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(Circulation. 1997;96:288-294.)
© 1997 American Heart Association, Inc.

Articles

Mobile Thromboses of the Aortic Arch Without Aortic Debris

A Transesophageal Echocardiographic Finding Associated With Unexplained Arterial Embolism

Thierry Laperche, MD; Claude Laurian, MD; Raymond Roudaut, MD; P. Gabriel Steg, MD; ; for the Filiale Echocardiographie de la Société Française de Cardiologie¹

From the cardiology departments of Hôpital Beaujon (T.L.), Clichy, Hôpital du Haut-Lévèque (R.R.), Pessac, and Hôpital Bichat (P.G.S.), Paris; and the Cardiovascular Surgery Department of Hôpital Saint-Joseph (C.L.), Paris, France.

	Abstract

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Background 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.

Methods and Results 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.

Conclusions Thromboses of the aortic arch appear to be a variant form of aortic atherosclerotic disease associated with arterial embolism in young patients.

Key Words: echocardiography • aortic arch syndromes • thrombosis • embolism

	Introduction

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
The etiologic diagnosis of arterial emboli remains difficult. Emphasis has been placed on the value of transesophageal echocardiography (TEE) for the detection of cardiac thrombi, patent foramen ovale (associated with paradoxical embolism), atrial septal aneurysms,^{1 2 3 4} and, more recently, atherosclerotic lesions of the aortic arch as potential sources of arterial embolism.^{5 6 7 8 9 10 11} TEE generally permits the precise delineation of mobile aortic debris and of their insertion site. Rare cases of pedunculated aortic arch thromboses (AATs), generally associated with diffuse atherosclerosis of the aortic arch, have been detected in elderly patients.^{12 13 14 15 16} However, the presence of mobile thrombi in the aortic arch in young patients without diffuse atherosclerosis has only recently been reported and appears to be rare.^{17 18}

We describe a series of young patients with unexplained arterial embolism in whom TEE revealed mobile pedunculated AATs without clear diffuse, atherosclerotic lesions.

	Methods

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
This retrospective study involved all academic cardiology centers of the echocardiography branch of the French Cardiology Society (Filiale Echocardiographie de la Société Française de Cardiologie). All TEE files, recorded on videotapes, collected between January 1991 and April 1995 were reviewed to identify patients who fulfilled the following criteria: (1) an arterial embolic event in the preceding weeks; (2) a mobile, pedunculated AAT on TEE, defined as a well-demarcated homogenous mass of echoes attached to the aortic wall and protruding into the lumen of the aorta, of a cruoric nature, proven by surgical retrieval or autopsy, if possible; and (3) an absence of obvious diffuse atherosclerosis or debris on the aortic arch on TEE examination. The aortic arch was studied for the presence and degree of atherosclerosis as well as for the presence of calcifications. Aortic wall and plaque thicknesses were measured perpendicularly to the far wall as the distance between the media-intima border and the lumen. The aortic wall was considered normal when the intimal surface was smooth and continuous with a thickness <1 mm. The presence of mild atherosclerotic plaque was defined echocardiographically as focal increased echo density and thickening of the intima extending <4 mm from the aortic wall into the aortic lumen. The presence of aortic calcifications was defined echocardiographically as bright echoes that caused acoustic masking and signal dropout distally. Furthermore, plaques were classified as either complex, when associated with important surface irregularities and/or calcifications, or smooth otherwise. Because it has been shown previously that atherosclerotic plaques with a thickness 4 mm are a possible source of cerebral emboli owing to their association with ischemic stroke,⁹ such patients were excluded from the study. Finally, aortic aneurysms were excluded.

All TEE videotapes corresponding to patients who fulfilled these criteria were reviewed in consensus by two experienced echocardiographers from the core laboratory, and the clinical and biological characteristics and follow-up data on the patients were retrieved from the hospital files.

