J Thorac Cardiovasc Surg 1995;110:1136-1139
© 1995 Mosby, Inc.
TRAUMATIC AORTOPULMONARY COMMUNICATION: CLINICOPATHOLOGIC CORRELATION
Tzong-Luen Wang, MD,a,
Jiunn-Lee Lin, MD,a,
Shoei-Shen Wang, MD,b,
Huei-Ming Ma, MD,a,
Juey-Jen Hwang, MD,a,
Wen-Pien Lien, MD, FACC,a
Taipei, Taiwan, Republic of China
This report concerns a young man in whom traumatic aortopulmonary communication occurred that mimicked congenital aortopulmonary window. To our knowledge, this has never been reported in the literature. The precise preoperative diagnosis and the adequate surgical treatment may provide a good clinical experience.
A 32-year-old male patient had a stabbing injury over the left side of the upper chest 4 years ago. Emergency surgical repair of a cardiac rupture was done immediately at that time at another hospital. The patient led an independent daily life after hospital discharge. He was told that an intracardiac shunt might be necessary; however, he did not request this therapy.
He had progressive exercise intolerance and exertional dyspnea (Canadian cardiovascular functional class II to III) during the past year. In addition, he had fever and deterioration of functional performance during the past month. After he visited our clinic, we suggested he be admitted to the hospital with possible ruptured coronary sinuses of Valvasa with infective endocarditis. At hospital admission, he appeared chronically ill. The blood pressure was 120/50 mm Hg, pulse rate 84 beats/min, respiratory rate 18 breaths/min, and body temperature 37.8° C. A 0.5 x 2.5 cm 2 scar of the previous stabbing injury was found at the second intercostal space over the left parasternal border. A grade 4/6 to-and-fro murmur with a superficial thrill was detected at the aortic area. Mild bounding pulse was also noted. The white blood cell count was 13,000 cells/ml.
The electrocardiogram revealed normal sinus rhythm and left ventricular hypertrophy with diastolic overload pattern. The transthoracic echocardiogram showed a dilated left ventricle and right ventricle, an estimated left ventricular ejection fraction of 72%, rupture of the left coronary cusp of the aortic valve with severe aortic regurgitation, severe pulmonary regurgitation, possible vegetations over the left and noncoronary cusps of the aortic valve and left pulmonary cusp, and a left-to-right shunt across the aortopulmonary septum (Fig. 1). A transesophageal echocardiogram furthermore confirmed that the exact location of the left-to-right shunt was across the aortopulmonary septum and just distal to the pulmonary anulus (Fig. 2). The profiles of pressure tracings and oxygen saturation are shown in 
Table I. The ratio of pulmonic to systemic flow of the left-to-right shunt was estimated to be 2.8.
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Fig. 1. Parasternal short-axis view with transthoracic echocardiography showed possible defect across aortopulmonary septum (arrow). AV, Aortic valves; RVOT, right ventricular outflow tract; PA, main pulmonary artery; LA, left atrium; RA, right atrium.
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Fig. 2. Longitudinal section of right ventricular outflow tract (RVOT) by transesophageal echocardiography demonstrated that exact site of left-to-right shunt was just distal to pulmonary anulus (arrow). PV, Pulmonary valves; AO, aortic root.
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After intensive medical control of infective endocarditis, the patient underwent surgical intervention. The operative findings included severe adhesion of the aorta and the surrounding tissue, complete destruction of the left coronary cusp of the aortic valve and left pulmonary cusp, multiple vegetations and fibrogranulomatous tissue over the aforementioned cusps, and a 2 x 0.5 cm 2 fistula tract from the site near the left coronary orifice to the pulmonary trunk just distal to the anulus (Fig. 3, A, B, and C). Complete debridement, aortic valvular replacement with a No. 19 St. Jude Medical valve, and pulmonary valvular replacement with a No. 21 St. Jude Medical valve (St. Jude Medical, Inc., St. Paul, Minn.) were done. The pathologic findings of both valves revealed fibrinous coating with focal bacterial clumps, foamy histiocyte and multinucleated giant cell aggregation, mononuclear cell infiltration, degenerative mesenchymal cells, and neovascularization. The picture was compatible with the diagnosis of bacterial endocarditis over both aortic and pulmonary valves.
Traumatic cardiology is a special category that includes a broad spectrum of disease entities. The manifestations of cardiac trauma vary case by case and its management should also be individualized. In this report, we provide at least two clinical implications, as follows. First, adequate surgical intervention depends on correct preoperative diagnosis. In our case report, the clinical differential diagnoses included subaortic ventricular septum rupture combined with severe aortic regurgitation, ruptured coronary sinuses of Valsalva, and traumatic aortopulmonary communication. The methods of operation differ from each other in these circumstances. 1-3 Detailed preoperative evaluation may provide excellent surgical planning and thus reduce perioperative risks. Second, transesophageal echocardiography provides a new avenue of imaging of the heart and mediastinal contents because of the lack of chest wall interference and the use of high-frequency transducers with less beam dispersion and better resolution. 4 The close anatomic relationship of the esophagus and the aorta allows imaging of the aortic root, the arch, and great vessels. 4 The pathologic delineation of the structures around the aortopulmonary anulus can be therefore defined clearly by this noninvasive tool. In addition, transesophageal echocardiography may be superior to cardiac catheterization and angiography, as in our case. The latter sometimes cannot define exactly the location of intracardiac shunting because of the interference of a large regurgitant flow to the oxygen-saturated nearby chambers or because of unsatisfactory angulation in the performance of angiography.
Footnotes
From the Divisions of Cardiologya and Cardiac Surgery,b National Taiwan University Hospital, Taipei, Taiwan, Republic of China. 
J THORAC CARDIOVASC SURG 1995;110:1136-9
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