Ann Thorac Surg 2008;86:1987-1989. doi:10.1016/j.athoracsur.2008.05.046
© 2008 The Society of Thoracic Surgeons
Case Reports
Extrinsic Compression of the Left Main Coronary Artery by Atrial Septal Defect
Yusuke Jo, MDa,
Akio Kawamura, MDa,*,
Masahiro Jinzaki, MDb,
Takashi Kohno, MDa,
Toshihisa Anzai, MDa,
Shiro Iwanaga, MDa,
Kiyokazu Kokaji, MDc,
Tsutomu Yoshikawa, MDa,
Ryohei Yozu, MDc,
Sachio Kuribayashi, MDb,
Satoshi Ogawa, MDa
a Division of Cardiology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan
b Department of Cardiovascular Surgery, Keio University School of Medicine, Tokyo, Japan
c Department of Radiology, Keio University School of Medicine, Tokyo, Japan
Accepted for publication May 15, 2008.
* Address correspondence to Dr Kawamura, Division of Cardiology, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan (Email: kawamura{at}cpnet.med.keio.ac.jp).
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Abstract
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On rare occasions, extrinsic compression of the coronary artery can cause significant stenosis. We report a 42-year-old woman who was referred to our hospital for surgical repair of atrial septal defect. Cardiac 64-slice multi-detector computed tomography before the operation revealed the extrinsic compression of the proximal left main coronary artery by the marked dilatation of pulmonary trunk. The patient eventually underwent atrial septal defect closure and coronary artery bypass simultaneously. Four months after the operation, multi-detector computed tomographic scan revealed reduction of pulmonary trunk diameter and resolution of left main coronary artery narrowing.
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Introduction
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Coronary artery stenosis is usually caused by atherosclerotic disease. However, on rare occasions, extrinsic compression of the left main coronary artery (LMCA) is caused by pulmonary artery dilatation and the best management is not well defined [1–3]. In this article, we report a 42-year-old patient with atrial septal defect (ASD) who had extrinsic compression of the LMCA by an enlarged pulmonary trunk due to long-standing pulmonary hypertension.
A 42-year-old woman who had been diagnosed with ASD was referred to our hospital for surgical repair. Recently, she had been suffering from progressive dyspnea on exertion, but never experienced chest pain suggestive of typical angina. On physical examination, there were right ventricle heave, right ventricular S3 and fixed splitting S2 and a grade III/VI systolic murmur. Chest roentgenogram showed cardiomegaly and dilated pulmonary artery. Electrocardiography revealed sinus rhythm with the right axis deviation, signs of right ventricular hypertrophy and negative T waves in anterior and inferior leads. Echocardiography revealed a large secundum ASD (diameter, 44 mm) with bidirectional shunt flow, moderate tricuspid regurgitation, right ventricle enlargement and significant pulmonary trunk dilatation (44 mm). Estimated pulmonary arterial pressure was 89/17 mm Hg. Brain natriuretic peptide level was 346 pg/mL.
The patient underwent cardiac catheterization. Pulmonary artery pressure was 73/24 mm Hg (mean, 40 mm Hg), mean pulmonary capillary wedge pressure was 8 mm Hg. Blood gas sampling revealed O2 step up at the level of the right atrium (Qp/Qs = 2.4). Although she had no coronary risk factor, coronary angiography unexpectedly revealed a 75% long, smooth narrowing of the LMCA ostium (Fig 1). The remainder of the coronary artery was free of significant disease. Subsequently, a cardiac 64-slice multi-detector computed tomography (MDCT) confirmed extrinsic compression of the proximal LMCA by marked dilatation of the pulmonary trunk (Fig 2A). The pulmonary trunk diameter was 47 mm. Curved planner reconstruction of the MDCT images revealed that atherosclerotic plaque was absent inside LMCA. Eventually, the patient underwent surgical ASD closure and coronary artery bypass to the left anterior descending coronary artery with the left internal mammary artery simultaneously. Two weeks after the operation, her dyspnea on exertion disappeared completely and chest roentgenogram revealed improvement of cardiomegaly. The cardiac MDCT did show reduction of pulmonary trunk diameter to 38 mm, but the narrowing of the LMCA did not change at this point. Estimated pulmonary arterial pressure on echocardiography after the operation improved from 89/17 mm Hg to 31/20 mm Hg. However, 4 months later the cardiac MDCT finally disclosed the complete resolution of LMCA narrowing (Fig 2B).
