Mobile Aortic Arch Research Articles

Abstract 13392: 3D TEE Aids in Assessment of Embolic Stroke Due to Aortic Atherosclerotic Plaque

Case Presentation: A 69-year-old right-handed man presented with new left-sided weakness and recurrent ischemic strokes. His had history of coronary artery disease, diabetes mellitus, hypertension, dyslipidemia, chronic kidney disease stage 3, obstructive sleep apnea and obesity. Plasma low-density lipoprotein was 127 mg/dL. Brain MRI showed diffusion restriction in the left caudate head, left corona radiata, left anterior lentiform nucleus, and left periventricular white matter from acute to subacute infarction. CT angiogram showed diffuse atheromatous disease in the anterior and posterior circulation, bilateral mild cervical internal carotid artery stenosis, and calcifications in the aortic arch ( Figure 1 ). Transthoracic echocardiogram (TTE) showed mild generalized left ventricular hypokinesis (ejection fraction 45%) without thrombus. Transesophageal echocardiogram (TEE) showed complex mobile atherosclerotic plaques in the aortic arch ( Figure 2 ) after which Apixaban & Clopidogrel were started and statins increased. At 1-year follow-up there was no recurrent stroke. Discussion: This case highlights the role of 3D TEE in the detection of complex aortic arch atherosclerotic plaque with mobile components as the etiology of recurrent embolic stroke. 2D TTE & TEE and CT chest were unable to show mobile components in the aortic arch plaque. Many patients identified as having “cryptogenic stroke” after 2D TTE & TEE may in fact have mobile aortic arch plaques which can only be delineated by 3D TEE, thus reducing the need for further workup and expediting appropriate treatment.

Vacuum to the Rescue: Aspiration of a Large Mobile Aortic Arch Thrombus With the AngioVac System Utilizing Transcaval Access

Vacuum to the Rescue: Aspiration of a Large Mobile Aortic Arch Thrombus With the AngioVac System Utilizing Transcaval Access

P2469The yield of transoesophageal echocardiography in embolic stroke of unknown source

Abstract Purpose Transthoracic echocardiography (TTE) and transoesophageal (TOE) are the main diagnostic tools for the detection of potential cardiac and aortic sources of embolism (PCSE). TOE is superior to TTE. However, its therapeutic impact is questioned. TOE is no longer recommended in ESUS (embolic stroke of unknown source), which is thought to be caused by undiagnosed atrial fibrillation (AF). Recent studies however report an about 10% change in therapeutic management due to TOE. We aimed to assess prospectively, in patients admitted to our stoke unit and diagnosed ESUS, the rate of treatment change induced by TOE. Methods Patients diagnosed with acute (≤7 days) ESUS were included to undergo TOE. ON TTE, PCSE, left ventricular ejection fraction (LVEF, %), left atrial area (LA-A, cm2), indexed left atrial volume (LAV, ml/m2) were recorded. On TOE, PCSE, left atrial appendage area (LAA-A, cm2), left atrial appendage emptying velocity (LAA-EV, cm/s) were recorded. PCSE on TTE and TOE were classified according to EAE guidelines. Results Between October 2016 and May 2018, 1322 TTEs were performed in patients admitted to our newly labelled stroke unit. ESUS was diagnosed in 152 patients, who underwent TOE. Mean delay (95% CI) between stroke onset and TTE was 2.2 days (1.9–2.5). Mean (95% CI) age was 61 years (58–63). 56/152 were female (37%). On TTE, mean (95% CI) LVEF was 62% (61–64), mean LA-A was 19 cm2 (19–20) and mean LA-V was 32 ml/m2 (31–34) ml/m2. In 38 patients, a major PCSE was identified by TTE. In 4 cases, there were 2 potential major PCSE and in one case 3. In 79 patients, at least one minor PCSE was identified by TTE, among which 35 PFO. On TEE, mean (95% CI) LAA-A and LAA-EV were: 5.2 cm2 (4.9–5.5) % and 76 cm/s (72–80) cm/s. In 50 patients, a major PCSE was identified by TOE. Eleven patients had 2 major PCSE. In 115 patients, at least one minor PCSE was identified by TOE, among which 34 PFO. According to EAE guidelines, a treatment change induced by TOE occurred in 12 patients. Anticoagulation in 5 patients (aortic arch thrombus in 2, thrombus of the proximal descending aorta in 1, LAA thrombus in 1, and thrombotic non-infectious vegetations in 2). Surgery in one patient (LAA fibroelastoma), antibiotics in two patients with infectious endocarditis, One patient had aortic fibroelastoma not seen on TTE. Finally, two patients with mobile aortic arch debris had dual antiplatelet therapy (DAT). In two other patients, TOE showed a mitral fibroelastoma and a mobile aortic arch thrombus, but these abnormalities were already seen on TTE, hence not taken into account. When considering the eight patients who had, at neurologist's discretion, the instauration of DAT for complex aortic arch atheroma, 12+8 patients had therapeutic modifications induced by TOE (13%). Conclusion Major PCSE on TOE lead to a treatment change in 12/152 patients (8%) according to EAE guidelines, and 13% when complex aortic arch atheroma was considered.