	Results

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Twenty-four centers provided the TEE files used in this study. Twenty-three cases fulfilling the definition criteria were collected, two of which have been published previously,¹⁷ originating from 15 centers in which a total of 27 855 TEE examinations were performed between January 1991 and April 1995. TEE examinations had been performed with the use of commercially available imaging systems with a 5-MHz monoplane ultrasound probe in 11 patients, a biplane probe in 3, and a multiplane probe in 9. In all patients, TEE examination revealed a mobile pedunculated thrombus protruding in the aortic arch. The echocardiographic appearance always consisted of a highly mobile, ovoid echogenic mass in the lumen of the aorta (largest dimension ranging from 3 to 40 mm) with a narrow insertion base on the aortic wall (Fig 1). The insertion site could be identified in all but 1 patient. It was located on the horizontal aorta in 3 patients, near the ostium of the left subclavian artery in 5, and on the concavity of the posterior segment of the aortic arch (in the isthmus) in 14 (Fig 2). In the last patient, in whom the insertion site was not directly seen, visualization of the thrombus on TEE was strictly restricted to the horizontal portion of the aorta, strongly suggesting insertion in that area. In 14 (64%) of 22 patients, the insertion site was a small atherosclerotic plaque (1 but <4 mm) with increased mural echo density. In 7 patients, the insertion site was a more irregular and complex plaque (Fig 3), with calcifications in 5 patients. Finally, in 1 patient, the insertion site appeared normal. In 17 patients (74%), the echocardiographic appearance of the adjacent aortic wall was normal, whereas in the other 6 cases (26%), mild intimal thickening was observed that ranged from 1 to 2 mm, suggesting mild atherosclerotic infiltration of the aortic wall. The diameter of the aorta in the arch and its other portions was normal in all patients. All patients were in sinus rhythm, and none had any other identifiable source of arterial embolism; specifically, there were no other visible sites of thrombi on TEE examination. In the patients with a history of stroke, Doppler ultrasound examination of the carotid arteries did not reveal any stenosis 30% in diameter.

View larger version (54K): [in this window] [in a new window]   Figure 1. A, Transesophageal echocardiographic (TEE) view of the aortic arch in a 50-year-old woman who had an embolism of the inferior mesenteric artery and both legs (patient 20). A highly mobile thrombosis was seen in the horizontal portion of the aortic arch. The aortic wall had a normal echocardiographic aspect. B, TEE view of a mobile thrombosis in the horizontal aortic arch in a 61-year-old patient (patient 23).

View larger version (11K): [in this window] [in a new window]   Figure 2. Schematic representation of the location of the insertion site of the thromboses in aortic arch. IA indicates innominate artery; LCA, left carotid artery; and LSCA, left subclavian artery.

View larger version (58K): [in this window] [in a new window]   Figure 3. A, Transesophageal echocardiographic (TEE) view of the insertion site in a 38-year-old patient (patient 2), showing a small plaque and the pedunculus of the thrombosis. The aortic wall had a normal echocardiographic aspect. B, TEE view of the insertion site of the thrombosis in a 59-year old patient (patient 22). The thrombosis was inserted on a complex plaque on the isthmic portion of the arch, whereas the remaining aortic wall appeared mildly atherosclerotic.

Patients
The clinical characteristics of the 23 patients are summarized in Table 1. There were 13 men and 10 women, with a mean age of 45±8.4 years (range, 26 to 61 years). All but 3 patients had one or more cardiovascular risk factors: smoking in 16, hypercholesterolemia in 11 (mean plasma cholesterol, 6.1±1.8 mmol/L), hypertension in 6, and diabetes mellitus in 3. Assays for antithrombin III, proteins C and S, fibrinogen, and antiphospholipid antibodies had been performed in all patients, but only 4 (17%) had evidence of a hemostatic disorder (protein C deficiency in 2 and antiphospholipid antibody syndrome in 2). Fibrinogen levels were >4 g/L in 10 patients (mean, 4.5±1.5 g/L). The initial arterial embolic event was ischemic stroke in 5 patients, embolism in the arms in 10 (right superior limb in 3), embolism in the legs in 11, and visceral artery embolism in 4. Ten patients had multiple emboli affecting more than one territory. In most of the patients (19 [83%] of 23), clinical onset of the embolic event was sudden. However, in 2 patients, the initial manifestation was subacute limb ischemia (evolving over 3 months), and in 2 patients the initial symptoms were limited to dysesthesia of one hand.

