Aortic Arch Plaque and Ischemic Stroke Detection Modalities and Statin Effects

Editorial

Austin J Cerebrovasc Dis & Stroke. 2014;1(5): 1025.

Aortic Arch Plaque and Ischemic Stroke Detection Modalities and Statin Effects

Kazuyoshi Kaneko1*

Department of Cardiology, Kitamurayama Municipal Hospital, Japan

*Corresponding author: Kazuyoshi Kaneko, Department of Cardiology, Kitamurayama Municipal Hospital, 2-15-1, Onsen-machi, Higashine, Yamagata 999-3792, Japan

Received: August 18, 2014; Accepted: September 26, 2014; Published: September 29, 2014

Keywords

Aortic Arch Plaque; Ischemic Stroke; Transesophageal Echocardiography; Statin

Abbreviations

CAP: Complicated Aortic Arch Plaque; TEE: Transesophageal Echocardiography; LDL-C: Low-Density Lipoprotein-Cholesterol; HDL-C: High-Density Lipoprotein-Cholesterol; Apoa-1: Apolipoprotein A-1; Apob: Apolipoprotein B

What should we do when severe aortic arch atheroma is detected on Transesophageal Echocardiography (TEE) in patients with ischemic stroke? Aortic arch atheroma is associated with atherosclerotic risk factors such as advanced age, hypertension, hypercholesterolemia, diabetes mellitus, and smoking [1,2]. In addition the importance of apolipoprotein A-1 (ApoA-1) and the ratio apolipoprotein B/A-1 on lipid profiles in thoracic aortic plaque detected by TEE has also been described in a recent clinical report [3]. Accordingly, aggressive and strict control of hypertension, hypercholesterolemia, diabetes mellitus and smoking cessation may be required.

What is the rationale for treating severe aortic arch atheroma? The answer has been shown over the past 20 years in many previous clinical reports concerning the correlation between aortic atheroma and ischemic stroke recurrence and death [1,4,5]. In these reports, aortic arch intima media thickness ≥4 mm increased ischemic stroke relative risk 4-9 fold, and aortic arch intima media thickness ≥5 mm increased all cause mortality [6]. Furthermore, characteristics of aortic arch atheroma such as low echoic status, lack of calcification, or presence of ulcerated and mobile plaques increased risk further [4]. Progression of aortic arch atheroma assessed by TEE over a 12 month period was associated with recurrent vascular events, suggesting the need for medical intervention such as use of statins, which may improve prognosis [7]. Recently new recommendations for treatment for aortic arch atheroma in patients with stroke and transient ischemic attacks published in the AHA/ASA guidelines have received widespread recognition [8]. According to theguidelines, prophylactic endarterectomy, aortic arch stenting, and anticoagulation with warfarin for purposes of stroke prevention are not recommended, whereas antiplatelet and statin therapies arerecommended with assignment to high grade evidence levels and recommendation class. Nevertheless, no randomized clinical trials have yet been reported which specifically examine the effectiveness of statin therapy for reducing the risk of first or recurrent stroke among patients with complex aortic plaque. However, observational studies among patients with a recent embolic event including stroke or transit ischemic attack suggest that statins may be effective in preventing recurrent events [9]. Although there are clinical reports showing that statins may reduce plaque volume and morphology based on intravascular ultrasound study of coronary arteries [10] or magnetic resonance imaging study of descending aortic plaque [11], few reports concerning aortic arch plaque regression have been published. Recently, we have reported that rosuvastatin improves aortic arch plaque morphology concomitant with improving lipid profiles in cerebral embolism patients with normal low-density Lipoprotein-Cholesterol (LDL-c) levels [12]. In this paper we studied Complicated Aortic Arch Plaque (CAP) morphology, defined as presence of atheromatous plaque with ≥4 mm wall thickness or presence of ulcerated or mobile plaque in the aortic arch. In a group of 56 acute cerebral embolism patients without hypercholesterolemia, defined as LDL-c below 140 mg/dl, CAP was detected in 24 patients (43%) despite their non-hypercholesterolemia status. However they were older and had lower serum levels of ApoA-1 and High- Density Lipoprotein-Cholesterol (HDL-c) than the group of 32 patients without CAP. Rosuvastatin was given to these 24 patients for 6 months, with a follow-up TEE in 18 of them. The results showed that aortic arch plaque surfaces were improved (Figure) in 11 of the 18 patients (61%) with no change in the other 6 of the 18 (33%). CAP diameter was significantly decreased, and was accompanied by an increase in ApoA-1 and HDL-c. No patients had recurrent ischemic stroke or died during the 6-month treatment period. The data suggest that rosuvastatin therapy may lead to CAP regression and inhibit progression to acute ischemic stroke in patients without hypercholesterolemia, and that rosuvastatin therapy may represent a beneficial option for treating CAP. Therefore when severe aortic arch atheroma is detected, statin therapy may be considered as additional antithrombotic therapy in not only dyslipidemic but also non-dyslipidemic ischemic stroke patients [9,12,13,14].

Citation: Kaneko K. Aortic Arch Plaque and Ischemic Stroke Detection Modalities and Statin Effects. Austin J Cerebrovasc Dis & Stroke. 2014;1(5): 1025. ISSN: 2381-9103.