Article Text

Catastrophic embolisation via a thrombus in the left ventricular outflow tract and ascending aorta
  1. Diana Adrião1,
  2. Érico Costa1,
  3. Marisa Silva2 and
  4. Isabel Jesus Pereira1,3
  1. 1Department of Intensive Care, Centro Hospitalar de Vila Nova de Gaia Espinho EPE, Vila Nova de Gaia, Portugal
  2. 2Department of Cardiology, Centro Hospitalar de Vila Nova de Gaia Espinho EPE, Vila Nova de Gaia, Portugal
  3. 3Faculdade de Medicina, Universidade do Porto, Porto, Portugal
  1. Correspondence to Dr Diana Adrião; diana_adriao{at}

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A male patient in his mid-50s with a history of arterial hypertension and smoking presented to the emergency department after falling from a height of 1 m. He had a thoracic trauma with fractures of the 1st–6th ribs bilaterally and was discharged with painkillers. Two days later, he was readmitted with an inferior ST elevation myocardial infarction and an acute ischaemic stroke in the territory of the right middle cerebral artery. Given the patient’s haemodynamic stability and high likelihood of an embolic aetiology to the clinical condition, it was decided not to perform coronary angiography and stroke treatment was prioritised instead.

After endovascular thrombectomy, contrast-enhanced CT was performed revealing a mass (18×10×25 mm) in the ascending aortic lumen, without evidence of aortic dissection, aneurysm or tortuosity of the aorta (figure 1). An infarction of the right kidney was also reported. Transoesophageal echocardiography (TEE) confirmed the presence of a pedunculated highly mobile echogenic mass attached to the anterior region of the aortic root, near the right coronary ostium, measuring >15 mm, suggestive of a thrombus. A 12 mm mobile echogenic mass in the anterior region of the left ventricular outflow tract (LVOT) was also identified, suggestive of a thrombus (online supplemental videos 1 and 2). Other findings included left ventricular inferior wall hypokinesia with normal left ventricular function, akinesia of the free wall and diaphragmatic wall of the right ventricle with severe right ventricular dysfunction and small patent foramen ovale with minimal shunt.

Supplementary video

Supplementary video

Figure 1

Contrast-enhanced CT scan in coronal view showing a thrombus in the ascending aortic lumen (yellow arrow) and kidney infarction (red arrow).

He was admitted to the intensive care unit where he developed cardiogenic shock with multiorgan dysfunction. Given the high risk of cardiac surgery, a multidisciplinary decision was taken to start anticoagulation with unfractionated heparin after repeating the head CT to exclude haemorrhagic complications. Despite adequate medical management, the patient deteriorated and died after 48 hours. The patient was deemed unsuitable for ventricular support due to his advanced myocardial infarction and significant neurological deficits.

Thrombus formation in LVOT and in a non-aneurysmal ascending aorta is extremely rare due to the high blood flow environment.1–3 It has potentially life-threatening complications arising from coronary, cerebral and systemic embolisation. Few cases of aortic mural thrombus have been described in the absence of severe atherosclerosis, aneurysmal disease and aortic dissection.1 2 Moreover, cases of LVOT thrombi related to chest trauma have rarely been reported.3 4

Diagnostic evaluation of these patients should include a combination of imaging studies, such as TEE and CT. Because there are no clear consensus and established recommendations, managing this condition is difficult. Some authors have advised anticoagulation as a primary therapeutic approach, or surgical intervention as an alternative.1

Learning points

  • Thrombus in left ventricular outflow tract and in a non-aneurysmal ascending aorta is an uncommon condition, but should be considered in patients with unexplained systemic embolism.

  • Transoesophageal echocardiography is an important diagnostic tool that permits detailed assessment of the left ventricular and aortic thrombus.

  • Guidelines regarding the best treatment approach for this clinical entity are yet to be established.

Ethics statements

Patient consent for publication


Supplementary materials

  • Supplementary Data

    This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.


  • Contributors The following authors were responsible for drafting of the text, sourcing and editing of clinical images, investigation results, drawing original diagrams and algorithms, and critical revision for important intellectual content: DA, ÉC, MS and IJP. The following authors gave final approval of the manuscript: DA, ÉC, MS and IJP.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.