View this table: [in this window] [in a new window]   Table 1. Demographic, Clinical, and Therapeutic Data of Patients Enrolled in the Study

Treatment
Management of the embolic events included intravenous heparin in all cases. However, in 4 patients, embolic events recurred despite intravenous heparin. Peripheral embolectomy was performed in 13 patients. One patient underwent small-bowel resection for mesenteric ischemia.

Surgical ablation of the aortic mass was performed in 10 patients an average of 6.8±3.6 days (range, 0 to 12 days) after discovery. The decision to operate was based on the persistence of the mass on a repeat TEE (n=4) or the highly mobile appearance of the thrombosis (n=6, 2 of whom had evidence of recurrent embolism). In all cases, surgery showed a mobile thrombosis inserted on the aortic wall (Fig 4). Histological examination of the surgical sample always confirmed a fibrinocruoric thrombus inserted on an atherosclerotic plaque (Fig 5). The site of insertion showed atherosclerosis in all 10 patients, of whom 5 had calcifications and 3 had ulcerations (Table 2). This insertion site was located at the distal part of the aortic arch in the region of the ligamentum arteriosum (n=6), 1 cm above this region (n=1), around the ostium of the left subclavian artery (n=2), or facing the origin of the left carotid artery (n=1). The surgical appearance of the rest of the aortic wall was judged normal or mildly atherosclerotic. In all but 3 patients, these findings correlated well with TEE findings, both regarding the site of the thrombosis and the macroscopic appearance of the insertion site (Table 2). The surgical procedure consisted of thrombectomy in all the patients, associated with resection of atherosclerotic plaque in 5, of whom 3 underwent combined repair of the aortic wall (using either a patch of polytetrafluoroethylene [n=2] or a prosthetic tube [n=1]). All the patients survived. The complications of surgery were one axillo-femoral bypass infection and one deep venous thrombosis of the lower limb. Six patients were discharged from the hospital with warfarin therapy and the remaining 4 patients with aspirin therapy.

View larger version (106K): [in this window] [in a new window]   Figure 4. Surgical view showing a thrombosis into the lumen of the aorta (patient 10).

View larger version (130K): [in this window] [in a new window]   Figure 5. Histological view showing a fibrinocruoric thrombosis (T) protruding in the aortic lumen, inserted on an atherosclerotic lesion. The intima (I) appears thick. The atherosclerotic nature of the insertion site is demonstrated by the presence of cholesterol clefts (black arrowheads) in the intima.

View this table: [in this window] [in a new window]   Table 2. Correlations Between Transesophageal Echocardiography and Macroscopic (Surgery or Autopsy) Findings

In 13 patients, there was no surgical removal of the AAT, which was exclusively treated with anticoagulant therapy (intravenous heparin followed by warfarin). One patient died 24 hours after initial TEE, despite emergency laparotomy, of massive mesenteric infarction due to embolism in the superior and inferior mesenteric arteries. Postmortem examination confirmed the existence of a thrombosis located on an atherosclerotic plaque in the isthmic portion of the aortic arch, while the remainder of the aortic wall appeared normal. In the remaining 12 patients, a repeat TEE performed 3 days to 6 months after the first showed disappearance of the thrombosis in 11 patients. In the last patient, the TEE appearance was unchanged 2 years later, and the patient had no evidence of subsequent embolism.

Altogether, the cruoric nature of the mass on TEE was formally confirmed in 18 (78%) of 23 patients by surgical (n=10) or autopsy (n=1) examination of the thrombosis itself (in 6 of these 11 patients, it was further confirmed by direct analysis of the thrombus retrieved by embolectomy) or by surgical embolectomy (n=7). In the remaining 5 patients, the cruoric nature of the embolus or mass was not formally proven, but the echocardiographic appearance of the mass was highly suggestive of a thrombus.

