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Reprinted by permission from Primary Cardiology, 1995.

Paul Barone DO, Daniel Shindler MD, John Kostis MD.


An 84 year old white man presented with crescendo angina. He had a long history of hypertension and diabetes. During the hospital stay he ruled in for myocardial infarction and underwent cardiac catheterization which reveled triple vessel coronary artery disease. It was decided to send him for coronary bypass surgery. At the time of surgery he underwent a transesophageal echocardiogram (TEE), which showed diffuse aortic plaques with a mobile atheroma. He underwent bypass surgery uneventfully, but on the second postoperative day he was found to be aphasic with new left sided weakness. CT scan confirmed a new left side CVA.


There are many methods of detecting and quantifying aortic atherosclerotic plaques. Roentgenographic studies such as chest X-ray, CT scans, MRI and angiography have all been used. These studies do not provide real-time images. The use of transesophageal echocardiography has shown great promise because it does provide real-time images and is able to image arterial wall structure permitting plaque and wall characterization.

Aortic atherosclerosis by TEE has been clinically useful in the field of systemic and peripheral embolization.(1) Many studies have shown that protruding atheromas in the thoracic aorta are an independent risk factor for embolism.(2-5) Stroke data banks show that no cause can be found in 26-40% of all cerebral infarcts.(5) In this subgroup of patients, TEE is the study of choice to define the embolic source.(6) TEE has also found its way into the operating room. With respect to cardiopulmonary bypass surgery it has been shown that use of TEE has decreased the incidence of perioperative stroke.(7) Recent studies have also been done showing a relationship between aortic atherosclerotic disease and coronary artery disease.(8,9)

The following is a review of the history of TEE visualization of aortic atherosclerosis, of the present classifications of aortic plaques, and of the limitations of TEE in this area.


Early studies of arterial atherosclerosis utilized ultrasonic tissue characterization. The use of techniques such as, analysis of attenuation properties, backscattered radio frequency signals and more recently pixel gray scale level brought new insights.

Picano et. al (10) studied formalin-fixed human aortic walls and found that by using backscattered signals they were able to differentiate normal from fibrofatty and calcific subsets. They went on to study the attenuation properties of human fresh aortic walls. This in vitro approach showed that integrated attenuation index was lowest in normal walls and progressively increased in fibrous, fibrofatty and calcific subsets.(11) Sarnelli et. al.(12) did comparative histology on aortic specimens utilizing both attenuated and backscattered indexes. This had the ability to differentiate deposition of biochemical components, such as collagen, and calcium from fatty tissue.

Grey level statistics by Pandian et. al. have been used to differentiate myocardium before and after infarction. McPherson et al. who were able to distinguish perivascular fat from atheroma or normal wall in human coronary arteries.(13,14) McPherson et. al used grey scale levels to differentiate plaques from plaque free regions in the aorta.(15) They were able to do so when comparisons were made in the same patient. In comparable visualization between patients, the plaques with lower mean gray scale levels required slightly higher gain settings to offset the lower brightness. As a result, the gray scale levels of the plaques and normal aorta were nearly identical. This finding reflects the difficulty in applying gray scale statistics across patients when there is no internal standardization of equipment for comparison.


Studies done looking at aortic atherosclerosis and systemic embolization utilized other criteria to diagnose atherosclerosis. One such criterion is intimal and medial thickness. Pignoli et. al. utilizing B mode images of intimal and medial thickness defined this area as two parallel echogenic lines separated by a hypoechoic space.(16) They showed that the inner line was the luminal/intimal transition and the outer line represented the adventitia. They also set out to determine the accuracy of intimal/medial thickness measurements by B mode imaging and correlating this with the thickness of different combinations of tunicae evaluated by gross and microscopic exam. They found, by gross pathologic exam, no statistically significant difference between the two measurements. There was a statistical difference when compared to the histologic measurements. This discrepancy may be due to artifacts introduced during the processing of tissue for histologic evaluation.

Nishino et. al. utilized maximal thickness of the intimal/medial complex as an index of atherosis.(17) They also compared the TEE results with pathologic measurements and found a linear relationship. Toyoda et. al. also utilizing intimal-medial thickness compared measurements recorded with TEE and histologic specimens. They found a sensitivity of echo detection of a complicated lesion to be 74% with a specificity of 94%.(4)

Thus, multiple studies have found the use of ultrasonic images in the measurement of intima/media complex to be pathologically accurate. However, none of the above studies supply pathological support for the concept of thickened intimal/media complex as it applies to atherosclerosis.

