European Journal of Echocardiography Advance Access published online on June 16, 2008
European Journal of Echocardiography, doi:10.1093/ejechocard/jen193
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Complicated course consequences of a floating thrombus in ascending aorta
Mohammad Hossein Mandegar,
Farideh Roshanali* and
Armin Kocharian
Day General Hospital, Vali Asr Avenue, Tavanir street, Tehran 14466, Iran
Received 12 April 2008; accepted after revision 30 May 2008.
* Corresponding author. Tel: +98 912 3093151; fax: +98 21 88797353.E-mail address: farideh_roshanali{at}yahoo.com
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Abstract
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The ascending aorta may be the site of origin of systemic embolization
of an unidentifiable cause. We report a case in which a free-floating
thrombus of an unknown cause was detected in the ascending aorta
via transesophageal echocardiography. The removal of this pedunculated
thrombus, which was attached onto a macroscopically and histologically
mildly atherosclerotic aortic wall, led to an uneventful recovery
for the patient.
Keywords: Aortic root; Thrombosis; Embolism
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Introduction
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We report a particularly interesting case in which a pedunculated
free-floating thrombus of an unknown cause in the ascending
aorta was attached to a mildly atherosclerotic aortic wall.
The thrombus was thought to have been the origin of a previous
left tibial artery embolic event.
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Case report
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A 50-year-old woman was apparently in good health until she
was admitted to the emergency department of another centre for
sudden ischaemia of the left leg. A left tibial artery occlusion
was demonstrated by angiographic examinations. The patient was
treated successfully with a trans-tibial embolectomy. The patient
had no previous history of thrombotic events, had never been
exposed to heparin, and was on no medication at the time. A
histological examination of the embolus disclosed a fresh thrombus
composed of platelets, red-blood cells, polymorphonuclear cells,
and fibrin. No evidence of malignant cells was found, nor did
physical examination, chest roentgenogram, electrocardiogram,
and Holter monitoring show any abnormalities. Two-dimensional
transthoracic echocardiography (TTE) excluded pericardial effusion,
mitral valve abnormality, and the presence of a thrombus in
the left atrial appendage. The aortic valve was tricuspid with
mild insufficiency and no stenosis. The four cardiac chambers
and the ascending aorta were of normal dimensions. The left
and right ventricular wall thickness and contractility were
normal. No patent foramen ovale was detected on a colour Doppler
echocardiogram. The patient, having been given heparin and then
warfarin, was discharged from hospital.
A week later, however, she came to our hospital for further evaluation. The patient underwent transesophageal echocardiography (TEE), which confirmed the previous TTE findings but revealed the presence of a very mobile lobulated mass >2.5 cm in diameter and attached with a 5-mm base to the posterior wall of the ascending aorta 1.5 cm above the sinotubular junction (Figure 1) and it confirmed by 64-slice CT angiography (Figure 2).
Urgent surgery for the prevention of a recurrent embolic event,
particularly brain embolization, seemed to be the only choice.
Two hours later, she was in the operating room with her chest
open. To ensure the safety of cannulation and find an appropriate
clamp site, an epicardial echocardiography probe was employed
to evaluate the mass. Unfortunately, the base of the mass had
thinned to 1 mm, causing a very exaggerated motion (
Figure 3,
see
Supplementary material online, Video S1). A safe clamp site
was found, and through atrial cannulation, the patient was placed
on cardiopulmonary bypass pump and her aorta was clamped with
minimal manipulation. A cardioplegic injection was then administered
followed by a transverse aortotomy 3 cm above the right coronary
artery, which failed to reveal the mass. It was tragedy. The
aortic wall and leaflets appeared mildly thickened, and mild
macroscopic atherosclerotic changes were found on the implantation
site of the mass. The left ventricle was explored through the
aortic valve, but no thrombus was found. The mitral valve was
intact.
Immediately afterwards, the aortic arch was opened directly
with total circulatory arrest to expose the origin of the neck
vessels. The mass, however, was nowhere to be seen. The patient’s
chest was closed and her limbs’ vessels were evaluated
with Doppler sonography on the operating table; there were still
no signs of the elusive mass. Then, the patient being rushed
to the CT scan ward with ambulatory mechanical ventilation.
A 64-slice MSCT for an abdominal evaluation detected the mass
6 mm from the origin of the superior mesenteric artery (
Figure 4).
