Atherosclerotic Disease of the Aortic Arch and the Risk of Ischemic Stroke
Pierre Amarenco, Ariel Cohen, Christophe Tzourio, Bernard Bertrand, Marc Hommel, Gerard Besson, Christophe Chauvel, Pierre-Jean Touboul, and Marie-Germaine Bousser
Background Atherosclerotic disease of the aortic arch has beensuspected to be a potential source of cerebral emboli. We conducteda study to quantify the risk of ischemic stroke associated withatherosclerotic disease of the aortic arch.
Methods Using transesophageal echocardiography, we performeda prospective case-control study of the frequency and thicknessof atherosclerotic plaques in the ascending aorta and proximalarch in 250 consecutive patients admitted to the hospital withischemic stroke and 250 consecutive controls, all over the ageof 60 years.
Results Atherosclerotic plaques 4 mm in thickness were foundin 14.4 percent of the patients but in only 2 percent of thecontrols. After adjustment for atherosclerotic risk factors,the odds ratio for ischemic stroke among patients with suchplaques was 9.1 (95 percent confidence interval, 3.3 to 25.2;P<0.001). Among the 78 patients who had brain infarcts withno obvious cause, 28.2 percent had plaques 4 mm in thickness,as compared with 8.1 percent of the 172 patients who had infarctswhose possible or likely causes were known (odds ratio, 4.7;95 percent confidence interval, 2.2 to 10.1; P<0.001). Plaquesof 4 mm in the aortic arch were not associated with the presenceof atrial fibrillation or stenosis of the extracranial internalcarotid artery. In contrast, plaques that were 1 to 3.9 mm thickwere frequently associated with carotid stenosis of 70 percent.
Conclusions These results indicate a strong, independent associationbetween atherosclerotic disease of the aortic arch and the riskof ischemic stroke. The association was particularly strongwith thick plaques. Atherosclerotic disease of the aortic archshould be regarded as a risk factor for ischemic stroke andas a possible source of cerebral emboli.
Until recently, atherosclerotic disease of the aortic arch wasnot regarded as a source of cerebral emboli1. We have reportedon the basis of autopsy studies that the presence of ulceratedplaques in the aorta is an independent risk factor for ischemicstroke, particularly in patients with strokes of unknown cause,and that ulcerated plaques are predominantly found in patientswho are 60 years of age or older2. The advent of transesophagealechocardiography has made it possible to detect protruding atheroscleroticplaques in the aortic arch and descending aorta3,4. Althougha causal link between pedunculated and highly mobile plaquesand cerebral emboli seems likely,5 only retrospective studiesof this association have been reported6,7. One of these studiesfound a threefold increase in the risk of embolic disease inpatients with protruding plaques7. However, since these seriesincluded selected patients referred for echocardiography todetect the sources of the emboli, they may have been biased.In particular, atherosclerotic disease of the thoracic aortamay simply be a marker for general atherosclerotic disease8and for the actual cause of the stroke9. The aims of our studywere to determine with transesophageal echocardiography thefrequency of plaques in the aortic arch in consecutively admittedpatients with brain infarcts, as compared with the frequencyin controls, and to evaluate the clinical importance of theseplaques as possible sources of cerebral emboli.
Methods
This was a prospective case-control study of consecutively admittedpatients with ischemic stroke and consecutively admitted controls.
Patients and Controls
All patients over the age of 60 years with brain infarcts whowere hospitalized between September 1991 and October 1993 wereenrolled in the study. The following risk factors were noted:hypertension, hypercholesterolemia, cigarette smoking, diabetesmellitus, a high body-mass index, a previous myocardial infarction,peripheral vascular disease, and known atrial fibrillation oratrial fibrillation recorded within eight days after the detectionof the brain infarct. The patients underwent a diagnostic workupthat included cranial computed tomographic (CT) imaging or magneticresonance imaging (MRI) of the brain (or both), ultrasound examinationof the internal carotid and vertebral arteries (according toa standard protocol), transcranial Doppler examination, 12-leadelectrocardiographic studies, and transesophageal echocardiographicstudies, including an assessment of the thoracic aorta within15 days after the onset of the stroke.