Pathologic studies have been done looking at aortic intimal thickness and correlating it with atheronecrosis and coronary artery disease.(18,19) Fibroplastic intimal thickening is thought to be driven in experimental animals by smooth-muscle cells proliferating in situ. Studies done on postmaturity intimal changes have found that at a certain intimal thickness: 200-299um, the increase in cell number is complete.(19)

Tracy et. al. have shown that the probability of atheronecrosis emerging in the aorta was related to age and fibroplastic intimal thickness. Aortas with a mean thickness grater than 300um have a high probability of developing some foci of atheronecrosis. They also defined a threshold for necrosis as a mathematical equation, in which age and fibroplasia are variables. When years times the mean intimal thickness exceeded 17,000um-years the odds of finding a necrotic core exceeded unity.(18,19)

Thus, there is some pathological support for the theory of increased intimal/medial complex as a sign for atherosclerosis. This also supplies a intimal/medial critical thickness that is required to produce an atheronecrotic lesion. Whether this can be utilized as pathologic basis for ultrasound characterization of plaques remains to be answered by further study.


As stated earlier, a majority of studies done defined atherosclerosis as an increase of the thickening of the intima with luminal irregularities. Fazio et. al.(8) and Tribouilloy et. al.(9) were more specific in their respective studies and defined aortic atherosclerosis in grades I-IV and I-III respectively. Fazio et. al. do not place a figure on the exact measurement of the I/M complex. Tribouilloy et al. state that an I/M thickness of less than 5mm is stage II and greater than 5mm is stage III. The measurement of 5mm was used in an earlier study by Katz et. al. (7) Toyoda et. al.(4) looking at aortogenic embolic strokes, delineated a measurement of 3mm. Again, none of the above studies define any pathologic basis for these measurements.

Plaque thickening and its association with embolic events were looked at by Amarenco.(20) In a group of 78 patients with no known cause of cerebral infarction, 28% had plaques >4mm in thickness, as compared to 8.1% who had infarcts of known cause. They concluded that the association between atherosclerotic plaques in the aortic arch and the risk of ischemic strokes increased from less than 5 to more than 13 when plaque thickness was greater than 4.2 mm.

A final characterization first described by Karalis et. al.(3) and later studied by Tunick et. al is a protruding or mobile component to the atherosclerotic lesion, such as our patient.(1-3)

Multiple studies have shown that protruding atheroma to be an independent risk factor for systemic embolization.(2,6) Tunick et. al. showed that in the presence of a protruding atheroma, one was at a 3 times greater risk of having an embolic event.(2) Karalis showed and incidence of embolic events to be 31% with such a lesion. A prospective study by Tunick et. al. in which patients with protruding aortic plaques were followed for 13 months found that 33% developed embolic complaints compared to only 7% of the controls.(3,6)

No studies have been done to characterize the form of the atheroma, ie whether it is ulcerated. Amarenco et. al. determined the frequency of ulcerated plaques in the aortic arch in 500 postmortem patients with history of CVA and found the prevalence of ulcerated plaques was 26%.(21) TEE is, as shown in our patient, able to visualize plaques protruding into the lumen, but it is unable to identify ulcerations. With the advent of 3-D and 4-D imaging of the aorta, more accurate description of plaque morphology is expected.(22)


As is true for all diagnostic tests, there are also limitations to TEE imaging of the aorta. A major limitation is the inability to visualize the ascending aorta due to the air filled trachea interposed between the esophagus and the aorta. One pathologic study has shown that in 97 specimens of ascending aorta from adults with coronary artery disease, the prevalence of atherosclerotic plaques was 38%.(23) Amarenco showed that plaques in the ascending aorta and proximal arch were associated with a greater increase in the risk of stoke than those found in the distal arch or descending aorta. With the use of biplane and multiplane probes the blind spot in the ascending aorta is even smaller.

Another limitation, artifacts, are inborn to all ultrasonic images. They are especially troublesome in the ascending aorta. As with all echocardiography, artifacts arise at multiple levels in the acquisition, processing, display, and recording of reflected ultrasound signals.(24) The ability to diminish the effects of artifacts on studies depends as much on the technique and skill of the echocardiographer performing and interpreting ultrasound images as on the anatomic challanges posed by a particular esophagus.

Other limitations include, the lack of a large scale study comparing TEE images with histologic or gross pathologic specimens, the inability to visualize the aortic wall that is closest to the transducer, and if a protruding atheroma is found, what is the optimal treatment? Only the anecdotal use of oral anticoagulants has been published with good results.(25)


The use of transesophageal echocardiography for aortic dissection, valvular pathology and visualizing posterior cardiac structures is well documented.(26) The use of TEE in the study of aortic atherosclerosis and its clinical implications is still in its infancy. The use of TEE for undiagnosed causes of CVA is well documented and should be utilized. Further study is needed in the aspect of effective treatment in patients with mobile or protruding atheromas. TEE in the operating room for cardiopulmonary surgery appears to be effective in decreasing post-operative stroke. The age of patients undergoing coronary artery bypass grafting has increased and the incidence of stroke after the procedure increases linearly with age.(27,28) TEE inspection of the aorta prior to cannulation is becoming routine. The emerging technology of 3-D and 4-D imaging will better depict the aorta, and more exactly characterize atherosclerotic plaques.


1. Tunick P, Kronzon I. Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: A new finding seen by transesophageal echocardiography. Am Heart J 1990;120:658-660.

