of a healthy cerebral artery (Figure A‐D).…”

Section: Pathogenesis Of Iasmentioning

confidence: 99%

Role of hemodynamics in initiation/growth of intracranial aneurysms

Diagbouga

Morel

Bijlenga

et al. 2018

Eur J Clin Investigation

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Background: Intracranial aneurysm (IA) is a disease of the vascular wall resulting in abnormal enlargement of the vessel lumen. It is a common pathology with a prevalence of 2%-3% in the adult population. IAs are mostly small, quiescent and asymptomatic; yet, upon rupture, severe brain damage or even death is frequently encountered. In addition to clinical factors, hemodynamic forces, mainly wall shear stress (WSS), have been associated with the initiation of IAs and possibly with their risk of rupture. However, the mechanism by which WSS contributes to aneurysm growth and rupture is not completely understood. Design: PubMed and Ovid MEDLINE databases were searched. In addition, key review articles were screened for relevant original publications. Results: Current knowledge about the relation between WSS and IA has been obtained from both computational fluid dynamic studies in patients and experimental models of IA formation and growth. It is increasingly recognized that a high wall shear stress (gradient) participates to IA formation and that both low and high WSS can drive IA growth. Primary cilia (PC) play an important role as mechanosensors as patients with polycystic kidney disease, which is characterized by the absence or dysfunction of PC, have increased risk to develop IAs as well as increased risk of rupture. Conclusion: Wall shear stress is a key player in IA initiation and progression. It is involved in vascular wall remodelling and inflammation, processes underlying aneurysm pathophysiology. K E Y W O R D Sendothelium, intracranial aneurysms, primary cilium, wall shear stress

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Section: Pathogenesis Of Iasmentioning

confidence: 99%

Role of hemodynamics in initiation/growth of intracranial aneurysms

Diagbouga

Morel

Bijlenga

et al. 2018

Eur J Clin Investigation

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“…Venous hypertension may lead to bleeding into the subarachnoid space or brain parenchyma due to rupture of fragile, thin-walled cortical veins (Pradhan et al, 2007). Moreover, the sinus thrombosis, due to thrombophilia in some patients, may produce dilatation of the cortical veins, which may rupture and bleed into the subarachnoid space and produce subsequent SAH (Cheng et al, 2014; de Bruijn et al, 2000; Etminan et al, 2014). However, the precise mechanism of vein-induced hemorrhage remains unknown.…”

Section: Vein-mediated Pathophysiology After Acute Brain Injurymentioning

confidence: 99%

Venous system in acute brain injury: Mechanisms of pathophysiological change and function

Chen

et al. 2015

Experimental Neurology

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Cerebral vascular injury is a major component of acute brain injury. Currently, neuroprotective strategies primarily focus on the recanalization of cerebral arteries and capillaries, and the protection of insulted neurons. Hitherto, the role of vein drainage in the pathophysiology of acute brain injury has been overlooked, due to an under appreciation of the magnitude of the impact of veins in circulation. In this review, we summarize the changes in the vein morphology and functions that are known, or likely to occur related to acute brain injury, and aim to advance the therapeutic management of acute brain injury by shifting the focus from reperfusion to another term: recirculation. Recent progress in the neurobiological understanding of the vascular neural network has demonstrated that cerebral venous systems are able to respond to acute brain injury by regulating the blood flow disharmony following brain edema, blood brain barrier disruption, ischemia, and hemorrhage. With the evidence presented in this review, future clinical management of acutely brain injured patients will expand to include the recirculation concept, establishing a harmony between arterial and venous systems, in addition to the established recanalization and reperfusion strategies.

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Section: Introductionmentioning

confidence: 99%

“…1 Subarachnoid hemorrhage, following rupture of CA, is a major cause of death or disability in these patients. 1 The etiology of CA involves hemodynamic stress and inflammation, with similarities and important differences to abdominal aortic aneurysms (AAA). 1–4 Treatment for both unruptured and ruptured CA is surgical, with coiling and clipping to prevent rupture and re-rupture; there is no pharmacological treatment.…”

Section: Introductionmentioning

confidence: 99%

Myeloperoxidase Is Increased in Human Cerebral Aneurysms and Increases Formation and Rupture of Cerebral Aneurysms in Mice

Chu

Wilson

et al. 2015

Stroke

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Background and purpose Cerebral aneurysm (CA) affects 3% of the population and is associated with hemodynamic stress and inflammation. Myeloperoxidase (MPO), a major oxidative enzyme associated with inflammation, is increased in CA patients, but whether MPO contributes to CA is not known. We tested the hypotheses that MPO is increased within human CA and is critical for formation and rupture of CA in mice. Methods Blood was drawn from the lumen of CAs and femoral arteries of 25 patients who underwent endovascular coiling of CA, and plasma MPO concentrations were measured with ELISA. Effects of endogenous MPO on CA formation and rupture were studied in MPO knockout (KO) mice and wild-type (WT) mice using an angiotensin II-elastase induction model of CA. In addition, effects of MPO on inflammatory gene expression in endothelial cells were analyzed. Results Plasma concentrations of MPO were 2.7-fold higher within CA than in femoral arterial blood in CA patients. MPO-positive cells were increased in aneurysm tissue compared with superficial temporal artery of CA patients. Incidence of aneurysms and subarachnoid hemorrhage was significantly lower in MPO KO than in WT mice. In cerebral arteries, proinflammatory molecules including TNFα, COX2, CXCL1, MMP8, CD68 and MMP13, and leukocytes were increased, and α-smooth muscle actin was decreased, in WT but not in MPO KO mice after induction of CA. MPO per se increased expression of VCAM1 and ICAM1 in endothelial cells. Conclusions These findings suggest that MPO may contribute importantly to formation and rupture of CA.

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Cerebral Aneurysms: Formation, Progression, and Developmental Chronology

Cited by 56 publications

References 66 publications

Role of hemodynamics in initiation/growth of intracranial aneurysms

Role of hemodynamics in initiation/growth of intracranial aneurysms

Venous system in acute brain injury: Mechanisms of pathophysiological change and function

Myeloperoxidase Is Increased in Human Cerebral Aneurysms and Increases Formation and Rupture of Cerebral Aneurysms in Mice

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