3. Stames VA, Pitlick PT, Bernstein D, Griffin ML, Choy M, Shumway NE. Ebstein’s anomaly appearing in the neonate: a new surgical approach. J Thotac Cardiovasc Suq 1991:101:1082-1087. 4. Mair D. Ebstein’s anomaly: natural history and management. J Am Co// Cardi- ol 1992;19:1047-1048. 5. Plowden JS, Kimball TR, Bensky A, Savani R, Flake AW, Warner BW, All- men D, Ryckman FC. The use of extracorporeal membrane oxygenation in criti- cally ill neonates with Ebstein’s anomaly. Am Hem-r .I 1991;121:619-622. 6. Schober JG, Kellner M, Mocellin R, Schumacher G, Buhlmeyer K. Indications and pharmacological effects of therapy with prostaglandin El in the newborn. Ad\, Prosta&ndin Thrombmane Leukot Res 1980;7:905-91 I. 7. Cole RB, Abman S, Aziz KU, Bhamti S, LKV M. Prolonged prostaglandin El infusion: histolog’ic effects on the patent ductus ateriosus. Pedmtrics 1981;67: 81&819. 8. Lewis, Alan B, Freed MD, Heyman MA, Roehl SL, Kensey RC. Side effects

of therapy with prostaglandin E, in infants with critical congenital heart disease. Cimdation 1981;64:893-898. 9. Calder AL, Kirker JA, Neutze JM, Starling MB. Pathology of the ductus ate- riosus treated with prostaglandms: comparisons with untreated cases. Pediatr Car- dial 1984;5:85-92. 10. P&d N, Dagan 0, Baby” P, Silver M, Barker G, Hellmann I, Scolnik D, Karen G. Gastric-Outlet obstruction induced by prostaglandin therapy in neonates. N En,q/ .I Med 1992;327:505-5 IO. 11. Teixeira OP. Carpenter B, MacMurray SB, Vlad P. Long-term prostaglandin El therapy in congenital heart defects. J Am Co/l Cardiol 1984;3:83%843. 12. Emmanoulides GC, Moss AI, Duftie ER, Adams FH. Pulmonary arterial pres- sure changes in human newborn infants from bii. J Pediatr 1964:65:327-333. 13. Weesner KM. Hemodynamic effects of prostaglandin El in patients with con- genital heat disease and pulmonary hypertension. Cather Cardiovasr Diagn 1991;24: l&15.

How Many Patients with Acute Dissection of the Thoracic Aorta Would Erroneously Receive Thrombolytic Therapy Based on the Electrocardiographic Findings on Admission? Philip Weiss, MD, lmre Weiss, MD, Michael Zuber, MD, and Rudolf Ritz, MD

I n patients with myocardial infarction, thrombolytic therapy is now accepted as the standard care provid-

ed that ST-segment elevations in the electrocardiogram are present, whereas the benefit of thrombolytic therapy is questionable in patients with ST-segment depression.’ Acute dissection of the thoracic aorta can mimic the symptoms of myocardial infarction with pain, elevated serum creatinine kinase levels* and electrocardiographic abnormalities suggesting myocardial ischemia,3 and therefore lead to thrombolytic therapy with possibly dis- astrous results.4%5 However, to our knowledge there are no published data on the frequency of ST elevations in patients with acute aortic dissection.

To evaluate the incidence of electrocardiographic findings fulfilling the criteria for thromholysis (>l mm ST elevation in >I contiguous lead) in patients with acute dissection of the thoracic aorta, we analyzed retrospectively the initial electrocardiogram of patients admitted to our coronary care unit with chest pain subsequently proved to originate from aortic dissection. The computerized data jZe of the coronary care unit was searched for the diagnosis of aortic dissection in the years 1982 to 1991. Patients were included in the study if they filjlled the following 3 criteria: (I) acute dissection of the thoracic aorta proved by computer tomographic scan, angiography, echocardiography, surgery or autopsy; (2) admission electrocardiogram available; and (3) diagnosis not known on admission. Of IO1 patients with the diagnosis of aortic dissection, 51 did not conform to the inclusion criteria. The re- maining 50 patients (aged 62 IL II years, range 28 to 79, 8 women) form the basis of this analysis. A dissec- tion type A was found in 23 patients (10 died), and a dissection type B in 27 (4 died). Substernal chest pain suggesting myocardial infarction was present in 21 of 50 patients (42%, 95% confidence interval 25 to 59%); only 4 patients complained of pain radiating to the

