European Journal of Echocardiography 2008 9(1):56-57; doi:10.1016/j.euje.2006.08.013
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2006. For permissions please email: journals.permissions@oxfordjournals.org.
Aortic intramural haematoma and chronic anticoagulation: role of transoesophageal echocardiography
Alberto Ruggiero2,3,4,
Teresa González-Alujas1,
José Rodríguez1,
Eduardo Bossone2,3,4 and
Arturo Evangelista1,*
1 Servei de Cardiologia, Hospital Universitari Vall 
Hebron, P° Vall Hebron 119, 08035 Barcelona, Spain
2 Divison of Cardiology and Internal Medicine, Cava de Tirreni and Amalfi Coast Hospital ASL Salerno 1, Italy
3 Clinical Physiology Institute, National Research Council of Italy (IFC–CNR), Lecce, Italy
4 Department of Clinical and Experimental Medicine, Federico II University School of Medicine, Naples, Italy
Received 6 May 2006; accepted after revision 29 August 2007; online publish-ahead-of-print 13 October 2006.
* Corresponding author. Tel: +34 93 2746212; fax: +34 93 2746244. E-mail address: aevangel{at}vhebron.net
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Abstract
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The case of a 66-year-old patient with acute intramural haematoma
in descending aorta, receiving anticoagulant treatment with
warfarin for chronic atrial fibrillation, is presented. Transoesophageal
echocardiography was fundamental in the diagnosis of the intramural
haematoma, assessment of the cardioembolic risk of atrial fibrillation
and in follow-up the evolution of the intramural haematoma,
which facilitated therapeutic management. Although no established
recommendation exists on anticoagulation in aortic intramural
haematoma, individual risk-benefit assessment of anticoagulation
and follow-up with imaging techniques are essential to elect
the most appropriate therapeutic management.
Keywords: Transoesophageal echocardiography; Aortic intramural haematoma; Anticoagulation
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Introduction
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Aortic intramural haematoma (IMH) constitutes 15–20% of
acute aortic syndromes, mainly involves descending aorta and
has similar morbidity and mortality to aortic dissection.
1 Aortic
intramural haemorrhage is produced by vasa vasorum bleeding;
thus, anticoagulant treatment may be prejudicial. Transoesophageal
echocardiography (TEE) affords correct diagnosis and follow-up
of intramural haematoma thickness. To date, there is a paucity
of information on the risk of anticoagulation in the evolution
of intramural haematoma and the presence of complications such
as wall re-bleeding or aortic rupture.
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Case report
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A 66-year-old woman had a history of venous sinus-type atrial
septal defect operated on 6 years previously. She was receiving
anticoagulant treatment with warfarin for chronic atrial fibrillation.
The reason for the present admission was left lumbar pain of
sudden onset irradiated to epigastrium. Physical examination
revealed systemic blood pressure of 180/120 mmHg. ECG showed
atrial fibrillation 70 bpm and chest X-ray was normal. Laboratory
analysis revealed no alterations except an INR of 4.4, with
normal myocardial lesion markers. Abdominal echography performed
was normal. Transthoracic echocardiogram showed non-dilated
left ventricle with normal function and dilated left atrium
(55 mm). Transoesophageal echocardiogram disclosed an intramural
haematoma in descending aorta (
Figure 1A). Maximum thickness
of the haematoma was 12 mm. Severe spontaneous contrast was
observed at left atrium with absence of thrombi. Left atrial
appendage emptying flow velocity was diminished (18 cm/s). The
diagnosis of aortic intramural haematoma was confirmed by magnetic
resonance imaging (MRI) (
Figure 2A). The patient was admitted
and it was decided to temporarily suspend the anticoagulation.
At 5 days of uncomplicated evolution, with adequate systemic
blood pressure control and, after verifying by TEE that haematoma
thickness remained stable, anticoagulation was restarted with
subcutaneous heparin. TEE performed 4 days later showed a marked
increase in maximum thickness of the intramural haematoma (20
mm), in the absence of symptoms (
Figure 1B). It was decided
to suspend the anticoagulation, and the examination was repeated
5 days later; no changes in the aortic intramural haematoma
or left atrium were observed. Two weeks post-discharge, TEE
(
Figure 1C) showed a significant decrease in intramural
haematoma thickness (7 mm), confirmed by MRI 1 month after discharge
(
Figure 2B). At 6 months of evolution, the haematoma was
completely reabsorbed; thus, warfarin treatment was restarted,
with no new complications in the aortic wall observed on the
TEE performed at 1 year of follow-up.
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Figure 1 Intramural haematoma evolution by TEE. (A) Diagnostic study of the IMH in descending aorta. IMH thickness is 12 mm. (B) Study conducted 4 days after restoration of anticoagulant treatment, showing an increase in haematoma thickness to 20 mm. (C) Study 15 days after withdrawal of anticoagulant treatment, IMH thickness has decreased to 7 mm.
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Discussion
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This case demonstrates that anticoagulation in acute phase on
an IMH may lead to an increase in IMH thickness secondary to
re-bleeding of the aortic wall vasa vasorum. The haematoma stabilized
and later regressed progressively when anticoagulation was stopped
for 6 months. IMH reabsorb completely without complications
in 30 % of cases, with the remainder evolving to aortic dissection
or the formation of aortic aneurysms.
2 The indication for anticoagulant
treatment in patients over 60 years of age with chronic atrial
fibrillation and a history of arterial hypertension, left atrium
dilatation and spontaneous atrial contrast is well established.
3 Given the controversy of avoiding the embolic risk of atrial
fibrillation or increasing the risk of aortic intramural haemorrhage,
it was decided to initially suspend the anticoagulation. The
satisfactory clinical evolution, blood pressure control and
stabilization of the haematoma prompted the re-initiation of
anticoagulation, which led to an increase in thickness of the
haematoma, probably due to asymptomatic re-bleeding of the aorta
wall. Owing to this complication, and although the cardioembolic
risk of atrial fibrillation was significant, anticoagulation
was suspended until total reabsorption of the haematoma was
verified at 6 months of evolution.
This case illustrates the difficulty in decision-making in these circumstances. We believe that when the thromboembolic risk is intermediate or low, interruption of anticoagulant treatment is advisable until the haematoma regresses significantly. If the thromboembolic risk is very high, as in patients with valvular prostheses, close monitoring with imaging techniques should be performed, and if evolution is not satisfactory, endovascular or surgical treatment should be considered.
In conclusion, anticoagulant therapy in patients with an acute IMH may facilitate re-bleeding of the aorta wall. Individualization of the risk/benefit of anticoagulation and monitoring of haematoma thickness by imaging techniques may facilitate the choice of the most appropriate therapeutic management.
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References
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- Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P, Kotler MN. Meta-analysis of 143 reported cases of aortic intramural hematoma. Am J Cardiol (2000) 86:664–8.[CrossRef][Web of Science][Medline]
- Evangelista A, Domínguez R, Sebastià C, Salas A, Permanyer-Miralda G, Avegliano G, et al. Long-term follow-up of aortic intramural hematoma. Predictors of outcome. Circulation (2003) 108:583–9.[Abstract/Free Full Text]
- Ezekowitz MD, Falk RH. The increasing need for anticoagulation therapy to prevent stroke in patients with atrial fibrillation. Mayo Clin Proc (2004) 79:904–13.[Abstract/Free Full Text]
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Abstract
Introduction