Follow-up
All surviving patients (n=22) were discharged with either warfarin (n=18) or aspirin (n=4) therapy and were followed up for an average of 18±14 months (range, 3 to 48 months). In 1 patient receiving aspirin therapy, embolism recurred 11 months after thrombectomy. TEE examination revealed recurrent thrombosis at the same site on the aortic arch. Repeat thrombectomy was performed, associated with resection of the atherosclerotic site of insertion and patch repair. No symptomatic embolic events occurred in the remaining patient. Sequelae were observed in 11 patients (50%) in the form of neurological deficits (6 patients), lower-limb amputation (2), or intermittent claudication (3). Eleven patients (50%) remained asymptomatic.

	Discussion

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Thromboses of the aortic arch are infrequent causes of systemic emboli. Rare cases have been reported in the literature,^{12 13 14 15 16 17 18} and to the best of our knowledge, this is the largest series of cases. Twenty-three cases were collected from >27 855 TEE examinations. Although the actual frequency in patients with arterial embolism is probably underestimated here (there is no "gold standard" for diagnosis, and some patients with unexplained arterial embolic events probably did not undergo TEE examination), AAT appears rare.

Aortic arch is now recognized as a source of systemic embolisms that complicate atherosclerotic plaques.^{9 11 19} The high prevalence of insertion of thrombi on the wall opposite the ostia of the aortic arch is striking. There was no obvious morphological feature visible on echocardiography that would explain why the majority of thromboses were attached to this area. This may be related to the fact that areas of low wall shear stress (such as this area) are predisposed to the development of atherosclerotic plaques, which, even when minute, are likely sites for attachment of thrombi. Several studies have demonstrated the impact of flow-velocity profiles and wall shear stress on plaque localization.^{20 21 22} Amarenco and colleagues⁹ found mobile components on complex aortic plaques, but these cases were infrequent (7 of 250 patients) and occurred on severe plaques (with a thickness 4 mm). Furthermore, although aortic atherosclerosis may be complicated by thrombosis of ulcerated plaques, it usually occurs in elderly patients.^{13 16} In their anatomic series, Amarenco and colleagues²³ did not find any ulcerated plaque on the aortic arch of stroke patients aged <60 years. In previous large studies of atherosclerotic plaques or debris, the average age was always >70 years.^{5 8 11 19 23 24} In contrast, AAT can affect younger patients: in the present study, the oldest patient was 61 years old, and the mean age was 45. In contrast to aortic debris, atheromas or calcified plaques were limited to the thrombus insertion site on the aortic wall. The remaining aortic wall was otherwise either normal or mildly atherosclerotic on TEE (in fact, its thickness never exceeded 2 mm). Furthermore, in elderly patients with embolic events and diffuse aortic atherosclerosis, the distinction between thromboembolic occlusion of a major artery, thromboembolic microembolization, and atheromatous microembolization is frequently difficult to perceive. In the AAT cases described here, we found evidence of the cruoric nature of the embolism. The mobile mass observed on TEE in the aortic lumen was indeed a clot. Its cruoric nature was proven by surgical retrieval (of the embolus and/or the mass) or by autopsy in 78% of cases; in the remainder, TEE images were highly evocative. Both the clinical and the echocardiographic appearances of AAT differed from those of aortic dissection with thrombosis of the false lumen, dissecting flaps,^{25 26} traumatic aortic disruption,^{27 28} intramural hemorrhages,^{29 30} or other rare causes of aortic masses.

Although AAT appears morphologically distinct from "classic" aortic arch debris, the insertion site always appeared to involve an atheromatous plaque, and this was confirmed by postoperative pathological examination of the aortic wall in seven patients and by autopsy in one patient, in whom the aortic insertion site always showed typical features of atherosclerosis. AAT therefore appears to be a complication of atherosclerosis. Aortic atherosclerosis may constitute a spectrum of disease ranging from pure atherosclerotic debris floating in the aorta (most prevalent in elderly patients) to nearly pure clot formations (often found in younger patients). Considering the high thrombogenic potential of atherosclerotic plaques,³¹ it is extremely likely that these clots are inserted on atherosclerotic plaques, even when they are not visible on echocardiography. It is likely that many patients in fact have aortic atherosclerosis complicated by clot formation. We point out, however, that the population in our study (whose inclusion criteria did not include age per se) were young patients who did have extensive clot formations floating in the aorta, without TEE evidence of profuse atherosclerosis but with a history of embolic events. Therefore, this does represent a specific variant of aortic atherosclerosis with high embolic potential, different in its presentation from that previously described by other groups in older patients, even though the pathophysiology may be common.

