Patent ductus arteriosus

To compare the accuracy of transesophageal echocardiography (TEE) with that of transthoracie echocardiography (TTE) in the detection of patent ductus arteriosus (PDA) in the adolescent and the adult, 40 patients with PDA and 50 patients with other congenital heart diseases were studied. All echocardiograms were recorded before cardiac catheterization and surgery. The echocardiographic diagnosis of PDA was made by direct visualization of a shunt How in the duct. A mosaic flow in the pulmonary artery without direct visualization of the duct was considered possible but not definitely diagnostic of PDA. TEE showed greater sensitivity and negative predictive value than TTE (97% vs 42%, and 98% vs 68%, respectively; p<0.001) in confirming the diagnosis of PDA. The specificity and positive predictive value in establishing the diagnosis of PDA were the same for both techniques. In the subgroup of patients with Eisenmenger's syndrome, the sensitivity of TEE and TTE in confirming diagnosis of PDA was 100% and 12% (p<0.01), respectively. The sensitivity of monoplane and biplane TEE in the diagnosis of PDA was comparable (95% and 100%, respectively; p=NS). In conclusion, TEE was highly sensitive and specific in detecting PDA in adolescents and adults. It was also highly valuable for detecting the cause of pulmonary hypertension in patients with Eisenmenger's syndrome.

(CHEST 1995; 108:1201-05)

PDA = patent ductus arteriosus; TEE = transesophageal echocardiography; TTE = transthoracic echocardiography

Key words: Eisenmerger's syndrome; patent ductus arteriosus; transesophageal echocardiography; transthoracic echocardiography

Patent ductus arteriosus (PDA) is a frequent congenital cardiovascular abnormality connecting the origin of the left pulmonary artery with the descending aorta just distal to the left subclavian artery.[1] PDA is usually identified early in life. However, there is an increasing awareness of PDA presenting in adulthood and even in the elderly.[2-5] PDA in infants and children can often be diagnosed by transthoracic two-dimensional and color Doppler echocardiography through detecting a shunt flow from the descending aorta into the pulmonary artery through a ductal structure.[6-9] However, since the PDA is far from the transducer on the chest wall and because of interference from lung tissue and ribs in adults, it is usually difficult to show clearly this structure and the flow in it.[10-11] Thus, diagnosing PDA by transthoracic echocardiography (TTE) is difficult, highly technique-dependent, and sometimes even an impossible task in adolescents and adults.

With the advent of transesophageal echocardiography (TEE), there is a much better window to the posterior structures of the thoracic cardiovascular system.[12-14] Although TEE has been employed to evaluate various cardiac anomalies,[15-16] experience with its use in PDA is limited[17,18] and its accuracy for the diagnosis of PDA is not known. Therefore, we conducted a prospective study to evaluate the sensitivity and specificity of TEE and to compare the accuracy of TTE and TEE in the diagnosis of PDA in adolescents and adults.

MATERIALS AND METHODS

Study Patients

This study was a prospectively designed study. A total of 90 patients form the basis of the study, and they were subdivided into two groups. Group 1 (40 patients) comprised all patients studied at our echocardiography laboratory with both TTE and TEE in whom PDA was proved by cardiac catheterization and surgery (n=21), cardiac catheterization alone (n=18), or surgery alone (n=1) in a 3-year period. Six patients who refused cardiac catheterization and did not undergo cardiac surgery were excluded in the same period. Patients referred for echocardiographic examination in our laboratory were above age 15. Group 2 (50 patients) comprised all patients with other congenital heart diseases studied with both TTE and TEE in whom absence of PDA was verified by cardiac catheterization. All group 2 patients underwent cardiac surgery.

Group 1 contained 10 men and 30 women (age range, 17 to 65 years; mean age, 33 years). The clinical diagnosis was PDA in 24, ventricular septal defect with pulmonary hypertension in 5, aortic regurgitation in 3, atrial septal defect in 3, ventricular septal defect with rupture of sinus of Valsalva in 1, unexplained pulmonary hypertension in 2, and cyanotic congenital heart disease in 2 patients. Only 20 patients had typical continuous murmurs. The clinical manifestations included dyspnea and exercise intolerance in 18, palpitation in 4, and chest pain in 3. Fifteen patients were asymptomatic. Eight of the 40 patients had Eisenmenger's syndrome confirmed by cardiac catheterization. Of the eight patients, three had ventricular septal defect and one had coarctation of the aorta besides PDA. Of the 32 patients without Eisenmenger's syndrome, 2 also had ventricular septal defect.

