Focal histopathological progression of porcine experimental abdominal aortic aneurysm is mitigated by atorvastatin.

AIM: Observational studies in human patients and animal experiments suggested that statins have a potential in slowing the growth of small abdominal aortic aneurysms (AAA). Our aim was to quantify histological postoperative changes of AAA in porcine experimental model of AAA with and without administration of atorvastatin. METHODS: The AAA was induced by intraaortic infusion of porcine pancreatic elastase and subrenal application of plastic cuff. The AAA statin group (N.=14) received atorvastatin 1 mg/kg daily for 28 days, the other AAA group (N.=13) did not. The aortic diameter was measured by ultrasonography. Aortic samples were described using eleven quantitative histological parameters and compared with healthy aortae. RESULTS: There was no difference in aortic diameter between the AAA with statin when compared to AAA without statin. Administration of atorvastatin led to a better postoperative histological condition of the aortic elastin network, preservation of contractile phenotype of vascular smooth muscle, a higher density of vasa vasorum, it prevented thickening of intima and media. The increase in wall thickness in AAA without atorvastatin has not been accompanied by a proportional increase in number of vasa vasorum. CONCLUSION: The effects of atorvastatin seem to prevent the histopathological progression of AAA.

Quantification of plasminogen activator inhibitor type 1 in the aortic wall.

AIM: Plasminogen activator inhibitor type 1 (PAI-1) plays a key role in regulation of fibrinolytic system, cell-associated proteolysis and migration of smooth muscle cells (SMC). This study is focused on the types of PAI-1 expressing cells, quantification of PAI-1 expression in the walls of aneurysmatic abdominal aortas (AAA) and correlation between histological and clinical findings. METHODS: A group of nine patients who underwent surgery for AAA: asymptomatic (aAAA), symptomatic (sAAA) and ruptured (rAAA) and one control specimen (CA) were included in the study. Samples underwent histological processing and immunohistochemistry in comparison with in situ hybridisation. In order to assess the PAI-1 area fraction in histological sections through the aortic wall the Line System module of Ellipse software was used. PAI-1 expressing cells were measured in CA and AAA: endothelium, SMC, and foam cells. Photomicrographs with a total area of 0.7 mm(2) for each specimen were analysed by two independent observers. Mean values of PAI-1 positive components per section area were calculated as average values. RESULTS: The results of both observers are as follows: 28.6% in CA; 18.1% in aAAA; 10.9% in sAAA; 11.0% in rAAA. During the progression of AAA, the SMC (PAI-1 expression was found mainly in them) became less abundant in agreement with the values of PAI-1 area fraction. In rAAA immunohistochemistry detected PAI-1 in necrotic centres of atheromathous plaques. CONCLUSIONS: AAA may be evaluated as the result of gradual changes in regulation of fibrinolysis that is observed as redistribution of cells expressing PAI-1. The area fraction of PAI-1 positive components correlates with clinical classification of AAA.