Variations in intracranial arterial anatomy of the circle of Willis and their association with arteriosclerosis in patients with ischemic cerebrovascular disease

Abstract

Introduction: An estimated 20-31% of all people are born with a textbook anatomical configuration of the intracranial arteries comprising the Circle of Willis. Individuals with specific anatomical variants may be at elevated risk of intracranial arteriosclerosis, and possibly its sequelae of stroke and dementia, as the distribution of blood flow and pressure is known to be different in variants with missing arteries or arterial segments. Therefore, we studied the association of anatomical variation of intracranial arteries with arteriosclerosis.

Methods: Between December 2005 and October 2010, 1126 patients (mean age: 62.3 (SD: ±14.0) years, 48.0% female) were recruited, 59.9% of whom had ischemic stroke and 40.1% a transient ischemic attack (TIA). Within the routine diagnostic work-up for stroke, patients underwent cranial computed tomography (CT) angiography. These images enabled a detailed visualization of intracranial arteries, which allowed for the assessment of the anatomical configuration of the cerebral arteries, the anterior and posterior communicating arteries, the internal carotids, and the vertebrobasilar arteries. In addition, these images facilitated the identification of intracranial arterial calcifications, the defining feature of intracranial arteriosclerosis. Binomial logistic regression models adjusting for age, sex, and ethnicity were constructed to assess associations between intracranial artery variations and presence of intracranial arterial calcifications.

Results: An incomplete Circle of Willis, defined by aplasia of any arterial segment, was present in 875 (77.7%) patients. The most common variation found was aplasia of the right posterior communicating artery, in 52.0% of patients. Men more often presented with an incomplete anatomy as compared to women (adjusted odds ratio: 1.36 (95% CI = 1.02-1.81)). Intracranial artery calcification was present in 59.2% of patients. Incompleteness of the intracranial arteries was not associated with the presence of any intracranial artery calcification (0.95 (0.68-1.34)). However, specific variants were associated with specific locations of intracranial artery calcification: The prevalence of vertebrobasilar artery calcification was lower among those with fetal-type posterior cerebral artery compared to individuals with a normal posterior cerebral artery (0.61 (0.38-0.99)). The prevalence of vertebrobasilar artery calcification was higher among those with a-/hypoplasia of both posterior communicating arteries as compared to those with normal posterior communicating arteries (1.63 (1.00-2.66)). Furthermore, patients with a-/hypoplastic left A1-segments had a higher prevalence of right internal carotid artery calcification as compared to people with a normal left A1-segment (2.30 (1.00-5.26)).

Conclusion: The prevalence of arteriosclerosis in the intracranial arteries on CT imaging varies among patients with certain anatomical variants of the intracranial arterial system. Specifically, arteriosclerosis in the right internal carotid artery and the vertebrobasilar arteries was more frequently observed in patients who had an a-/hypoplastic left anterior cerebral artery or a-/hypoplasia of both posterior communicating arteries, respectively. In addition, arteriosclerosis was less frequently observed among vertebrobasilar arteries of patients with a fetal-type posterior cerebral artery. Future longitudinal research is warranted regarding the anatomical configuration of intracranial arteries and the development of intracranial arteriosclerosis, as this line of research may reveal a novel group of people at elevated risk of cerebrovascular disease.

Keywords: Stroke; anatomy; arteriosclerosis; intracranial arterial diseases; vascular calcification.

Graphical abstract

Figure 1.

Axial maximum intensity projection examples of specific variants of the intracranial arteries. Panel (a) aplastic right A1 segment, (b) aplastic right P1 segment, (c) aplastic posterior communicating arteries, (d) left vertebral artery terminating in a posterior inferior cerebellar artery.

Figure 2.

Combined histogram plot depicting frequency of combinations of variant arteries. Basilar, carotid and medial cerebral arteries left out due to low case numbers of variants.