MASSIVE AORTIC ATHEROMA AS CAUSE OF ISCHEMIC STROKE

Abstract

Therapeutic Area

CVD Prevention – Primary and Secondary

Case Presentation

A 78-year-old-male was referred for assessment of the etiology of a symptomatic ischemic stroke in the right cerebellum. Vascular imaging including CT angiogram of the head and neck as well as prolonged electrocardiogram monitoring did not reveal a cause of his stroke.

A transesophageal echocardiogram (TEE) demonstrated no embolic source in the cardiac chambers and no intra-atrial shunt was identified. However, upon inspection of the descending thoracic aorta, a large atheroma was visualized measuring 2 cm in diameter and 0.7 cm thick (Figure). This finding led to a CT to further characterize this lesion. CT demonstrated non-calcified atherosclerotic plaque in the descending thoracic aorta which was determined to be the likely etiology of the stroke.

The identification of significant atherosclerotic plaque led to aggressive secondary prevention with the addition of aspirin 81 mg and high-intensity statin therapy. The patient's LDL cholesterol decreased from 120 mg/dL prior to the event to 42 mg/dL 12 weeks after initiating high-intensity statin therapy. At 1-year follow-up the patient has had no neurologic events and is tolerating therapy well.

Background

After a cerebrovascular accident is diagnosed, testing is warranted to identify the etiology. Unless a known etiology is identified, testing typically includes laboratory studies, prolonged ambulatory cardiac monitoring, imaging of the head and neck vessels, and imaging of the cardiac structures. Cardiac imaging typically begins with a transthoracic echocardiogram (TTE). However, TTE lacks the spatial resolution to identify atheromatous disease in the descending thoracic aorta. Thus, further imaging with TEE is often necessary for imaging the aorta and to rule out an intra-cardiac shunt.

After the etiology of a stroke is defined, management focuses on aggressive risk factor modification. Recent guidelines recommend initiating high-intensity statin therapy with a goal of reducing LDL to reduce the risk of future sequela related to atherosclerosis. In this case, aggressive antiplatelet and lipid lowering therapy was initiated with a significant reduction in the patient's LDL cholesterol.

Conclusions

This case represents a massive descending aortic atheroma, identified on TEE, as the cause of an ischemic stroke that led to aggressive secondary risk factor modification.