After these studies had been performed, the patients were dividedinto four groups according to the presence of other potentiallycausal lesions. These assignments were made without knowledgeof the transesophageal echocardiographic assessment of the aorta.The first group included patients with brain infarcts likelyto have been caused by 70 percent stenosis of the ipsilateralinternal carotid artery or a definite cardiac source of embolism(acute anterior myocardial infarction, atrial fibrillation withleft atrial thrombus or spontaneous echo contrast, mural thrombusin left-heart cavities, mitral stenosis, a prosthetic heartvalve, or endocarditis). The second group included patientswith infarcts that may have been caused by 31 to 69 percentstenosis of the ipsilateral carotid artery, isolated atrialfibrillation, or atrial fibrillation occurring after the braininfarction. Patients in the third group were presumed to havelacunar infarcts due to lipohyalinosis of small deep intracranialarteries, with one of the four major lacunar syndromes (puremotor hemiplegia, pure sensory loss, hemiparesis and ataxia,or sensori-motor impairment) and with infarcts that were small(<15 mm) and deep or not demonstrable with two CT or MRIscans, in the absence of a cardiac or carotid source of embolism.Patients in the fourth group had no detectable lesions or theyhad lesions that have not been shown to increase the risk ofbrain infarction in subjects over the age of 60 years, suchas ipsilateral carotid stenosis of 30 percent, patent foramenovale, atrial septal aneurysm, or mitral-valve prolapse.
A total of 263 patients were enrolled in the study. Patientswith impaired consciousness for more than 15 days were excluded,as well as patients with respiratory failure and those in whomintroduction of the echocardiographic probe was technicallyimpossible. After these exclusions, there were 250 patientsin the study group.
The control group consisted of 250 consecutively enrolled patientsover 60 years of age with no history of ischemic stroke whounderwent transesophageal echocardiography for assessment ofcardiac conditions such as mitral or aortic valvulopathy, possibleimpairment of a prosthetic valve, myocardial infarction, atrialfibrillation, or suspected endocarditis. Patients with aorticdiseases, such as dissection or a saccular aneurysm, were excluded.Risk factors were noted at the time of examination.
Transesophageal Echocardiographic Assessment of the Aorta
Patients and controls underwent transesophageal echocardiographyperformed by trained cardiologists who were given informationabout the cause of brain infarction. The examinations were recordedon videotape. Transesophageal echocardiography was performedwithin two weeks after the onset of the stroke, according tostandard techniques8. We used commercially available imagingsystems with a 5-MHz single-plane probe (in the first 346 patients),biplane probe (in the next 97 patients), or multiplane probe(in the last 57 patients). After examination of the cardiacstructures, the transducer was gradually withdrawn to a pointabove the level of the aortic valve to obtain serial short-axisviews of the ascending aorta (with a single-plane probe). Witha counterclockwise rotation of the entire probe in the transverseplane, a short-axis image of the descending aorta was then obtained(40 to 45 cm from the incisors). The probe was progressivelypulled back to the curve of the distal arch (18 to 20 cm fromthe incisors). This portion was important to visualize in orderto differentiate the distal and proximal segments of the aorticarch. The probe was then rotated clockwise to study the proximalarch and, in some patients, the distal part of the ascendingaorta.
Videotapes of the transesophageal examinations of all 500 subjectswere reviewed by one of us (a senior echocardiographer) randomlyand without knowledge of the status of the patient (case orcontrol) or the classification of the cause of the stroke. Inaddition, the videotaped examinations of 100 randomly selectedpatients and controls were reviewed by two of us (also seniorechocardiographers) according to the same protocol.
We measured the thickness of the intimal and medial layers ofthe far wall during systole on a freeze frame, as previouslydescribed10,11,12. Wall thickness was measured in the descendingaorta, distal arch, proximal arch, and ascending aorta, withthe largest measured at all levels (Figure 1 and Figure 2).Since the ascending part of the aorta and the proximal archare both more likely to be sources of cerebral emboli than theother regions, we decided to pool the studies of lesions locatedin these two parts of the thoracic aorta.
Figure 1. Transesophageal Echocardiogram of the Aortic Arch Obtained with a Single-Plane Probe (Transverse View).
