With a 3% prevalence in the general population, intracranial aneurysms (IA) are not rare. Asymptomatic and unruptured aneurysms are harmless, but growth is associated with rupture risk. Other characteristics, such as their location, morphology and certain risk factors can also increase their rupture risk, and small aneurysms can also sometimes rupture. Inflammation which drives their formation might also cause aneurysm to rupture. Aneurysms prone to rupture should be identified more efficiently, as an aneurysmal subarachnoid haemorrhage (aSAH) can be fatal or cause permanent disability. Although the pathophysiology of IA formation is yet incompletely understood, inflammation, endothelial dysfunction and loss of structural integrity have been found to be important pathophysiological issues.

Atherosclerosis is the common and well-established aetiology for the majority of cardiovascular diseases (CVD). Inflammation, lipid-accumulation, endothelial dysfunction and alterations in artery intima and media are all hallmarks of it’s pathophysiology. Atherosclerotic CVD is a widespread health issue associated with varying risk factors and comorbidities, and patients with IAs are one of the most recently found subpopulations to carry an excess burden of atherosclerotic CVDs.

The first study (I) of this dissertation investigates aortic calcification as a marker of atherosclerosis in IA patients and shows that aortic calcification is greater among IA patients than among matched controls. The second study (II) establishes the potential of aortic calcification as a prognostic factor in atherosclerotic population. The third study (III) investigates the association between the classical ankle-brachial index (ABI) and IAs and shows that IAs are clearly more prevalent among patients with low or borderline ABI values than among those with normal ABI values. The fourth study (IV) explores the soluble inflammatory profile of aortic atherosclerosis.