Apolipoprotein(A) expression in intracranial aneurysms

Elevated serum levels of lipoprotein(a), a risk factor for atherosclerosis (AS), are also associated with the presence of asymptomatic intracranial aneurysms. AS is present in some aneurysms, but its contribution to aneurysm formation and growth is unclear. Apolipoprotein(a) [apo(a)], the active moiety of lipoprotein(a), is present in atherosclerotic circle of Willis vessels but not in normal circle of Willis vessels. We wished to determine whether apo(a) is present in intracranial aneurysms independently of AS.

With a purified anti-apo(a) monoclonal antibody, aneurysms (n = 25) and feeding vessels (n = 23) were examined for apo(a) expression by immunohistochemical analysis. Circle of Willis arteries with and without AS (n = 19), cavernous angiomas (n = 5), and arteriovenous malformations (n = 6) acted as control samples.

AS was present in 32% of aneurysms, and all of those aneurysms demonstrated mural immunopositivity for apo(a). However, aneurysms devoid of AS also demonstrated apo(a) immunopositivity. Apo(a) was demonstrated in 86% of available feeding vessels. Apo(a) deposition was not observed in cavernous angiomas but was present in arteriovenous malformations. Eleven Circle of Willis arteries (57.9%) were devoid of AS and demonstrated no apo(a) immunostaining, whereas the eight (42.1%) with AS were immunopositive for apo(a).

Apo(a) expression in intracranial aneurysms may occur independently of AS. Apo(a) in feeding vessels suggests a possible role for apo(a) in early events leading to aneurysm formation. Multilayered transmural apo(a) deposition in established aneurysms suggests apo(a) involvement in aneurysm growth, possibly via cycles of injury and repair. The absence of apo(a) in cavernous angiomas suggests that such injury might be pressure-mediated.