Ascending aorta thrombus adjacent to a cholesterol-rich plaque as the source of multiple emboli

Abstract

Ascending aortic thrombus causing thromboembolism in the absence of hyper-coagulable states is a rare occurrence. We present a case of a 40-year old healthy female smoker who presented with a 6-month history of three transient ischaemic attacks, hand pain and numbness despite being on dual anti-platelet therapy. Computed tomography revealed a mid-ascending aorta thrombus. She underwent ascending aorta replacement on cardiopulmonary bypass, but without the use of circulatory arrest. She recovered uneventfully. We identified a fresh thrombus adjacent to a soft, cholesterol-rich plaque as the culprit lesion. We advocate surgical excision of such lesions as the only way of removing the underlying cause of thromboembolism. In addition, rupture-prone aortic plaques may lead to a penetrating aortic ulcer or an intramural haematoma and ultimately aortic dissection.

INTRODUCTION

The presence of a thrombus in the ascending aorta is a rare cause of peripheral embolization, especially in the absence of hyper-coagulable states. We present a case of a floating thrombus in the ascending aorta adjacent to a lipid-laden atherosclerotic plaque that caused multiple embolic phenomena.

CLINICAL SUMMARY

A 40-year old female presented to the Emergency Department with a 1-day history of pain and numbness in her left hand. She was under investigation by her family doctor, having experienced three transient ischaemic attacks over the preceding 6-month period. She was already on dual anti-platelet therapy. Her past medical history was unremarkable, and there was no family history of vascular disease. She continued to smoke 20 cigarettes per day. On examination, all peripheral pulses were present and there was no carotid or subclavian bruit. She was in sinus rhythm and heart sounds were normal. She was noted to have a dusky appearance of the fingertips in her left hand. Neurological examination was normal.

Blood profiles were normal, as were screening tests for vasculitis, anti-phospholipid syndrome, lupus anticoagulant and paroxysmal nocturnal haemoglobinuria. Transthoracic echocardiography revealed good biventricular systolic function with a normal ascending aorta with no evidence of thrombus or dissection. Duplex assessment demonstrated normal carotid and upper limb arteries. A computed tomography (CT) scan of the thoracic aorta was performed, which showed a mural thrombus in the ascending aorta at the level of the pulmonary trunk (Fig. 1). Neither significant coronary vessel disease nor valvular abnormalities were identified. A brain CT scan was normal.

Figure 1:

(A) CT aortogram shows a filling defect in the mid-ascending aorta highly suggestive of thrombus (lateral view). (B) Three-dimensional reconstruction (antero-posterior view).

The patient underwent replacement of the ascending aorta. An intraoperative transoesophageal echocardiography and epiaortic ultrasound confirmed the presence of a hyperechoic mass in the mid-ascending aorta. A transverse aortotomy was performed and a fresh friable thrombus with adjacent gelatinous platelet aggregates next to a soft cholesterol-rich atherosclerotic plaque was identified (Fig. 2). The aorta was otherwise unremarkable. A 3-cm segment of the ascending aorta was excised and replaced with a Dacron graft. Pathological examination confirmed the findings mentioned above. The patient made a good recovery and was discharged home on the sixth postoperative day.

Figure 2:

(A) Transverse aortotomy revealed a thrombus on the left lateral wall of a non-atherosclerotic mid-ascending aorta. (B) Surgical specimen of the excised ascending aorta. (C and D) Soft, cholesterol-rich plaque (thick arrow) with adjacent fresh thrombus and multiple small gelatinous platelet aggregates (thin arrows).

DISCUSSION

Floating thrombi in the ascending aorta are extremely rare in the absence of hyper-coagulable states [1]. The underlying mechanism dictates management. Conservative management with anticoagulation or antiplatelet therapy has been suggested. However, although this addresses the already formed thrombus and may prevent an increase in its size and thromboembolism, it does not treat the underlying cause. In the absence of hyper-coagulable states, the most common cause is atherosclerosis of the ascending aorta and/or aortic arch [2]. Although high-dose statins may have an anti-inflammatory effect on atherosclerosis [3], it has been suggested that atherothrombosis in the ascending aorta may be treated best with surgery [4, 5]. Sodian et al. [4] have treated a similar case with aspiration of the thrombus only. Our approach was more aggressive, as we believe that removal of the diseased aorta was the only way of preventing further thromboembolic phenomena. Indeed, intraoperative findings confirmed the presence of an ‘active’, cholesterol-rich atherosclerotic plaque with adjacent thrombus and platelet aggregates as the cause of multiple thromboembolisms (Fig. 2). In addition, such plaques are rupture-prone, which may lead to a penetrating aortic ulcer or an intramural haematoma with the ultimate potential for aortic dissection.

In summary, we present a case of a vulnerable ascending aortic plaque with an adjacent floating thrombus causing multiple thromboembolic phenomena. We believe that surgical removal of the underlying cause with replacement of the relevant aortic segment is the most appropriate treatment for the prevention of peripheral thromboembolism and dissection.