Jaechun Hwang

Characterization of the Infarct Pattern Caused by Vulnerable Aortic Arch Atheroma: DWI and Multidetector Row CT Study

Background: Aortic arch atheroma (AAA) has been accepted as a possible embolic source in patients with ischemic stroke, especially cryptogenic stroke. However, despite its well-known role as a risk factor for stroke, research focused on the mechanism or characteristics of stroke caused by AAA is insufficient. In this study, we aimed to evaluate clinical and radiological characteristics including lesion pattern on DWI in acute stroke patients associated with vulnerable AAA detected by multidetector row computed tomography (MDCT). Methods: From September 2008 through May 2011, patients who presented with acute ischemic stroke and underwent MDCT were found in a prospective stroke registry. Patients without evident stroke etiology were included and classified by presence of vulnerable AAA. Vulnerable AAA was defined as (i) at least 6 mm thick adjacent to the aortic wall; (ii) ulcerated plaque, or (iii) soft plaque. Soft plaque was defined as the presence of clearly visualized area of hypoattenuation (<80 Hounsfield units) suggestive of thrombus. The patients without vulnerable AAA were classified as no/simple AAA group. The characteristics of diffusion-weighted MRI (DWI) lesions were analyzed in terms of the number and size of the lesions, and the involved vascular territories. Results: A total of 63 cryptogenic stroke patients were included in this study. Vulnerable AAA was observed in 15 (23.8%) patients. The patients with vulnerable AAA were older than those with no/simple AAA (p = 0.026). DWI analysis revealed that the vulnerable AAA group had a greater chance of having multiple and small lesions in multiple vascular territories that were mainly located in cortical and border-zone regions than the no/simple AAA group. Multiple logistic regression analysis showed that age (odds ratio 1.17; 95% confidence interval 1.02–1.34) and multiple small lesions in multiple vascular territories (odds ratio 33.18; 95% confidence interval 4.26–258.45) were independently associated with vulnerable AAA. Conclusion: Vulnerable AAA is independently associated with a DWI pattern characterized by multiple small scattered lesions in multiple vascular territories in conjunction with age. It may help determine stroke mechanism quickly and easily, and provide more information about the pathomechanism of vulnerable AAA-related stroke.

Microembolic Signals in Acute Posterior Circulation Cerebral Ischemia Sources and Consequences

Background and Purpose— The clinical significance of microembolic signals (MES) in the posterior circulation remains unclear. The aim of this study was to investigate the sources and consequences of MES in acute posterior circulation cerebral ischemia. Methods— We evaluated a total of 140 consecutive patients (93 males, mean age 62.9 years) who had acute posterior circulation cerebral ischemia. The MES monitoring was conducted at the basilar artery through the suboccipital window for a 30-minute period. Results— MES were detected in 18 (12.9%) of the 140 patients. Clinical characteristics and laboratory data did not differ between the MES-positive and MES-negative groups. Intracranial vertebrobasilar artery (VBA) stenosis was independently associated with the presence of MES (odds ratio, 9.85; 95% confidence interval, 1.22–79.48; P=0.032), whereas the patients with vertebral artery stenosis that was limited to the extracranial portion did not show an association. Microembolic signals occurred significantly more frequently in patients with severe degree of VBA stenosis compared to those with nonsignificant stenosis (odds ratio, 9.88; 95% confidence interval, 1.23–79.07; P=0.031). In a subgroup analysis of the 79 patients who had lesions on diffusion-weighted images and relevant VBA stenosis, the MES-positive group showed more frequent embolic infarction (P=0.010) and multiple lesion patterns (P=0.007) than single perforating infarctions. Conclusions— In acute posterior circulation cerebral ischemia, intracranial and severe VBA stenosis is associated with MES and may be its root causes. The presence of MES in VBA stenosis suggests that multiple and embolic type infarctions are the mechanisms of stroke.

Echoing Plaque Activity of the Coronary and Intracranial Arteries in Patients With Stroke

Background and Purpose— Atherosclerosis is a systemic disease, and both coronary and intracranial atherosclerosis are common in the elderly. Unlike coronary artery disease (CAD), intracranial atherosclerotic disease can cause intracranial atherosclerotic stroke by branch occlusive disease (B-type) and coronary-type rupture of plaque (C-type). We hypothesized that plaque characteristics of intracranial arteries are associated with those of coronary arteries. Methods— Eighty-one patients with acute cerebral infarcts caused by intracranial atherosclerotic disease without history of CAD were analyzed. Asymptomatic CAD burden (number and degree of stenosis) and plaque characteristics (calcified, mixed, and noncalcified) were measured with multidetector computed tomography, whereas the asymptomatic intracranial atherosclerotic disease burden was measured using magnetic resonance angiography. The symptomatic intracranial artery was analyzed using high-resolution magnetic resonance imaging for vascular morphology (stenosis degree, remodeling index, and wall index) and plaque activation (enhancement pattern and volume). Results— The asymptomatic CAD burden was correlated with the asymptomatic intracranial atherosclerotic disease burden. The overall CAD burden did not differ between B- and C-type intracranial atherosclerotic stroke. However, the prevalence of noncalcified coronary plaque was much higher in C-type intracranial atherosclerotic stroke and the presence of coronary noncalcified plaque was independently associated with C-type intracranial atherosclerotic stroke (odds ratio, 3.38; 95% confidence interval, 1.05–10.85; P=0.041). As the number of coronary noncalcified plaques increased, positive remodeling and plaque enhancement increased in the symptomatic intracranial artery on high-resolution magnetic resonance imaging. Conclusions— Plaques within the intracranial and coronary arteries behave in similar ways. Our results suggest the need to evaluate and treat other vascular trees in patients with vulnerable plaques within a single arterial system.

Implications of CHA2DS2-VASc Score in Stroke Patients with Atrial Fibrillation: An Analysis of 938 Korean Patients.

Background and Aims: The aim of this study was to investigate the stroke mechanisms and associated conditions influencing the decision regarding stroke thromboprophylaxis in patients with atrial fibrillation (AF) plus ischemic stroke, according to the CHA2DS2-VASc score. Methods: We evaluated 938 consecutive patients with a diagnosis of AF plus transient ischemic attack/ischemic stroke. Based on the CHA2DS2-VASc scores, patients were stratified as score 0 or 1 (n = 151), score 2 (n = 146), score 3 (n = 213), score 4 (n = 185), or score ≥5 (n = 243). Results: Patients with a higher CHA2DS2-VASc score were more likely to have noncardioembolic stroke mechanism (p = 0.001). Large-artery atherosclerosis causing stenosis >50% was more frequently observed in the high CHA2DS2-VASc group (p < 0.001). Coronary artery disease and the use of antiplatelet agents were more prevalent in the higher group (p < 0.001). A high CHA2DS2-VASc score was associated with a higher frequency of cerebral microbleeds and a higher Fazekas grade for leukoaraiosis (p < 0.001). The HAS-BLED score was correlated with the CHA2DS2-VASc score (γ = 0.650; p < 0.001). Conclusions: A higher CHA2DS2-VASc score is associated with noncardioembolic mechanisms of stroke and with a higher risk of bleeding. Strategies to treat macro/microangiopathy such as use of statin for plaque stabilization, as well as oral anticoagulants with a lower bleeding risk, are needed in these patients.