Abdominal aortic aneurysm (AAA) is a prevalent and potentially life threatening disease. Many animal models have been developed to simulate the natural history of the disease or test preclinical endovascular devices and surgical procedures. The aim of this review is to describe different methods of AAA induction in animal models and report on the effectiveness of the methods described in inducing an analogue of a human AAA. The PubMed database was searched for publications with titles containing the following terms “animal” or ‘‘animal model(s)’’ and keywords “research”, “aneurysm(s)’’, “aorta”, “pancreatic elastase’’, “Angiotensin”, “AngII” “calcium chloride” or “CaCl2”. Starting date for this search was set to 2004, since previously bibliography was already covered by the review of Daugherty and Cassis (2004). We focused on animal studies that reported a model of aneurysm development and progression. A number of different approaches of AAA induction in animal models has been developed, used and combined since the first report in the 1960’s. Although specific methods are successful in AAA induction in animal models, it is necessary that these methods and their respective results are in line with the pathophysiology and the mechanisms involved in human AAA development. A researcher should know the advantages/disadvantages of each animal model and choose the appropriate model.
Cerebrovascular reserve capacity (CVRC) is a hemodynamic parameter indicating the brain’s capacity to overcome ischemia. Transcranial Doppler
(TCD) is a useful device to measure CVRC, with high availability and low cost. The aim of the study is to investigate asymptomatic patients with affected CVRC, who could benefit from CEA. One hundred and forty five consecutive patients (60 symptomatic and 65 asymptomatic), with internal
carotid artery (ICA) stenosis >70 % and 20 healthy individuals without internal carotid stenosis underwent TCD-inhalation CO2 tests in order to measure the CVRC in both hemispheres of each patient. CVRC between asymptomatic and symptomatic patients were significantly different in the 95% confidence interval (CI) as well as the mean CVRC value in contralateral carotid artery. The correlation between CVRC in the carotid
artery with stenosis and the existence of symptoms is significant at the 0.01
level. Additionally, symptoms and CVRC of the contralateral carotid artery are also significant at the 0.05 level and CVRC values in asymptomatic patients and the control group at the 0.01 level. None of the covariant factors, except the age, are significantly correlated with CRVC. CVRC could be an early mark-index to evaluate the risk of stroke in this group of patients
and to design their therapeutic approach.