Abstract P573: The Interplay Between Mineral and Skeletal Metabolism Biomarkers and Intracranial Internal Carotid Artery Calcifications in Stroke Patients

Abstract

Background: Intracranial internal carotid artery calcifications (IICAC), considered a phenomenon within the spectrum of atherosclerosis and vascular aging, are frequently encountered in ischemic stroke patients. While intimal IICAC directly contributes to ischemic stroke pathophysiology, the medial counterpart is generally deemed as a risk factor for vascular end-points. Apart from aging and cardiovascular risk factors, the underlying pathophysiology that contributes to development of IICAC is not well understood; herein we studied the interplay between mineral and skeletal metabolism biomarkers, and IICAC presence and pattern. Methods: In a prospective series of 194 ischemic stroke patients (mean±SD age: 69±14 yr), blood samples were collected to determine calcium, phosphorus, magnesium, osteocalcin, parathyroid hormone, and vitamin D levels within 72 hours of symptom onset. IICAC presence and type was determined on admission CT-angiography source images; a medial or intimal type of IICAC category was assigned according to Kockelkoren criteria. Results: A total of 45 (23%) patients had no calcifications, while 95 (49%) had an intimal pattern and 54 (28%) had non-intimal (or medial) pattern. Apart from the well-known factors related with IICAC, such as age, lower glomerular filtration rate (GFR), history of hypertension, diabetes mellitus, coronary artery disease and atrial fibrillation, we identified admission magnesium levels to be associated with IICAC presence and pattern (no calcification: 1.96±0.18 mEq/L, intimal calcification 1.93±0.19 mEq/L, medial calcification: 1.81±0.28 mEq/L; p=0.006). None of the other biomarkers had any significant relationship to IICAC. In multivariate models, a lower magnesium level was significantly associated with medial calcification (each 0.1 mEq/L drop increased the odds by 1.2 (95% CI 1.0-1.4; p=0.046)), in addition to older age, history of diabetes mellitus and lower GFR. Conclusion: Hypomagnesemia is one of the factors well-known to be associated with vascular calcifications in the body. Our findings, extend this relationship to the intracranial vascular bed. No similar association was observed for other biomarkers related to mineral and skeletal metabolism. (Funding: TUBITAK grant 218S753)