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Ann Thorac Surg 2001;72:1371-1373
© 2001 The Society of Thoracic Surgeons
a Division of Cardiovascular and Thoracic Surgery, University of Minnesota Hospital and Clinics, Minneapolis, Minnesota, USA
b Division of Cardiology, University of Minnesota Hospital and Clinics, Minneapolis, Minnesota, USA
Accepted for publication November 13, 2000.
Address reprint requests to Dr Park, Division of Cardiovascular and Thoracic Surgery, University of Minnesota, MMC #207, 420 Delaware St SE, Minneapolis, MN 55455
e-mail: parkx021{at}maroon.tc.umn.edu
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A 37-year-old man was admitted after a 16-month history of exertional substernal chest pain. Occasionally, the chest pain occurred at rest and was associated with left arm numbness. The patient had significant cardiac risk factors, including hyperlipidemia, hypertension, and a family history of coronary artery disease. He had no prior history of trauma to the thorax. Initial evaluation of the patient included a chest radiograph which showed an unusual cardiac contour with a bulging left ventricle. A myocardial perfusion scan showed no significant abnormality. Cardiac catheterization, performed at an outside institution, at that time demonstrated two-vessel coronary artery disease involving the left anterior descending artery (80% stenosis proximally, 75% stenosis mid-level, and total occlusion distally) and the circumflex artery (50% stenosis mid-level). The left ventricular ejection fraction was estimated to be 64%.
Despite maximal medical therapy with ß-blockers and nitrates, he required multiple hospitalizations for persistent chest pain. Electrocardiograms performed during these chest pain episodes demonstrated mild ST-segment and T-wave changes in the lateral and anterior leads consistent with myocardial ischemia. There was no evidence of myocardial infarction based on cardiac enzyme studies. Repeat catheterization, 11 months after the initial evaluation, demonstrated similar two-vessel coronary disease. In this study, however, there was evidence of dynamic complete compression of the mid-left anterior descending artery (LAD), first diagonal branch, and mid-circumflex arteries during diastole (Fig 1), which resolved during systole (Fig 2). Angioplasty and stent deployment were performed on these three lesions in addition to a lesion in the proximal LAD. There was improvement in the extent compression at these "stenotic" areas. However, after a brief period of resolution of the symptoms, the chest pain recurred. Two subsequent catheterizations, at 3 months and 5 months after stenting, demonstrated re-stenoses at the same areas along the mid-LAD, first diagonal, and mid-circumflex. Re-stenting of these lesions was only temporarily successful and did not relieve the patient’s symptoms. The patient also had a magnetic resonance imaging study to evaluate the dynamic compression of the coronary vessels. The exam revealed focal enlargement of the apical and lateral portions of the left ventricle. In addition, a kink was noted in the lateral wall of the left ventricle near the base of the heart (Fig 3).
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The most prevalent symptom reported among patients with congenital pericardial defects is chest pain. The mechanisms of the chest pain are postulated to be secondary to (1) impingement of the fibrous pericardial rim on the coronary arteries, causing myocardial ischemia; (2) torsion of the great vessels; (3) lack of a cushioning effect of the pericardium; and (4) tension on pleuropericardial adhesions [2]. There has been debate whether the chest pain experienced by these patients represents true myocardial ischemia, whereby the edge of the pericardial defect impinges on the epicardial coronary arteries and causes obstruction to blood flow. In the present case, because the patient had concomitant atherosclerotic disease, it is difficult to ascertain the exact etiology of the chest pain. However, we were able to document dynamic complete compression of three coronary vessels, including the LAD, first diagonal branch, and circumflex arteries by the pericardial defect. It is likely that the chest pain experienced by this patient was true myocardial ischemia, caused in part by the congenital pericardial defect.
Diagnosis of a congenital pericardial defect may be difficult to establish, particularly in patients with concomitant atherosclerotic coronary artery disease. Electrocardiographic findings are usually nonspecific, but may demonstrate evidence of myocardial ischemia, as in the case with our patient. Chest radiography can show a convex prominence of the left heart border. Echocardiography is rarely diagnostic. Other imaging modalities, including computed tomography and magnetic resonance imaging, have been useful in establishing the diagnosis [3, 4]. Coronary angiography may demonstrate the presence of dynamic migratory obstructions that are suggestive of a pericardial defect [5]. In the present case, the pericardial defect was not diagnosed preoperatively despite suggestive evidence from several studies. Undoubtedly, concomitant atherosclerotic coronary artery disease complicated the clinical picture, leading to a delay in diagnosis. It is important to note that the management of this patient may have been different had the diagnosis been made at the initial evaluation. He underwent several attempts at treating the dynamic obstructions with stent placement, which proved to be inadequate. Surgical intervention, either to repair or to enlarge the defect, is recommended for patients with symptomatic pericardial defects. In this patient, surgical repair of the defect along with coronary artery grafting to bypass the atherosclerotic lesions should have been the only required intervention.
In conclusion, myocardial ischemia may be caused by a congenital pericardial defect if its fibrous rim impinges enough on the coronary arteries to cause significant obstruction to blood flow. The diagnosis of the pericardial defect is suggested by the presence of migratory dynamic obstructions on coronary angiography. A high index of suspicion is required to make the diagnosis of a congenital pericardial defect in a patient who has concomitant atherosclerotic coronary artery disease.
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