The correlation between medial pattern of intracranial arterial calcification and white matter hyperintensities

Background Despite previously reported correlations between intracranial arterial calcification (IAC) and white matter hyperintensities (WMH), little is known about the relationship between IAC pattern and WMH. By differentiating intimal and medical IAC, we aimed to investigate the relationship between IAC pattern and WMH. Methods Consecutive patients with acute ischemic stroke were included. IAC pattern was categorized as intimal or medial on plain brain CT. The number of cerebral arteries involved by IAC for each patient was recorded. IAC severity of each artery was defined as focal or diffuse. On brain MRI, the burden of WMH was graded on a visual rating scale and classified as absent mild, moderate and severe. Multiple logistic regression was performed to examine the relationship between IAC and WMH. Results Among 265 recruited patients, intimal IAC was detected in 54.7% patients, medial IAC in 48.5% patients and coexistent (intimal and medial) IAC in 52.1% patients. Diffuse IAC was in 27.9% patients, all of which were medial IACs. WMH was found in 75.5% patients, including 105 patients (39.6%) with mild WMH, 69 (26.0%) with moderate WMH and 26 (9.8%) with severe WMH. The presence and severity of medial IAC were correlated with WMH occurrence ( p <0.001, respectively). Chi-square linear trend suggested the number of arteries involved by medial IAC ( p <0.001) and the severity of medial IAC ( p <0.001) were correlated with WMH burden. After adjusting age, hypertension, history of stroke and history of ischemic heart disease, multiple ordinal regression demonstrated a positive correlation between the number of arteries involved by medial IAC ( p <0.001) and the severity of medial IAC ( p <0.001) with the overall burden of WMH. Conclusions Medial IAC was correlated with the burden of WMH. The dose-effect relationship between IAC and WMH suggests the need of further investigations on shared underlying mechanisms of intracranial large artery disease and cerebral small vessel disease.