The plaque thickness, measured perpendicularly to the far wall, is calculated as the distance between the medial-adventitial border and the internal side of the lesion. The thickest portion is 5.9 mm (large arrow) and is located in the distal part of the aortic arch. The second lesion (arrowhead), which is more echogenic, is located in the proximal arch and is 4.5 mm thick. The two small arrows indicate an extensive plaque in the proximal arch and the upper part of the ascending aorta.
Figure 2. Transesophageal Echocardiogram of the Aortic Arch Obtained with a Biplane Probe (Transverse View).
A highly mobile component suggesting a thrombus (small arrows) is superimposed on a complex and extensive atherosclerotic plaque (large arrow). This free-floating thrombus is localized in the proximal arch.
Statistical Analysis
We used two-tailed t-tests for comparisons of means and chi-squaretests for comparisons of proportions. First, we performed aclassic case-control analysis. We compared the patients withbrain infarcts (case patients) and the controls with respectto various vascular risk factors and the presence of aorticplaques in the ascending aorta and proximal arch. Then we comparedthe frequency of high-grade plaques (those most likely to causeinfarction) with the frequency of atrial fibrillation and carotidstenosis in the case patients. Finally, we compared the frequencyof plaques in the patients who had ischemic strokes with knowncauses with the frequency in the patients who had infarcts withundetermined causes. Odds ratios were calculated by stepwiseunconditional multiple logistic regression, with adjustmentsfor age, sex, hypertension, cigarette smoking, cholesterol levels,diabetes, previous myocardial infarction, and atrial fibrillation.We used the kappa test to determine the degree of interobserveragreement on the assessment of plaques in the thoracic aorta.The data were analyzed with SAS software13.
Results
The case patients were older and had higher frequencies of hypertension,hypercholesterolemia, cigarette smoking, and diabetes than thecontrols (Table 1). The frequencies of atrial fibrillation andperipheral vascular disease did not differ significantly betweenthe two groups. The frequency of diseases of the coronary arteriesor valves was higher in the control group than in the infarctgroup. Table 2 shows the frequency of plaques in the ascendingaorta and proximal arch in patients and controls, accordingto the thickness of the plaque. We calculated the risk of cerebralinfarction for each category of plaque thickness relative tothe risk with a reference thickness of <1 mm, which was assignedan odds ratio of 1 (Table 2). Since a univariate analysis showedan abrupt increase in the odds ratio for stroke when plaqueswere 4 mm or thicker (crude odds ratio, 4.2 for plaques <4mm and 13.8 for those 4 mm), we performed an additional analysiswith this cutoff point.
Table 2. Risk of Cerebral Infarction According to the Thickness of Atherosclerotic Plaques in the Ascending Aorta or Proximal Arch.
Plaques with a Thickness of 1 to 3.9 mm
Patients with aortic plaques that were 1 to 3.9 mm thick differedfrom those with plaques under 1 mm thick only with respect tothe frequency of hypercholesterolemia, which was higher in thosewith thicker plaques. We found plaques 1 to 3.9 mm thick inthe ascending aorta or proximal arch in 46 percent of the patientswith brain infarcts and in 22 percent of the controls. The crudeodds ratio was 3.9 (Table 3), and the adjusted odds ratio was4.4 (P<0.001).
Table 3. Risk of Cerebral Infarction According to the Thickness of Plaques in the Thoracic Aorta.
Among the case patients, plaques that were 1 to 3.9 mm thickwere associated with the presence of carotid stenosis (Table 4).Such plaques were detected in 40 percent of the patientswith no carotid stenosis, in 49 percent of those with <70percent carotid stenosis, and in 61 percent of those with 70percent carotid stenosis (P = 0.03).
Table 4. Relation between Thickness of Plaques in the Ascending Aorta or Proximal Arch and the Extent of Carotid Stenosis in the 250 Patients with Brain Infarcts.
Plaques with a Thickness of 4 mm or More
Plaques 4 mm thick were found in the proximal part of the aortain 41 subjects: in the ascending aorta in 2, in the proximalarch in 38, and in both in 1. As compared with the patientswhose plaques were less thick, these patients had a higher frequencyof hypercholesterolemia and cigarette smoking and a lower frequencyof atrial fibrillation. The mean thickness of protruding lesionswas 5.8 mm, with a range of 4 to 13.2 mm. Plaques 4 mm in thicknesswere found in the distal arch in 64 patients and in the descendingaorta in 113. The kappa index for interobserver agreement onthe presence of plaques 4 mm thick ranged from 0.85 for thosein the distal arch to 0.95 for those in the ascending aortaand proximal arch.
