Clinical approaches in the treatment of extracranial carotid artery aneurysms

Abstract

Extracranial carotid artery aneurysms (ECAA) are rare and have an unknown incidence. Little is known about its natural clinical course, optimal treatment and its association with other aneurysms. The average age of patients with an ECAA is 50 years. A better understanding of the natural clinical course, optimal work-up and treatment of these relatively young patients is needed. To study the prevalence and the association with other vascular aneurysms, we investigated the co-prevalence of ECAA in patients with an intracranial aneurysm (IA). About 2-4% of patients with an IA seem to also have an ECAA. This is based on retrospective research with incomplete imaging of the carotid arteries, suggesting that ECAA may be even more prevalent. Most ECAA are reported to be caused by atherosclerosis and dissection. Factors influencing vessel wall changes and the formation of an ECAA remain unclear. We explored whether changes of nerve fiber density occurred in ECAA and popliteal artery aneurysms (PAA) and compared them to healthy arteries of both groups. ECAAs showed a non-significant higher overall nerve density as compared to PAAs. Healthy carotid arteries showed a higher nerve density then the popliteal arteries. Also, ECAA had a non-significant higher density of scattered nerve fibers then the healthy carotid arteries. This suggests that outgrowth of nerve fibers from pre-existing bundles may be related to inflammation and aneurysm formation. Another method for visualizing inflammation in aneurysms is administration of gadolinium during MRI. This results in enhancements of sites with inflammation. We investigated whether Gadolinium enhancement was present in patients with a conservatively treated ECAA. Enhancement was present in the majority of ECAA. This imaging method seems like a useful tool to study arterial wall behavior over time. We investigated whether microvascular cerebral damage was visible in ECAA patients, seen as white matter lesions (WML) on MRI. These WML were present in most asymptomatic ECAAs. It remains unclear whether the visual scale for the assessment of WML is accurate, if WML is a part is of a systemic disease and if it will increase over time. Increased arterial tortuosity has been suggested as a predisposing factor for carotid artery dissection, which is a risk factor for development of ECAA. We compared four different software packages for semi-automatic tortuosity measurements. All had reproducible and comparable measurements, with an acceptable inter-observer agreement, and are all therefore valid for measuring tortuosity. Our retrospective case series showed that patients with an asymptomatic ECAA have a rate of ischemic stroke in the aneurysm territory of 1.1 per 100 patient years. Most aneurysms do not grow over time and remain asymptomatic. Our systematic review shows the lack of evidence and treatment guidelines. The majority of the published data on ECAA report the surgical treatment and short-term outcome of symptomatic ECAA. A conservative strategy may be warranted for the asymptomatic, non-growing aneurysms, with or without medication. For symptomatic or growing aneurysm, the treatment of choice is surgical repair, with resection of the aneurysm and reconstruction of the blood flow. Endovascular techniques with stent placement is the alternative treatment for patients that cannot undergo surgery due to different comorbidities, high risk of surgical complications, or in patients with anatomical variations. Insights for the optimal treatment may be gained within a few years with the international registry.