Quantity of intracranial calcification is not an independent predictor of stroke
CHICAGO—After adjustment for age and sex, intracranial calcification in the symptomatic artery—found on a multidetector CT angiography (MDCTA)—was not independently associated with infarcts in the symptomatic hemisphere, according to a study presented Monday at the 94th annual meeting of the Radiological Society of North America (RSNA).
The researchers hypothesize that the presence of intracranial calcification in the symptomatic artery is related to the presence of infarct on CT in the symptomatic hemisphere.
Philip Homburg, MD, from Erasmus Medical Center, University Medical Center in Rotterdam, the Netherlands, who presented the findings, said that MDCTA was used to assess and quantify calcification of the intracranial segment of the internal carotid artery.
The researchers studied 351 consecutive patients (59.5 male; mean age 62.4 years), who had cerebrovascular symptoms in the carotid artery territory with MDCTA. Patients with a likely cardioembolic stroke etiology (30 patients) or occluded internal carotid artery (20 patients) were excluded.
Homburg said they reviewed CT brain images for the presence of recent and old infarcts, and quantified intracranial calcification by manually drawing contours on axial images with a custom-made software tool. The Mann-Whitney U test and Logistic Regression were applied for statistical analysis.
He reported that intracranial calcification was present in 58 percent of the symptomatic carotid arteries, and infarcts were present in 43 percent of the symptomatic hemispheres.
The quantity of intracranial calcification was significantly higher in the symptomatic carotid artery of patients with infarcts in the symptomatic hemisphere (36 mm3) than in patients without infarcts in the symptomatic hemisphere (21 mm3).
However, Homburg noted that in n multivariate analysis after adjustment for age and sex, no independent relationship was found between the quantity of intracranial calcification in the symptomatic artery and infarcts in the symptomatic hemisphere. Before adjustment the “quantity of intracranial calcification was significantly higher in the symptomatic carotid artery of patients with infarcts in the symptomatic hemisphere than in patients without infarcts in the symptomatic hemisphere,” he said.
As a result of their findings, Homburg and colleagues concluded that quantity of intracranial calcification is not an independent predictor of stroke.
The researchers hypothesize that the presence of intracranial calcification in the symptomatic artery is related to the presence of infarct on CT in the symptomatic hemisphere.
Philip Homburg, MD, from Erasmus Medical Center, University Medical Center in Rotterdam, the Netherlands, who presented the findings, said that MDCTA was used to assess and quantify calcification of the intracranial segment of the internal carotid artery.
The researchers studied 351 consecutive patients (59.5 male; mean age 62.4 years), who had cerebrovascular symptoms in the carotid artery territory with MDCTA. Patients with a likely cardioembolic stroke etiology (30 patients) or occluded internal carotid artery (20 patients) were excluded.
Homburg said they reviewed CT brain images for the presence of recent and old infarcts, and quantified intracranial calcification by manually drawing contours on axial images with a custom-made software tool. The Mann-Whitney U test and Logistic Regression were applied for statistical analysis.
He reported that intracranial calcification was present in 58 percent of the symptomatic carotid arteries, and infarcts were present in 43 percent of the symptomatic hemispheres.
The quantity of intracranial calcification was significantly higher in the symptomatic carotid artery of patients with infarcts in the symptomatic hemisphere (36 mm3) than in patients without infarcts in the symptomatic hemisphere (21 mm3).
However, Homburg noted that in n multivariate analysis after adjustment for age and sex, no independent relationship was found between the quantity of intracranial calcification in the symptomatic artery and infarcts in the symptomatic hemisphere. Before adjustment the “quantity of intracranial calcification was significantly higher in the symptomatic carotid artery of patients with infarcts in the symptomatic hemisphere than in patients without infarcts in the symptomatic hemisphere,” he said.
As a result of their findings, Homburg and colleagues concluded that quantity of intracranial calcification is not an independent predictor of stroke.