From the Divisions of Intensive Care and Cardiology, Department of Internal Medicine, University Hospital Basel, 31 Petersgraben, CH- 4031 Basel, Switzerland. Manuscript received March 19, 1993; revised manuscript received and accepted June 3, 1993.

back. In 30 of 50 patients (60%, 95% confidence in- terval 42 to 75%) electrocardiographic abnormalities were present on admission ranging from anterior (30%) or inferior (8%) ST-segment depression, or negative T waves (32 and 14%, respectively) to old Q waves (Wo), or a combination of these. However, no patient had ST- segment elevation (95% confidence interval 0 to 8%).

Acute dissection of the thoracic aorta is a rare event compared with the incidence of acute myocardial infarc- tion. In the analyzed period (1982 to 1991) when we treated the 101 patients with aortic dissection, 3,834 pa- tients with acute myocardial infarction were admitted to our coronary care unit. In the Anglo-Scandinavian Study of Early Thrombolysis trial, 0.26% of the 5,011 patients were found to have aortic dissection4 In a comprehen- sive pathologic review of 505 cases of acute dissection of the aorta, involvement of the coronary arteries in the dissection was found in 39 patients (7.7%).6 However, not all of these patients will have concomitant ST ele- vations in the electrocardiogram as 1 of our patients demonstrated: His dissection reached well into the left main coronary artery but the electrocardiogram showed only unspecific ST-segment abnormalities.

In summary, ST-segment elevation is a relatively rare finding in patients with aortic dissection. The danger of erroneously administering thrombolytic therapy to a pa- tient with aortic dissection and ST-segment elevation suggesting acute myocardial infarction is very low given the low incidence of this finding in aortic dissection and the low prevalence of acute dissection of the thoracic aorta in patients admitted to a coronary care unit. The history of chest pain of recent onset and the finding of ST-segment elevation suggestive of evolving myocardial infarction in the absence of physical signs of aortic dissection will very rarely mislead the clinician. Losing time by ordering additional examinations before initiat- ing thrombolysis may decrease myocardial salvage and worsen the outcome of many patients.

1. Pastemak RC, Bmunwald E, Sobel BE. Acute myocardial infarction. In: Braun- wald E, ed. Heart Disease. 4th ed. Philadelphia: WB Saunders, 1992:1230-1291.

BRIEF REPORTS 1329

2. Davidson E, Weinixrger I, Rote&erg Z, Fuchs J, M&r S, Agmon J. Elevated serum creatine kinase levels: an early diagnostic sign of acute dissection of the

4. Wilcox RG, Olsson CG, Skew AM, van der Lippe G, Jensen G, Hampton JR. Trial of plasminogen activator for mortality reduction in acute myocardiaJ infarc-

aorta. Arch Intern Med 1988;148:2184-2186. tion. Lancer 1988;2:525-530. 2. Satler FL, Levine S, Kent KM, Pea& DL, Green CE, Del Negro A, Rackley 1. Butler J, Davies AH, Westaby S. Streptokinase in acute aortic dissection. or CE. Aotic dissection masquerading as acute myocardial infarction: implication for Med J 1990;300:517-519. thmmbolytic therapy without cardiac catheterization. Am J Cardiol 1984;54: 6. Hint AE, Johns VJ, Kime SW. Dissecting anemysm of the aorta. A review of 1134-l 145. 505 cases. Medicine 1958;37:217-279.

