Abstract

Background: Atherosclerosis is a systemic disease, and both coronary and intracranial atherosclerosis are common in elderly. Unlikely to coronary artery disease (CAD), intracranial atherosclerotic disease (ICAD) can cause stroke by branch occlusive disease-type (B-type ICAS), subcortical infarcts caused by parent arterial disease occluding perforator’s orifice as well as coronary type rupture of plaque (C-type ICAS).Vascular pathophysiology of coronary atherosclerosis in relationship with different phenotypes of intracranial atherosclerosis is unknown. Methods: We prospectively recruited 69 patients with acute cerebral infarcts caused by ICAS who had no history of CAD. Patients underwent both cardiac multidetector computed tomography (MDTC) and brain high-resolution MRI (HR-MRI). Symptomatic steno-occlusive intracranial artery at the maximal stenosis on MRA was analyzed in terms of vascular morphology (stenosis degree, remodeling index, and wall index) and activation (enhancement pattern and volume) using HR-MRI. Asymptomatic CAD burden (number and degree of stenosis) and plaque characteristics (calcified, mixed, and non-calcified) were measured with MDCT. The degree of asymptomatic ICAD was also measured in each patient (number of stenotic arteries and degree of stenosis). Results: The mean age of the patients were 65.1±1.5 years, 59.4% were male, and 35 (51.7%) were diagnosed with C-type ICAS. Asymptomatic CAD was observed in most patients, and increase in CAD burden was associated with increased asymptomatic ICAD (p<0.01). Overall CAD burden were not different between B-type and C-type ICAS. However, prevalence of non-calcified coronary plaque were much higher in C-type ICAS (35.3% vs 62.9%, p=0.02). C-type ICAS group also showed higher degree of stenosis (40.4 ±34.5 vs 77.3±17.3, p<0.001), increased positive remodeling index (1.0±0.3 vs 1.3±0.5, p=0.03), and larger proportion of vessels with enhancement (73.5% vs 97.1%, p<0.01) in cerebral arteries compared to B-type ICAS. Conclusions: Plaque characteristics of intracranial and coronary behave in same way. Further studies are needed to find systemic factors associated both intracranial and coronary plaque progression.

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