Mobile Aortic Arch Thrombi: Radiographic Image With Gross Pathology Correlation

60-year-old woman, a smoker, with a body mass 2 Aindex of 45 kg/m and a history of pulmonary embolism and taking warfarin, presented with chest pain. Computed tomography showed two filling defects on the aortic arch. Magnetic resonance angiography revealed a highly mobile 28 16 17-mm defect opposite the left common carotid artery (Fig 1A) and a 13 4.6-mm defect distal to the left subclavian artery (Fig 1B). The maximal aortic dimension was 37 36 mm. No gadolinium enhancement was seen. Aortic arch thrombi were diagnosed. She had no history of thromboembolic events,

Recurrent Cerebral Infarction Caused by Mobile Aortic Arch Thrombus Refractory to Warfarin Therapy

The mobile thrombus in the aortic arch is a rare condition, which becomes rarer when associated with cerebral infarction, resulting in disabling complications. Transesophageal echocardiography is useful for detecting the source of thrombi in the heart and aortic arch. Here, we report a case of a patient who suffered from recurrent cerebral infarction four times during the previous 18 months due to mobile thrombus in the aortic arch despite anticoagulant therapy. The thrombus with rocking motion (9.6 and 8 mm) was laid in the top of the aortic arch, and surgical resection was not allowed due to the location. We began anticoagulation therapy initially with heparin followed by a combination of warfarin, aspirin, and atorvastatin with an international normalized ratio between 2 and 3. The size of the aortic thrombi was significantly decreased by 3 mm and stabilized after 18 months.

Managing Severe Upper Extremity Ischemia from Mobile Aortic Arch Thrombus: A Novel Approach Using Isolated Limb Perfusion with Tissue Plasminogen Activator

Etiologies of upper extremity ischemia are numerous and include embolic aortic pathology. Traditional operative management for this entity includes open thrombectomy, catheter directed thrombolysis and/or percutaneous mechanical thrombectomy. These conventional options, however, may not be ideal for patients having unstable aortic arch thrombus and profound distal arterial thrombosis of the hand. An alternative approach for such patients is isolated limb perfusion (ILP) with tissue plasminogen activator (tPA). A 37-year-old female presented with sudden onset acute left hand ischemia associated with sensory and motor deficits. An axillary pulse was present and distal pulses were absent as were radial, ulnar and palmar signals. Her medical history was unremarkable but she was a 1 pack/day smoker. Her evaluation included a chest CT-angiogram showing a pedunculated aortic arch thrombus that was confirmed on transthoracic echocardiogram (TTE) and was mobile (Fig 1). Her hand ischemia was presumed to be caused by an embolus originating from the aortic arch. Given the severity of distal forearm and hand ischemia with the presence of mobile aortic thrombus, catheter directed thrombolysis was felt to be contraindicated and the patient was taken to the operating room (OR) for emergent brachial, radial and ulnar thrombectomy. This yielded some thrombus; however, an intraoperative angiogram (Fig 2, A) post-thrombectomy still showed significant residual hand thrombus with absent radial, ulnar and palmar signals. Further thrombectomy was felt to be ineffective and ILP with tPA was felt to be most appropriate. A perfusion circuit was constructed and connected to the patient via brachial artery and vein cannulas. A proximal arm tourniquet was placed. The perfusate was charged with 25 mg tPA/hour for a total circulation time of 2 hours at a flow rate of 200 cc/min. Fibrinogen levels remain unchanged during perfusion. After completing perfusion, a repeat angiogram (Fig 2, B) was performed showing marked thrombus resolution. The cannula sites and incision were closed. The patient then underwent left postero-lateral thoracotomy and open aortic thrombectomy without cardiopulmonary bypass. At 6 months follow-up, radial and ulnar pulses are present and without sensory or motor hand deficits. Prompt open surgical thrombectomy remains first line therapy for cases of acute severe upper extremity ischemia due to thromboembolism although it may be ineffective for distal arterial bed thrombus. Alternatively, catheter-directed thrombolysis is effective for distal bed thrombus. However, this is precluded in advanced ischemia and when systemic tPA exposure is contraindicated due to risk of further embolization from proximal thrombus. ILP with tPA allows for rapid distal bed thrombolysis while theoretically limiting systemic exposure. In circumstances where perfusion circuits are readily available, it is possible to utilize ILP with tPA as an alternative strategy when conventional treatment methods are deemed to be suboptimal.

Mobile aortic arch thrombus: Conservative management with ticlopidine?

Diffuse aortic atherosclerotic disease (AAD) is now well recognized as a potential source of cerebral and peripheral emboli. Its clinical importance has been demonstrated in patients over 60. We focus on an unusual presentation of AAD in younger patients free from significant diffuse aortic atherosclerosis, where the outstanding lesion was a large and highly mobile thrombus. Two cases of mobile aortic thrombi, which were conservatively managed with ticlopidine, a potent antiplatelet agent, are reported. Our two cases suggest a possible place of antiplatelet therapy with thienopyridine in the management of isolated large mobile aortic thrombus.