Group 2 was composed of 19 men and 31 women (age range, 17 to 64 years; mean age, 34 years). None of the patients had a clinically suspected PDA. The diagnosis, as confirmed by cardiac catheterization and surgery, was atrial septal defect in 37, ventricular septal defect in 9, Ebstein's anomaly in 2, and pulmonary stenosis and pseudotruncus each in 1 patient.

Echocardiographic Examinations

Transthoracic and transesophageal echocardiograms were recorded for all patients before cardiac catheterization or cardiac surgery. An echocardiographic imaging system (Toshiba SSH-65A; Toshiba Corp; Tokyo) was used in 22 of the group 1 and 26 of the group 2 patients and another imaging system (Aloka SSD-870; Aloka Corp; Tokyo) was used in 18 of the group 1 and 24 of the group 2 patients. Transthoracic studies were performed prior to, but as on the same day as, transesophageal studies. These studies were performed after patients gave informed consent. All studies were recorded on 3/4-in tapes (Sony U-matic) or 1/2-in VHS tapes (Panasonic) for further analysis. The echocardiograms were interpreted by two experienced echocardiographers unaware of the results of cardiac catheterization or surgery. Any differences in the interpretation were resolved by a third observer who also did not know any findings.

Transthoracic Echocardiographic Studies

Both 2.5- and 3.75-MHz phased-array transducers connected to an echocardiographic imaging system (Toshiba SSH-65A or an Aloka SSD-870) machine were used for transthoracic echocardiographic examinations. Standard parasternal long-axis and short-axis views, apical four-chamber, and suprasternal long-axis views were used to examine every patient with both two-dimensional and color Doppler flow mapping methods. Special attention was paid to various high parasternal short-axis views at the level of the pulmonary artery. Any mosaic flow in the aorta and pulmonary artery was carefully sought. Both pulsed-wave and continuous-wave Doppler were used to analyse the flow pattern.

Transesophageal Echocardiographic Studies

A single-plane transesophageal 3.75-MHz transducer interfaced with the Toshiba SSH-65A imaging system was used in 22 of the group 1 and 26 of the group 2 patients and a biplane transesophageal 5.0-MHz transducer interfaced with the Aloka SSD-870 imaging system was used in 18 of the group 1 and 24 of the group 2 patients. The procedure of transesophageal study has been described previously.[19] After cardiac structures were systemically examined, the probe was rotated counterclockwise to visualize the decending thoracic aorta. A transverse scan transducer was used at a distance of 30 cm from the incisor. The probe was pulled out carefully and, at about 1-cm intervals, the probe was anteflexed and retroflexed to search for abnormal flow between the descending aorta and the pulmonary artery. Pulsed Doppler was then used to demonstrate the pattern of the abnormal flow. In biplane probe, a longitudinal scan transducer was used to search for ductal shunt flow after completion of the transverse scan examination. Transesophageal echocardiographic procedure time was within 15 min in all patients.

Diagnostic Criteria

In either transthoracic or transesophageal echocardiographic study, direct visualization of the mosaic flow from the descending aorta into the pulmonary artery was considered confirmatory diagnosis of PDA. A mosaic flow in the pulmonary artery without demonstrating its origin (indirect visualization) was considered possible, but not definitely diagnostic of, PDA.

Cardiac Catheterization

The presence of PDA was confirmed by direct passing of the catheter from the pulmonary artery into the aorta through the duct during right heart catheterization. Blood was sampled at multiple sites for the measurement of oxygen saturation. Pressure was recorded to detect the presence and severity of pulmonary hypertension. If the presence of PDA was still doubtful, angiographic confirmation was performed by injecting contrast media into the ascending aorta and taking both posteroanterior and lateral cineangiograms in patients without pulmonary vascular obstructive disease.

Statistical Analysis

The sensitivity, specificity, and positive and negative predictive values of TTE and TEE in the diagnosis of PDA were calculated. Statistical analysis was performed using [X.sup.2] with Yates' correction and unpaired t test, and a p value less than 0.05 was considered significant.

Results

Transthoracic Echocardiography

A mosaic flow was detected in the pulmonary artery in 28 of the 40 group 1 patients. In the other 12 patients, no abnormal flow could be found in the pulmonary artery. Of the 28 patients with a mosaic flow in the pulmonary artery, the diagnosis of PDA could be confirmed by direct visualization of the mosaic flow from the descending aorta into the pulmonary artery in 17 patients. In the other 11 patients, the presence of a mosaic flow in the pulmonary artery was a possible PDA, but the diagnosis could not be confirmed because the flow was not proved to come from the descending aorta. None of the group 2 patients had possible or diagnostic PDA. The sensitivity, specificity, and positive and negative predictive values of TTE in confirming the diagnosis of PDA were 42%, 100%, 100%, and 68%, respectively. When possible and confirmatory diagnosis of PDA was included, the sensitivity and negative predictive value increased to 70% and 81%, respectively (Fig 1).