We found plaques of 4 mm in the ascending aorta or proximalarch in 14.4 percent of the patients with brain infarcts andin 2 percent of the controls (P<0.001) (Table 2). After adjustmentfor atherosclerotic risk factors, the odds ratio for strokewas 9.1 (Table 2). Plaques of 4 mm were found in the distalarch or the descending aorta more frequently in patients thanin controls, but for plaques in the descending aorta, the differencewas not statistically significant (Table 3).
Among the case patients, plaques of 4 mm in the ascending aortaor proximal arch were detected equally frequently in patientswith 70 percent stenosis of the internal carotid artery (15percent of 33 patients) and in patients with <70 percentcarotid stenosis (15 percent of 93 patients) or no stenosis(14 percent of 124 patients; P = 0.9) (Table 4). Aortic plaqueswere detected less frequently in the patients with atrial fibrillation(7.9 percent of 76 patients) than in those without atrial fibrillation(17.3 percent of 174 patients).
Among the case patients, plaques of 4 mm in the ascending aortaor proximal arch were found in 5.5 percent of the patients withanother likely cause of ischemic stroke, in 9 percent of thosewith lacunar infarcts, in 11.5 percent of those with anotherpossible cause of stroke, and in 28 percent of those with noother detectable lesions (P<0.001) (Table 5). After adjustmentfor the covariates, the risk associated with a plaque of 4mm was 4.7 (95 percent confidence interval, 2.2 to 10.1) forpatients who had no other detectable lesions as possible causesof stroke, as compared with those who had other likely or possiblecauses or lacunar infarcts.
Table 5. Frequency of Plaques of greater than or equal to 4 mm in the Ascending Aorta or Proximal Arch in the 250 Patients with Ischemic Stroke, According to the Cause of the Stroke.
Among the patients with ischemic strokes and plaques of 4 mmin the ascending aorta or proximal arch, the brain infarctsinvolved the right hemisphere (in 15 patients) almost as frequentlyas the left (in 14); in 7 patients the infarcts were in theposterior circulation. Infarcts were more frequently cortical(in 25 patients) than deep (in 11). A mobile component was presentin the aortic plaques in 6 of the 78 patients with no detectablelesions and in 1 (presumably with a lacunar infarct) of theother 172 patients (P<0.001).
Discussion
Atherosclerotic disease of the aortic arch has been consideredas a possible but rare cause of embolic events in patients undergoingcardiac surgery, catheterization procedures, or anticoagulanttherapy1,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34.In a previous autopsy study, we found that ulcerated plaquesin the aortic arch may have played a part in causing brain infarction,especially in patients with cerebral infarction of no knowncause2. The presence of superimposed thrombi could not be assessedin the autopsy study2. It was important to confirm these resultsin live patients, and several studies have shown that transesophagealechocardiography is a reliable method of visualizing the aorticarch, protruding plaques, and thrombi3,5,35,36.
Our results indicate that the presence of atherosclerotic plaquesin the ascending aorta or proximal arch as detected by transesophagealechocardiography is a risk factor for ischemic stroke. The riskappeared to be particularly high for patients with plaques 4 mm in thickness and for the subgroup of patients who had noother detectable cause of ischemic stroke. However, severalmethodologic issues should be considered. Since the controlswere not referred for assessment of embolic disease, they mayhave had a lower frequency of plaques in the arch, thus leadingto an overestimation of the risk among the case patients. However,the case and control groups were remarkably similar with respectto the presence of peripheral vascular disease and atrial fibrillation,and the control group had a much higher frequency of coronaryartery disease. Since there is a strong link between atheroscleroticdisease of the thoracic aorta and diseases of both the coronaryand peripheral arteries,8,37 the high frequency of coronaryartery disease in our control group may have accounted for thefrequency of atherosclerotic plaques in the arch in this group.
