Discussion Until recently atherosclerosis was considered the primary cause for the formation of abdominal aorta aneurysms.1 Commonly observed atherosclerotic plaques in the intima of aneurysmatic aorta and processes associated with their formation and evolution, such as rupture and dissection secondary to the hemorrhagic conversion may influence the natural course of aneurysm, resulting in the reduction of wall strength and raise in the risk of aneurysm rupture. One of the main phenomenon taking place during blood vessel aging is the degradation of elastic fibers, which intensifies in such conditions as atherosclerosis, arterial hypertension and diabetes.3,4 Some studies indicated the high elastase activity in human aorta extracts, which increased exponentially with age and correlated with the severity of atherosclerotic lesions. The impairment of elastin/laminin receptor function and its permanent stimulation (e.g. during aging) was proven responsible for the overproduction of elastases and elastin degradation.4 The positive correlation between the concentration of elastin degradation products and aneurysm growth rate was found.5,6 The atherosclerosis-like process that was previously considered responsible for pathological aorta dilatation was not confirmed in recent studies.