Transthoracic Echocardiographic Diagnosis of Mobile Aortic Arch Atherothrombosis Associated with Stroke

Aortic arch atherosclerosis is associated with an increased risk of stroke or TIA. Up to now, transesophageal echocardiography has been the standard method for diagnosing protruding and/or mobile aortic arch atherosclerosis. We report a case where a mobile aortic arch atheroma was diagnosed using transthoracic echo in a patient with a recent stroke.

Endovascular treatment of traumatic thoracic aortic injury—should this be the new standard of treatment?

Blunt trauma to the thoracic aorta is a potentially life-threatening condition that can lead to death in 75% of cases at the time of injury, as a result of either aortic transection or acute rupture. Although it accounts for 1% of adult admissions to level I trauma centers, blunt aortic injury represents the second most common cause of death due to blunt trauma, second to head injury. It is estimated that only 25% of patients who sustain aortic injuries due to blunt thoracic trauma remain alive upon arrival to the hospital. The prognosis for patients who survive the initial injury remains poor: nearly 30% will die within the first 6 hours, and 50% of these patients will not live beyond the first 24 hours after the injury. This high mortality rate has previously prompted traditional management of blunt aortic injury to establish early diagnosis and rapid surgical intervention to prevent a catastrophic rupture. This belief has been modified to allow delay of the operative intervention to first manage other serious concomitant injuries and lessen the high surgical mortality rate associated with emergent aortic repair. Despite advances in modern trauma care, emergent operative intervention for blunt aortic injury is associated with significant cardiac, pulmonary, neurologic, and hemodynamic complications. The classic injury mechanism of blunt thoracic aorta is related to the combination of sudden deceleration and traction at the relatively immobile aortic isthmus, which represents the junction between the relatively mobile aortic arch and the fixed descending aorta. The isthmus is the most common location for rupture (50% to 70%), followed by the ascending aorta or aortic arch (18%) and the distal thoracic aorta (14%). Patients with blunt trauma to the thoracic aorta typically have multiple associated injuries to

Aortic arch replacement for recurrent cerebral embolization

Replacement of the aortic arch for atheroma with cerebral embolization is in its infancy. The appropriateness of such intervention is controversial. Over a 10-month period, a 58-year-old woman suffered multiple debilitating cerebral vascular accidents manifested by motor, sensory, and memory deficits and documented by computed tomographic scanning and magnetic resonance imaging. Carotid and vertebral arteries were free of arteriosclerotic disease. Transesophageal echocardiography demonstrated two large atheromas with friable, pedunculated forms, one in the aortic arch and one in the very proximal descending thoracic aorta. Transcranial ultrasound revealed recurrent cerebral microembolic events. Cerebrovascular events continued, and the atheromas increased in size, despite treatment with Coumadin and aspirin. Under deep hypothermic arrest, the segment of the aortic arch harboring the atheroma was excised and replaced with a Dacron graft. Repeat transcranial ultrasound revealed cessation of embolic signals. All cerebrovascular events ceased. No further anticoagulation therapy was required. The patient has made substantial recovery from the preoperative deficits and continues to do well 1 year after aortic arch replacement. Resection of mobile aortic arch atheromas is likely to become increasingly important in the future as transesophageal echocardiography leads to their more common identification as a cause of cerebral ischemic events.

Mobile aortic arch thrombus: Conservative management with ticlopidine?

Mobile aortic arch thrombus: Conservative management with ticlopidine?

Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Société Française de Cardiologie.

Atherosclerotic lesions of the aortic arch are potential sources of arterial embolism. Mobile thrombi in the aortic arch in young patients without diffuse atherosclerosis have been reported recently, but such cases remain exceptional. We describe a series of young patients with unexplained arterial embolism in whom transesophageal echocardiography detected mobile aortic arch thromboses. Transesophageal echocardiography files collected between 1991 and 1995 in French academic cardiology centers were reviewed to identify patients who fulfilled the following criteria: (1) an arterial embolic event in the preceding weeks; (2) a mobile pedunculated aortic arch thrombosis, defined as an echogenic mass protruding into the lumen of the aorta and inserted on the aortic arch; and (3) absence of obvious diffuse aortic atherosclerosis or of aortic debris on transesophageal echocardiography. Twenty-three cases were identified from 27 855 examinations. Thromboses were located on the horizontal aorta (n = 4), near the ostium of the left subclavian artery (n = 5), or on the concavity of the posterior segment of the aortic arch (in the isthmus) (n = 14). The insertion site was a small atherosclerotic plaque in 21 patients. The remaining aortic wall always appeared normal or mildly atherosclerotic. The mean age of the patients was 45 +/- 8.4 years (range, 26 to 61 years). All patients were treated with intravenous heparin after the diagnosis of aortic arch thrombosis, and surgical removal of the thrombosis was performed in 10 patients in whom histological examination confirmed an atherosclerotic process at the site of insertion of the thrombosis. The prognosis was mainly influenced by embolic events. Thromboses of the aortic arch appear to be a variant form of aortic atherosclerotic disease associated with arterial embolism in young patients.