Asymptomatic abdominal aortic aneurysms show histological signs of progression: a quantitative histochemical analysis.
OBJECTIVE
Abdominal aortic aneurysm (AAA) is a serious disease due to its covert nature, relatively high prevalence and fatal prognosis in the case of rupture. To obtain new insights into AAA pathogenesis, we examined the relationships between histopathology, multiplex in vitro immunoassay data, diameter and symptomatology.


METHODS
In a prospective, non-randomised study, we evaluated samples from 6 normal infrarenal aortae and 65 AAA patients (65 walls, 55 thrombi). The AAA patients were either asymptomatic (n = 44), symptomatic (n = 7) or with ruptured AAA (n = 14). The AAA diameter was classified as small (<5 cm, n = 18), medium (5-7 cm, n = 26) and large (>7 cm, n = 21). We quantified the histopathology of the AAA wall and the adjacent thrombus. We assessed the expression of proteins in the same samples.


RESULTS
Asymptomatic AAAs had walls with more abundant inflammatory infiltrates, lower amounts of PAI-1, a higher number of tPA-positive elements, a tendency towards decreased collagen content, whereas the adjacent thrombi had a greater concentration of VCAM-1 and MMP-2 when compared with symptomatic AAAs. Compared with the aneurysmatic aorta, the normal aorta contained less collagen and more elastin, actin, desmin and PAI-1-positive elements; in addition, it was more vascular. Medium-sized AAAs were the most actin and vimentin rich, and large AAAs were the most vascular.


CONCLUSIONS
Our results show that asymptomatic AAA walls often have more potentially deleterious histopathological alterations than symptomatic AAA walls. This result indicates that a progression from an asymptomatic AAA to rupture can be expected and screening patients who are at risk of rupture could be beneficial.
Department of Histology and Embryology, Faculty of Medicine in Pilsen, Charles University in Prague, Pilsen, Czech Republic.
Lada
L
Eberlová
Zbyněk
Z
Tonar
Kirsti
K
Witter
Věra
V
Křížková
Lukáš
L
Nedorost
Marie
M
Korabečná
Pavel
P
Tolinger
Jitka
J
Kočová
Ludmila
L
Boudová
Vladislav
V
Třeška
Karel
K
Houdek
Jiří
J
Moláček
Jindra
J
Vrzalová
Martin
M
Pešta
Ondřej
O
Topolčan
Jiří
J
Valenta
D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001012:Aorta, Abdominal / Q000378:metabolism / Q000473:pathology*; D017544:Aortic Aneurysm, Abdominal / Q000378:metabolism / Q000473:pathology*; D001019:Aortic Rupture / Q000378:metabolism / Q000473:pathology*; D058070:Asymptomatic Diseases; D003094:Collagen / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D018450:Disease Progression; D004549:Elastin / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism*; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011446:Prospective Studies; D013927:Thrombosis / Q000378:metabolism / Q000473:pathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D000199:Actins; D003893:Desmin; D017395:Plasminogen Activator Inhibitor 1; D019010:Vascular Cell Adhesion Molecule-1; D003094:Collagen; D004549:Elastin; D020778:Matrix Metalloproteinase 2