2. Tunick PA, Perez JL, Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991;115:423-427.

3. Karalis DG, Krishnaswamy C, Victor MF, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;17:73-8.

4. Toyoda K, Yasaka M, Nagata S, Yamaguchi T. Aortogenic embolic stroke: a transesophageal echocardiographic approach. Stroke 1992;23:1056-1061.

5. Amarenco P, Cohen A, Baudrimont M, Bousser MG. Transesophageal echocardiographic detection of aortic arch disease in patients with cerebral infarction. Stroke 1992;23:1005-1009.

6. Tunick PA, Rosenzweig BP, Katz ES, Freedberg RS, Perez JL, Kronzon I. High Risk for vascular events in patients with protruding aortic atheromas: a prospective study. J Am Coll Cardiol 1994;23:1085-90.

7. Katz ES, Tunick PA, Rusinek H, Ribakove G, Spencer FC, Kronzon I. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992;20:70-7.

8. Fazio GP, Redberg RF, Winslow T, Schiller NB. Transesophageal echocardiographically detected atherosclerotic aortic plaque is a marker for coronary artery disease. J Am Coll Cardiol 1993;21:144-50.

9. Tribouilloy C, Shen WF, Peltier M, Lesbre JP. Noninvasive prediction of coronary artery disease by transesophageal echocardiographic detection of thoracic aortic plaque in valvular heart disease. Am J Cardiol 1994;74:258-260.

10. Picano E, Landini L, Distante A, Sarnelli R, Benassi A, L'Abbate A. (1983a) In Vitro differentiation of human atherosclerotic aortic walls by backscattered ultrasound. (Abstr) J Am Coll Cardiol 1:670.

11. Picano E, Landini L, Distante A, et al. Fibosis, lipids, and calcium in the human atherosclerotic plaque. In vitro differentiation from normal aortic walls by ultrasound attenuation. Circ Res 1985;56:556-62.

12. Sarnelli R, Landini L, Squartini F. Atherosclerosis detection by ultrasound. a comparative histologic study on aortic specimens. Appl Pathol 1986;4:270-5.

13. Skorton DJ, Melton HE, Pandian NG, et al. Detection of acute myocardial infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray level distributions. CircRes 1983;52:36-44.

14. McPherson DD, Sirna SJ, Haugen JA, et al. Acoustic properties of normal and atherosclerotic human coronary arteries in vitro and in vivo observations (Abstract) Circulation 1987;76:43.

15. Lanza G, Zabalgoitia-Reyes M, Frazin L, Meyers SN, Spitzzeri Cl, et al. Plaque and structural characteristics of the descending thoracic aorta using transesophageal echocardiography. J Am Soc Echo 1991;4:19-28.

16. Pignoli P, Tremoli E, Poli A, Oreste P, Paoletti R. Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging. Circulation 1986;74, No. 6:1399-1406.

17. Nishino M, Masugata H, Yamada Y, Abe H, Hori M, Kamada T. Evaluation of thoracic aortic atherosclerosis by transesophageal echocardiography. Am Heart J 1994;127:336-44.

18. Tracy RE, Toca VT, Lopez CR, Kissling GE, Devaney K. Fibrous intimal thickening and atheronecrosis of the thoracic aorta in coronary heart disease. Laboratory Investigation 1983;48:303- 12.

19. Tracy RE, Kissling GE. Age and fibroplasia as preconditions for atheronecrosis in the human thoracic aorta. Arch Pathol Lab Med 1985;109:651-658.

20. Amarenco P, Cohen A, Tzourio C, et al. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 1994;331:1474-9.

21. Amarenco P, Duyckaerts C, Tzourio C, Henin D, Bousser MG, Hauw JJ. The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 1992;326:221-5.

22. Pandian NG, Nanda NC, Schwartz SL, et al. Three-Dimensional and Four-Dimensional transesophageal echocardiographic imaging of the heart and aorta in humans using a computed tomographic imaging probe. Echocardiography 1992;9:677-87.

23. Tobler HG, Edwards JE. Frequency and location of atherosclerotic plaques in the ascending aorta. J Thorac Cardiovasc Surg 1988;96:304-6.

24. Obeid A. Echocardiography in Clinical Practice. Philadelphia, PA: J.B. Lippincott Company;1992:16-17.

25. Bansal RC, Pauls GL, Shankel SW. Blue digit syndrome: transesophageal echocardiographic identification of thoracic aortic plaque-related thrombi and successful outcome with warfarin. J Am Soc Echocardiogr 1993;6:319-23.

26. Bansal RC, Shah PM. Transesophageal echocardiography. Curr Prob Cardiol 1990;15:647-720.

27. Hall RJ, Elayda MA, Gray A, et al. Coronary artery bypass: long term follow-up of 22,284 consecutive patients. Circulation 1983;68:(suppl II):II-20-6.

28. Gardner TJ, Horneffer PJ, Manolio TA, et al. Stroke following coronary artery bypass grafting: a ten-year study. Ann Thorac Surg 1985;40:574-81.

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