Predictors of Significant Coronary Artery Disease in Patients with Cerebral Artery Atherosclerosis

Objective: There are few existing data on the status of coronary artery disease (CAD) in patients with atherosclerosis of the cerebral artery detected by brain imaging studies. We aimed to analyze the predictors of asymptomatic angiographically significant CAD detected by simultaneous cerebral and coronary angiography. Methods: This retrospective cohort study screened data obtained between August 2009 and April 2019; 11,047 patients underwent cerebral angiography for atherosclerotic change (>50% stenosis or aneurysm) seen in brain magnetic resonance angiography (MRA) or computed tomography angiography (CTA) at a single center by endovascular neurosurgeon’s decision. Of these, 700 patients including 622 patients who underwent simultaneous coronary and cerebral angiography and 78 patients who underwent coronary angiography within a month were enrolled. We investigated the characteristics and predictors of angiographically significant CAD (>50% stenosis). Furthermore, we also analyzed the major adverse cardiovascular and cerebrovascular events (MACCE), including all-cause death, myocardial infarction, and stroke for 5 years. Results: The frequency of significant CAD was 59% (413/700), the mean age was 68.9 ± 10.3 years, and 60.6% were male. During mean follow-up of 50 months, the MACCE rate of our whole cohort was significantly higher in the CAD group (21.5%) than in the non-CAD group (14.6%; hazard ratio 1.65, 95% CI 1.17–2.33, p value = 0.005). Considering that the embolic stroke is less associated with atherosclerotic change, our predictive model of significant CAD was made without embolic stroke (n = 599). In our multivariate model 2 including univariate <0.1, the independent predictors of significant CAD were male (OR 1.62, 95% CI 1.11–2.35, p = 0.012), diabetes mellitus (OR 1.81, 95% CI 1.22–2.68, p = 0.003), previous stroke (OR 1.63, 95% CI 1.02–2.60, p = 0.039), low ankle-brachial index (ABI; <0.9; OR 3.25, 95% CI 1.21–8.73, p = 0.019), left ventricular ejection fraction (EF) <50% on echocardiography (OR 2.82, 95% CI 1.25–6.35, p = 0.012), troponin I or T positive (OR 2.76, 95% CI 1.69–4.53, p < 0.001), and complex features on cerebral angiography (OR 2.73, 95% CI 1.78–4.19, p < 0.001). Conclusions: Accurate coronary evaluation by coronary angiography might be considered when patients with atherosclerotic cerebral artery detected on brain MRA or CTA planned cerebral angiography were male or have diabetes mellitus, previous stroke, low ABI (<0.9), left ventricular EF <50% on echocardiography, troponin I or T positivity, and complex features on cerebral angiography.

Abstract T P171: Impaired Brachial Flow-mediated Dilatation in Patients With Symptomatic Nontraumatic Intracranial Arterial Dissections

Background: Non-traumatic intracranial arterial dissections (IADs) are characterized by the sudden disruption of the internal elastic lamina in intracranial arteries. It is still unknown why IADs occurs. There are few reports concerned with relationship between the endothelial function and IADs. Purpose: The purpose of our retrospective study was to investigate whether or not patients with nontraumatic IADs had normal endothelial function. Methods: Included for retrospective analysis were patients with symptomatic nontraumatic IADs (1) who were admitted to our institution from 2012 to 2013 and (2) who underwent an endothelial function test during hospitalization. Headache patients admitted to outpatient clinic were selected as a control matched for sex and age. The endothelial function was assessed using flow-mediated dilatation (FMD). We investigated ankle brachial index (ABI) and pulse wave velocity (PWV) to determine the degree of atherosclerosis. Patients’ characteristics, brachial FMD, ABI and PVW were assessed in two groups. Results: During study periods, there were 14 patients (median age 45.5 years, IQR 38-53.5 years) with nontraumatic IADs. Fourteen patients of the control had median age of 47 years (IQR: 44-53.5 years). The locations of IADs were the vertebral artery (n=10), the internal carotid artery (n=3) and the superior cerebellar artery (n=1). Between two groups, there were no significant differences of clinical features, atherosclerotic risk factors, ABI and PWV except FMD, indicating that most of them did not suffer from atherosclerosis. However, FMD in IADs was significantly lower than in control (4.85 vs. 7.4, p<0.01) Conclusion: ur results suggest that the endothelial function of intracranial arteries might be impaired in patients with symptomatic nontraumatic IADs in spite of no atherosclerotic change.

The Protective Effect of Apamin on LPS/Fat-Induced Atherosclerotic Mice

Apamin, a peptide component of bee venom (BV), has anti-inflammatory properties. However, the molecular mechanisms by which apamin prevents atherosclerosis are not fully understood. We examined the effect of apamin on atherosclerotic mice. Atherosclerotic mice received intraperitoneal (ip) injections of lipopolysaccharide (LPS, 2 mg/kg) to induce atherosclerotic change and were fed an atherogenic diet for 12 weeks. Apamin (0.05 mg/kg) was administered by ip injection. LPS-induced THP-1-derived macrophage inflammation treated with apamin reduced expression of tumor necrosis factor (TNF)-α, vascular cell adhesion molecule (VCAM)-1, and intracellular cell adhesion molecule (ICAM)-1, as well as the nuclear factor kappa B (NF-κB) signaling pathway. Apamin decreased the formation of atherosclerotic lesions as assessed by hematoxylin and elastic staining. Treatment with apamin reduced lipids, Ca2+levels, and TNF-αin the serum from atherosclerotic mice. Further, apamin significantly attenuated expression of VCAM-1, ICAM-1, TGF-β1, and fibronectin in the descending aorta from atherosclerotic mice. These results indicate that apamin plays an important role in monocyte/macrophage inflammatory processing and may be of potential value for preventing atherosclerosis.