Physician Use of Transesophageal Echocardiography Varies with Time After Introduction into a Hospital Setting Richard W. Ayres, BMBS, FRACP, Trudy L. Burns, PhD, John Stuhlmuller, MD, Richard E. Kerber, MD, and Byron F.-Vandenberg, MD -

T ransesophageal echocardiography (TEE) is useful in the diagnosis of intracardiac masses and tumors, veg-

etations, native and prosthetic valve dysfunction, tho- racic aorta disease and congenital heart disease.’ Recent reports suggest a variation in the use of TEE.24 These reports generally describe either initial experiences* or reviews over 6 to 7 months.5Jj Since new diagnostic techniques typically pass through stages before becom- ing part of established medical practice,7 we hypothe- sized that the use of TEE varies with time after intro- duction into a hospital setting.

We reviewed the reasons for requesting TEE in 312 awake patients studied in our echocardiography labora- tory and intensive care units in the initial 2 years after introducing TEE. There were 185 men and 127 women, with a mean age (k SD) of 54 f 17 years. Reasons for TEE requests were classtjied as: (1) cardiac source of embolus, (2) valve vegetation or abscess, (3) prosthetic valve dysfunction, (4) native valve dysfunction, or (5) miscellaneous (including thoracic aorta and congenital heart disease). The requests were reviewed during 4 six- month periods, beginning with January to June 1990 and ending with July to December 1991. Chi-square analysis was used to investigate the distribution of TEE indications over time. Di$erences were considered sta- tistically significant at p <O.Ol.

Reasons for requesting TEE varied overall with time ji-om introduction into our hospital setting (Table I). After the initial 6 months, requests for TEE for suspect- ed valve vegetation or abscess signtjicantly increased, whereas requests for suspected prosthetic valve dysfunc- tion decreased. There were no further significant changes in these indications during the next 3 time pe-

From the Cardiovascular Center, College of Medicine, University of Iowa, Iowa City, Iowa 52242. Manuscript received April 16, 1993; revised manuscript received and accepted June 7, 1993.

riods. Requests for TEE for suspected cardiac source of embolus and native valve dysfunction did not change over the 2-year study period.

Kotler and Diamond* proposed that clinicians’ per- ception of the role of a diagnostic technique may change over time. Possible explanations for the changing perception of TEE are: (1) a requirement for evidence of effectiveness in detecting valvular vegetation or ab- scess, and (2) early individual explorations of effective- ness in assessing prosthetic valve function.7 The subse- quent decrease in use of TEE to evaluate prosthetic valve function is consistent with the studies by Seward et al*Z (Table lI).

Differences in ordering patterns between the previously reported series may be related to patient se- lection. In our study, only 5% of patients had TEE per- formed to evaluate native valve function; however, Chandrasekeran et al4 reported that 25% of their patients had TEE for the same indication; half of them had TEE to provide additional information before surgery.

TABLE I Indications for Transesophageal Echocardiograms Performed Over Four Six-Month Time Periods

Time Periods

I II Ill IV - - - -

Indication n (%) n (%) n (%I n (%)

Source of embolus 16 (35) 32 (44) 55 (50) 37 (44) Vegetation or abscess 2 (4)* 18 (25) 31 (28) 27 (32)

Prosthetic valve function 13 (28)* 5 (7) 6 (6) 8 (9) Native valve function 2 (4) 6 (8) 4 (4) 3 (4) Miscellaneous 13 (28) ll(15) 13 (12) 10 (12)

Totals 46

*p < 0.005 WRUS periods II, III and IV.

72 109 85

TABLE II Indications for Transesophageal Echocardiograms Reported in Six Studies

Seward et al Chandrasekeran et al Pavlides et al Zabalgoitia et al Ayres et al

1988 1992 1990 1990 1990 (present (ref. 2) (ref. 3) (ref. 4) (ref. 5) (ref. 6) study)

Indication n = 100 n = 3,827 n = 230 n = 95 n = 88 n = 312

Source of embolus 16% 32% 9% N/A 53% 45% Vegetation or abscess 11 13 12 17% 18 25 Prosthetic valve function 18 8 34 15 15 10 Native valve function 8 13 25 25 7 5 Miscellaneous 47 34 20 43 7 15 Not available

1330 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 72 DECEMBER 1,1993