TEE was particularly effective for identifying AAT and provided important additional information such as size and mobility, insertion site, and the appearance of the remaining aortic wall. There was a good concordance between TEE and surgical or pathological findings regarding AAT location, insertion site, and appearance of the aortic wall.

Although the optimal treatment of AAT remains to be defined, anticoagulant therapy appears to be a logical component of medical therapy. However, recurrent embolic events may occur despite anticoagulant therapy in patients who do not undergo surgical removal of the AAT. In this series, embolism recurred in 4 (27%) of the 15 patients who had not originally undergone surgical removal of AAT, despite heparin therapy. In our experience, despite its own risk, surgical removal of both the thrombosis and the plaque does not appear to be associated with the high risk of surgical removal of aortic debris.³² Other therapeutic modalities include thrombolysis¹⁸ and balloon embolectomy.¹⁶

These therapeutic options emphasize the importance of identifying AAT and distinguishing it from aortic debris. It must be stressed that in our series, the prognosis appeared to be mainly related to the sequela of the embolic events: 1 patient died and 11 others had important sequelae, such as amputation or neurological deficits.

In conclusion, thromboses of the aortic arch appear to be a variant form of aortic atherosclerotic disease associated with arterial embolism in young patients. In these patients with unexplained systemic embolism, AAT is to be included among potential causes and can be identified by TEE.

View this table: [in this window] [in a new window]   Table 1A. Continued

	Acknowledgments

 
The authors are indebted to Rosine Merlet for her excellent technical assistance and Odile Groussard, MD, for her contribution to histological documents.

	Footnotes

 
Reprint requests to Thierry Laperche, MD, Service de Cardiologie, Hôpital Beaujon, 100 bd du Général Leclerc, 92118 Clichy, France.

¹ A complete list of the study investigators may be found in the "Appendix."

	Appendix 1

Top Abstract Introduction Methods Results Discussion Appendix 1 References

 
Investigators of this study were: Sami Anidjar, MD (Hôpital Saint-Michel, Paris); Yvette Bernard, MD (Hôpital Saint Jacques, Besançon); Bernard Bertrand, MD (Hôpital Albert Michallon, Grenoble); Christian Brandt, MD (Hôpital Civil, Strasbourg); Eric Brochet, MD (Hôpital Bichat, Paris); Jean-François Bruntz, MD (Hôpital Central, Nancy); Jean-Louis Bussière, MD (Hôpital du Val de Grâce, Paris); Ariel Cohen, MD (Hôpital Saint Antoine, Paris); Alain Cohen-Solal, MD (Hôpital Beaujon, Clichy); Jean-Michel Cormier (Hôpital La Roseraie, Aubervilliers); Daniel Czitrom, MD (Hôpital Bichat, Paris); Claude Deville, MD (Hôpital du Haut-Lévêque, Bordeaux); Jean-Jacques Doumeix, MD (Hôpital Dupuytren, Limoges); Guy Lesèche, MD (Hôpital Beaujon, Clichy); Etienne Maffert, MD (La Rochelle); Marie-Christine Malergue, MD (Centre Médico-Chirurgical de la Porte de Choisy, Paris); Jean-Luc Monin, MD (Hôpital Henri Mondor, Paris); Oscar Nusseaume, MD (Hôpital Rothschild, Paris); Marguerite Perinetti, MD (Hôpital Louis Pradel, Lyon); Hélène Petit, MD (Hôpital Civil, Strasbourg); Xavier Roques, MD (Hôpital du Haut-Lévêque, Bordeaux); Robert Sal, MD (Hôpital Corvisart, Charleville-Mézières); Christophe Tribouilloy, MD (Hôpital Sud, Amiens); and Olivier Wittenberg, MD (Hôpital Arnaud de Villeneuve, Montpellier).

Received November 14, 1996; revision received January 13, 1997; accepted January 21, 1997.

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