In the subgroup of eight patients with Eisenmenger's syndrome, the diagnosis of PDA was confirmed in one (sensitivity, 12%) and possible in two. No abnormal flow was detected in the other five patients with the syndrome. If these eight patients with Eisenmenger's syndrome were excluded, the sensitivity of TTE in detecting confirmatory diagnosis of PDA increased to 50% (Table 1) and in detecting possible plus confirmatory diagnosis of PDA increased to 78%.

REFERENCES

[1] Kelly DT. Patent ductus arteriosus in adults. Cardiovasc Clin 1979; 10:321-26 [2] Marguis RM, Miller H, McCormack R, et al. Persistence of ductus arteriosus with left to right shunt in die older patient. Br Heart J 1982; 48:469-84 [3] Fisher RG, Moodie DS, Sterba R, et al. Patent ductus arteriosus in adults - long-term follow-up: nonsurgical versus surgical treatment. J Am Coll Cardiol 1986; 8:280-84 [4] Zarich S, Leonardi H, Pippin J, et al. Patent ductus arteriosus in the elderly. Chest 1988; 94:1103-05 [5] Hang CL, Sullebarger JT. Patent ductus arteriosus presenting in old age. Cathet Cardiovase Diagn 1993; 28:228-30 [6] Huhta JC, Cohen M, Gutgesell HP. Patency of the ductus arteriosus in normal neonates: two-dimensional echocardiography versus Doppler assessment. J Am Coll Cardiol 1984; 4:561-64 [7] Sahn DJ, Allen HD. Real-time cross-sectional echocardiographic imaging and measurement of the patent ductus arteriosus in infants and children. Circulation 1978; 58:343-54 [8] Swensson RE, Valdes-Cruz LM, Sahn DJ, et al. Real-time Doppler color flow mapping for detection of patent ductus arteriosus. J Am Coll Cardiol 1986; 8:1105-12 [9] Milne MJ, Sung RYT, Fok TF, et al. Doppler echocardiographic assessment of shunting via the ductus arteriosus in newborn infants. Am J Cardiol 1989; 64:102-05 [10] Perez JE, Nordlicht SM, Geltman EM. Patent ductus arteriosus in adults: diagnosis by suprasternal and parasternal pulsed Doppler echocardiography. Am J Cardiol 1984; 53:1473-75 [11] Tunick PA, Kronzon I Diagnosis of patent ductus arteriosus by serendipity in the adult. J Am Soc Echocardiogr 1988; 6:446-49 [12] Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. Mayo Clin Proc 1988; 63:649-80 [13] Matsuzaki M, Toma Y, Kusukawa R. Clinical applications of transesophageal echocardiography. Circulation 1990; 82:709-22 [14] Fisher EA, Goldman ME. Transesophageal echocardiography: a new view of the heart. Ann Intern Med 1990; 113:91-3 [15] Sreeram N, Sutherland GR, Geuskens R, et al. The role of transesophageal echocardiogirapby in adolescents and adults with congenital heart disease. Eur Heart J 1991; 12:231-40 [16] Marelli AJ, Child JS, Perloff JK. Transesophageal echocardiography in congenital heart disease in the adult. Cardiol Clin 1993; 11:505-20 [17] Mugge A, Daniel WG, Lichtlen PR. Imaging of patent ductus arteriosus by transesophageal color-coded Doppler echocardiography. J Clin Ultrasound 1991; 19:128-29 [18] Takenaka K, Sakamota T, Shiota T, et al. Diagnosis of patent ductus arteriosus in adults by biplane transesophageal color Doppler flow mapping. Am J Cardiol 1991; 68:691-93 [19] Shyu KG, Hwang JJ, Lin SC, et al. Prospective study of blood culture during transesophageal echocardiography. Am Heart J 1992; 124:1541-44 [20] Lam J, Neirotti RA, Lubbers WJ, et al. Usefulness of biplane transesophageal echocardiography in neonates, infants and children with congenital heart disease. Am J Cardiol 1993; 72:699-706 [21] Neufeld HN, Lester RG, Adams PJ, et al. Congenital communication of a coronary artery with a cardiac chamber or the pulmonary trunk ('coronary artery fistula'). Circulation 1961; 23:171-79 [22] Daniels O, Hopman JCW, Knecht DE, et al. Pulsed Doppler echocardiography in patients with aortopulmonary connection. Acta Paediatr Scand 1986; 329 (suppl):44-52

(*) From the Department of Emergency Medicine, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, and the Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan, Republic of China.

Manuscript received February 15, 1995; revision accepted May 11. Reprint requests: Dr. Chen, Department of Internal Medicine, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei 100, Taiwan, ROC

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