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Fig 1. Coronary angiographic scan revealed a 75% long, smooth stenosis of the left main coronary artery ostium without other evidence of coronary artery disease.
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Fig 2. (A) The extrinsic compression of the proximal left main coronary artery (LMCA) by the marked dilatation of main pulmonary artery (47 mm in diameter) was shown in a cardiac 64-slice multi-detector computed tomographic scan on admission. Any atherosclerotic plaque was absent inside LMCA. (B) The narrowing of LMCA disappeared 4 months after the operation. The pulmonary trunk diameter decreased to 38 mm.
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Comment
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Prolonged left-to-right shunt in patients with ASD promotes right heart dilatation and pulmonary vascular changes. Extrinsic compression of the LMCA by an enlarged pulmonary trunk in patients with long-standing pulmonary hypertension has been previously reported [1–3]. Although LMCA narrowing is generally secondary to atherosclerotic disease, it is important to differentiate extrinsic compression from atherosclerosis in a patient with long-standing pulmonary hypertension. The optimal management of LMCA compression caused by a dilated pulmonary artery secondary to ASD is yet to be clarified. Some authors have proposed aggressive treatment such as coronary artery bypass surgery or stent implantation [1, 4–6]. However, the benefit of coronary revascularization remains controversial because simple surgical closure of ASD may relieve the LMCA compression by lowering the pulmonary artery pressure and resultant decrease in pulmonary artery diameter as in the present case. Fujiwara and colleagues [1] reported that the LMCA compression by the dilated pulmonary artery associated with ASD disappeared in postoperative coronary angiograms. These results suggest that markedly dilated pulmonary arteries easily compress the LMCA and cause narrowing, which can improve after ASD closure. On the other hand, it is possible that the pulmonary artery dilatation is not promptly improved after ASD closure because of the pulmonary artery vascular remodeling caused by chronic pulmonary artery hypertension, and as a consequence, the degree of LMCA compression may not change. As extrinsic compression of LMCA may cause angina and lead to malignant arrhythmia or sudden death, a precise assessment for LMCA narrowing is very important [7]. Pina and colleagues [8] used a pressure wire to guide the treatment of the compression of the LMCA secondary to pulmonary artery trunk dilatation. In another report, intravascular ultrasonography showed deformation of the LMCA due to extrinsic compression from a markedly dilated main pulmonary artery [6]. They proposed that these devices might be useful for the decision on coronary revascularization. In the present case, although the patient did not have typical angina, electrocardiography revealed negative T waves in precordial and inferior leads. We decided to perform the bypass surgery for LMCA compression as a safety tether, because it was not certain whether the compression would promptly disappear by ASD closure in a short period of time. In fact, although the degree of LMCA narrowing remained unchanged in cardiac MDCT 2 weeks after the operation, the complete resolution of the narrowing was achieved 4 months later.
In conclusion, surgical closure of ASD can relieve LMCA narrowing due to extrinsic compression by the enlarged pulmonary artery. Cardiac MDCT is a useful tool to assess etiology of LMCA narrowing as well as to monitor the postoperative course.
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References
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- Fujiwara K, Naito Y, Higashiue S, et al. Left main coronary trunk compression by dilated main pulmonary artery in atrial septal defect. Report of three cases. J Thorac Cardiovasc Surg 1992;104:449-452.[Abstract]
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Abstract
Introduction