Because of the interposition of the left bronchus, there isa blind region at the upper part of the ascending aorta, regardlessof the type of echocardiographic probe used. We may have missedsome lesions in this region, but since both patients and controlsunderwent the same type of examination, it is likely that theunderestimation was similar in the two groups. For lesions locatedin the proximal as well as the distal part of the arch, therewas a very high degree of agreement in the detection of plaques 4 mm thick (kappa index, 0.95). This distinction between thedistal and proximal locations is important, because lesionswere located more frequently in the distal part of the arch(distal to the ostium of the left subclavian artery) than inthe proximal part of the arch, and the lesions in the distalpart of the arch were less likely to give rise to cerebral emboli.
Although we found that plaques in the ascending aorta and proximalarch were associated with an increased risk of stroke, thisfinding does not establish a causal link. Indeed, plaques thatwere 1 to 3.9 mm thick were frequently associated with carotidstenosis, which may have been the actual source of the brainemboli. However, with plaques of 4 mm, a causal link is quitelikely for several reasons. First, one of the striking findingsof the present study is that the risk of stroke increased sharplyfrom less than 5 to more than 13 when the thickness of the plaqueswas 4 mm (Table 2). This large increase in risk was observedonly for lesions of 4 mm in the ascending aorta or proximalarch, not for those in the distal arch or descending aorta.Second, the high increase in the risk of ischemic stroke associatedwith plaques of 4 mm in the proximal arch was independent ofthe presence of the two major risk factors for stroke in theelderly: carotid stenosis and atrial fibrillation. We foundthat the frequency of plaques of 4 mm in the proximal archdid not differ according to the degree of carotid stenosis andthat the frequency of such plaques was lower in patients withatrial fibrillation than in those without fibrillation. Third,plaques of 4 mm in the proximal arch were also associated withan abrupt increase in the risk of stroke among patients whohad ischemic strokes with no other apparent cause. Furthermore,the presence of a mobile component of the plaque was associatedwith a risk ratio of 14 among patients with ischemic strokesof unknown cause. This clear-cut difference in the risk of strokebetween patients with plaques <4 mm thick and those withplaques 4 mm thick may be related to the composition of thelarger lesions in the aortic arch. Lesions 4 mm thick may containthrombotic material superimposed on the plaques, as shown duringsurgery38. The presence of a thrombus may also explain the morefrequent mobile component.
The substantial increase in the risk of ischemic stroke in associationwith plaques 4 mm in thickness in the aortic arch suggeststhat such lesions should be investigated as a risk factor forischemic stroke, particularly in the case of a stroke with noother likely or possible cause. Appropriate treatment of theselesions remains uncertain. Thrombolysis and surgical removalhave occasionally been reported to be successful in patientswith pedunculated and mobile thrombi in the aortic arch38,39.However, prospective studies are needed to determine the naturalhistory of these plaques and to evaluate the efficacy of varioustreatment regimens.
Supported by grants from the Institut National de la Sante etde la Recherche Medicale (CNEP 92CN23) and the Direction dela Recherche Clinique de l'Assistance Publique-Hopitaux de Paris(922601).
We are indebted to Dr. Annick Alperovitch for helpful criticismof this article.
Source Information
From the Services de Neurologie (P.A., P.-J.T., M.-G.B.) and Cardiologie (A.C., C.C.), Hopital Saint-Antoine, Universite Pierre et Marie Curie, Paris; INSERM, Unite 360, Recherches Epidemiologiques en Neurologie et Psychopathologie, Villejuif, France (C.T.); and the Cliniques Neurologique (M.H., G.B.) and Cardiologique (B.B.), Centre Hospitalier Universitaire de Grenoble, Grenoble, France.
Address reprint requests to Dr. Amarenco at the Service de Neurologie, Hopital Saint-Antoine, 184, rue du Faubourg Saint-Antoine, 75571 Paris CEDEX 12, France.
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Tunick, P. A., Kronzon, I.
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[Abstract][Full Text]
4 mm in thickness were found in 14.4 percent of the patients but in only 2 percent of the controls. After adjustment for atherosclerotic risk factors, the odds ratio for ischemic stroke among patients with such plaques was 9.1 (95 percent confidence interval, 3.3 to 25.2; P<0.001). Among the 78 patients who had brain infarcts with no obvious cause, 28.2 percent had plaques 
30 percent, patent foramen ovale, atrial septal aneurysm, or mitral-valve prolapse. 
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