Case Report

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American Journal of Emergency Medicine

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Thrombus in acute aortic dissection with atrial fibrillation: a treatment dilemma

Abstract

Type B Acute aortic dissection is often successfully managed with medical therapy, with a lower mortality rate, compared with type A AAD. Although the number of AAD patients complicated with Atrial fibrillation has increased, reflecting an aging society, there have only been a few reports regarding the association of AAD and AF. Furthermore, there is no consensus on anticoagulation therapy in ADD patients complicated with AF, despite the importance of anticoagula- tion therapy in AF treatment. Here, we discuss a 79-year-old man with type B AAD and chronic AF complicated with the rapid left atrial appendage (LAA) thrombus formation after discontinuation of antic- oagulation therapy. Emergent contrast-enhanced computed tomog- raphy revealed type B AAD with a partially thrombosed False lumen from the bifurcation of the aorta and the left subclavian artery to above the diaphragm. Ulcer-like projection was observed in the proximal thrombosed false lumen. Ten days after discontinuation of antic- oagulation therapy, LAA thrombus was detected on contrast-enhanced computed tomography, which was not observed on admission. After anticoagulation therapy was resumed, the LAA thrombus disappeared, but the partially thrombosed false lumen was enlarged. The second discontinuation of anticoagulation therapy stabilized the dissected aorta and did not cause recurrence of LAA thrombus. In conclusion, clinicians need to balance the prevention of LAA thrombus formation with the complete thrombosis of a false lumen in patients with AAD and AF.

type B acute aortic dissection is often successfully managed with medical therapy, with a lower mortality rate, compared with type A AAD, especially in cases of thrombosed type AAD [1]. Although the number of AAD patients complicated with Atrial fibrillation has increased, reflecting an aging society, there have only been a few reports regarding the association of AAD and AF [2,3]. Furthermore, there is no consensus on anticoagulation therapy in AAD patients complicated with AF, despite the importance of anticoagulation therapy in AF treatment. Here, we discuss a 79-year-old man with AAD and chronic AF complicated with the rapid left atrial appendage (LAA) thrombus formation after discontinuation of anticoagulation therapy, which was given for the prevention of thromboembolism caused by AF.

A 79-year-old man with chronic AF was admitted to the hospital for severe back pain. His blood pressure was 176/88 mm Hg and had an irregular heart rate of 71 beats/min at presentation. Emergent contrast-enhanced computed tomography (CECT) revealed type B AAD with a partially thrombosed false lumen from the bifurcation of the aorta and the left subclavian artery to above the diaphragm (Figs. 1A and 2A, D). Ulcer-like projection was observed in the proximal thrombosed false lumen. We discontinued administration

of warfarin and started administration of Antihypertensive drugs, which included a ?-blocker and Intravenous morphine hydrochlo- ride. The patient’s pain and blood pressure was controllable. Laboratory examination after admission showed that prolonged prothrombin time was normalized after warfarin discontinuation, but that the elevation of D-dimer levels was sustained. Follow-up CECT performed 3 and 10 days after admission did not reveal any extension or enlargement of the dissected aorta. However, LAA thrombus was detected on CECT 10 days after admission, which was not observed before (Fig. 1A, B). After concurrent administration of heparin and warfarin, the LAA thrombus completely disappeared on day 18 without any embolic events (Fig. 1C). However, the partially thrombosed false lumen was enlarged and exerted pressure on the true lumen (Fig. 2A-F), despite stabilization of blood pressure and cautious rehabilitation. With respect to anticoagulation therapy, we needed to take balance between the prevention of an LAA thrombus and the complete thrombosis in the false lumen; therefore, we decided to again discontinue anticoagulation therapy. Fortunately, careful follow-up CECT and echocardiogram showed that discontin- uation of anticoagulation therapy stabilized the dissected aorta without enlargement of the false lumen or extension of the dissected aorta and did not cause recurrence of an LAA thrombus. After confirmation of false lumen stabilization, we restarted warfarin on day 42 after AAD onset, and AAD remained stable without enlargement of the false lumen.

Although there are no current recommendations regarding the

use of anticoagulants for patients with AAD, many physicians believe it would have a negative effect on thrombosis formation and the Healing process in the dissected aorta’s false lumen. On the other hand, Song et al [4] have also reported favorable effects of early anticoagulation on the AAD; therefore, the effect of anticoagulation on AAD remains unknown. To the best of our knowledge, this is the first description of the rapid formation of LAA thrombus in a patient with AAD. This case emphasizes the careful management required for patients with AAD and AF. Clinicians need to balance the prevention of LAA thrombus formation with the complete thrombosis of a false lumen in patients with AAD and AF. In patients who have a partially thrombosed false lumen with ulcer-like projections, discontinuing anticoagulants may prevent enlargement of the false lumen of the dissected aorta, at least during the acute phase. However, AAD is associated with hypercoagulation reaction, as evidenced by a significant elevation in coagulation marker. If rapid formation of LAA thrombus is observed, anticoagulation therapy needs to be started with careful follow-up of the dissected aorta. We also need to keep in close communication with the cardiovascular surgery team to prepare for emergent surgical intervention, including surgical or thoracic endovascular Aortic repair.

0735-6757/(C) 2014

Fig. 1. Contrast-enhanced computed tomography showing thrombus in the LAA (B, arrow) on day 10 after AAD, which was not observed on admission (A). C, After resumption of anticoagulation therapy, LAA thrombus disappeared on day 18.

Fig. 2. Comparison of thrombosed aortic dissection seen on CECT on days 1 (A and D), 10 (B and E), and 18 (C and F). C and F, A partially thrombosed false lumen was enlarged (arrows) after resumption of anticoagulation therapy.

Yasuyuki Shiraishi, MD* Takashi Kohno, MD Toru Egashira, MD Yuichiro Maekawa, MD

Division of Cardiology, Department of Medicine, Keio University

School of Medicine, Tokyo, Japan

*Corresponding author. Tel.: +81 3 5843 6702; fax: +81 3 5363 3875

E-mail address: [email protected]

Yoshitake Yamada, MD

Department of Diagnostic Radiology Keio University School of Medicine Tokyo, Japan

Akihiro Yoshitake, MD Hideyuki Shimizu, MD

Division of Cardiovascular Surgery Keio University School of Medicine, Tokyo, Japan

Motoaki Sano, MD

Division of Cardiology, Department of Medicine, Keio University School of

Medicine, Tokyo, Japan

Masahiro Jinzaki, MD

Department of Diagnostic Radiology Keio University School of Medicine, Tokyo, Japan

Keiichi Fukuda, MD Division of Cardiology, Department of Medicine Keio University School of Medicine, Tokyo, Japan

http://dx.doi.org/10.1016/j.ajem.2014.07.040

References

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3. Chew HC, Lim SH. Aortic dissection presenting with atrial fibrillation. Am J Emerg Med 2006;24:379-80.
4. Song SW, Yoo KJ, Kim DK, Cho BK, Yi G, Chang BC. Effects of early anticoagulation on the degree of thrombosis after repair of acute Debakey type I aortic dissection. Ann Thorac Surg 2011;92:1367-74.