The patient was, subsequently, transferred back to the operating
room, where her abdomen was opened, revealing a change of colour
and no peristalsis in the small intestine. The mass was excised
7 mm from the origin of the superior mesenteric artery (within
2 h of embolization) (
Figures 5 and
6), as a result of
which the artery pulse and colour of intestine were restored.
The patient was transferred to ICU and 7 days later was discharged
home in good condition.
A histological examination of the mass revealed a fresh thrombus
composed of a fibrinous material with polymorphonuclear cells,
lymphocytes, and platelets. A histopathological evaluation of
the aortic wall demonstrated mild evidence of atherosclerosis.
No bacteria or fungus was present in the serial histological
sections, and cultures of the mass yielded negative findings.
An appropriate regimen of anticoagulation therapy with an antivitamin
K was commenced on the first postoperative day, and an international
normalized ratio of 2–2.5 was maintained to prevent recurrent
clot formation. The patient is doing well 5 months after surgery
without evidence of recurrent aortic thrombus in echocardiographic
controls. Subsequent serial haematologic and plasma coagulation
system tests in the follow-up period have not disclosed abnormalities.
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Discussion
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The most frequent non-cardiac sources of systemic embolism are
mural thrombi within proximal aneurysms, ulcerated atherosclerotic
plaques, and paradoxical emboli originating from the venous
side of the circulation. Floating masses in the ascending aorta
are uncommon sources of systemic embolism.
1,2
The diagnosis of a hypercoagulable state in our patient was excluded by the negative complete coagulation profile and lack of previously unexplained arterial or venous thrombosis in her and her family members. Our patients, however, had some atherosclerotic risk factors: smoking and mild diabetes. The histological aspect of a mildly atherosclerotic ascending aortic wall could be a cause of thrombus formation. But because the blood flow volume in the ascending aorta is extremely large, we are inclined to believe that a transient hypercoagulable state, which is not well understood at the present time, in a site such as the ascending aorta, where turbulence could act as a contributing factor, is a reasonable possibility.
The treatment of patients who suffer from systemic embolic events and in whom a floating thrombus or protruding atheroma has been detected remains problematic.3 We believe that the presence of an ascending aortic floating thrombus or mobile atherosclerotic debris in patients who have embolic events should prompt consideration for surgery.4,5
Some authors6 have hypothesized that atherosclerotic plaques and a hypercoagulable condition might cause a thrombus in the ascending aorta. In our patient, we found no hypercoaguable or systemic disorder that could have caused unusual thrombosis but only an atherosclerotic plaque, which could have led to endothelial injury and thrombus formation.7 Be that as it may, the exact mechanisms of giant thrombi in a high-flow environment such as the ascending aorta are not fully known.
Neither antiplatelet agents nor antivitamin K such as warfarin has been shown to effectively prevent recurrent embolic episodes from aortic atheroma.8 On the one hand, therapeutic anticoagulation may paradoxically induce further embolic events by causing plaque haemorrhage, particularly in the presence of protruding atheroma,9,10 or by lysing the thin pedicle of the thrombus more rapidly than the mass itself. On the other hand, the efficacy of the anticoagulation in the presence of mobile atherosclerotic debris is questionable. In our patient, it is very likely that warfarin facilitated the embolization of the clot by lysing the base of the thrombus.
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Conclusion
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It is advisable that unusual sources of embolization be sought
diligently and thoroughly during diagnostic evaluations because
today the majority of sources is detectable and treatable, hence
the preventability of the recurrent systemic embolism.
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Supplementary material
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Supplementary material is available at
EJECHO online.
Conflict of interest: none declared.
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References
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- Muehrcke DD, Grimm RA, Nissen SE, Cosgrove DM 3rd. Recurrent cerebral vascular accidents are an indication for ascending aortic endarterectomy. Ann Thorac Surg (1996) 61:1516–8.[Abstract/Free Full Text]
- Sadony V, Walz M, Löhr E, Rimpel J, Richter HJ. Unusual cause of recurrent arterial embolism: floating thrombus in the aortic arch surgically removed under hypothermic cardiocirculatory arrest. Eur J Cardiothoracic Surg (1988) 2:469–71.[Abstract]
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- Amarenco P, Cohen A, Tzourio C, Bertrand B, Hommel M, Besson G, et al. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med (1994) 331:1474–9.[Abstract/Free Full Text]
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Abstract
Introduction
