Ann Thorac Surg 2009;87:642-643. doi:10.1016/j.athoracsur.2008.07.028
© 2009 The Society of Thoracic Surgeons
Case Reports
Early Constrictive Epicarditis After Coronary Artery Bypass Surgery
Curtis A. Anderson, MDa,*,
Evelio Rodriguez, MDa,
Ronny L. Shammas, MDb,
Alan P. Kypson, MDa
a Division of Cardiothoracic Surgery, Department of Cardiovascular Sciences, The Brody School of Medicine, East Carolina University, Greenville, North Carolina
b Division of Cardiology, Department of Cardiovascular Sciences, The Brody School of Medicine, East Carolina University, Greenville, North Carolina
Accepted for publication July 9, 2008.
* Address correspondence to Dr Anderson, Division of Cardiovascular Sciences, The Brody School of Medicine, East Carolina University, 600 Moye Blvd, Room 252, Greenville, NC 27834 (Email: andersoncu{at}ecu.edu).
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Abstract
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A patient with constrictive pericarditis early after coronary bypass surgery is presented. At reoperation a dense inflammatory process was encountered on the epicardial surface of the heart with minimal pericardial thickening. Crosshatching of the epicardial scar tissue produced an immediate and durable clinical response.
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Introduction
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Constrictive pericarditis impairs filling of cardiac chambers, resulting in venous congestion and diminished cardiac output. The visceral pericardium, or epicardium, contributes variably to this process. We present a patient with postoperative constrictive physiology early after coronary artery bypass surgery. At the time of reoperation, the patient was found to have pronounced constrictive epicarditis.
A 62-year-old man underwent coronary artery bypass surgery for severe three-vessel disease. The operation was uneventful and no pericardial abnormalities were noted. He was discharged on day 4 and had an unremarkable early postoperative recovery. At week 6 he began experiencing exertional dyspnea. Echocardiography showed normal ventricular contraction with early septal collapse and diminished respiratory variation of the inferior vena cava. Contrast enhanced computed tomography of the chest was unremarkable except for small bilateral pleural effusions, a small pericardial effusion, and normal postoperative changes. No pericardial thickening was evident on computed tomography. Despite intravenous diuretic therapy and a short course of intravenous steroids, the patient experienced worsening dyspnea and continued to gain weight. Cardiac catheterization revealed equalization of left and right ventricular diastolic pressures, a central venous pressure of 19 mm Hg, and a cardiac index of 1.73 L · min–1
· m–2. All three grafts were widely patent.
The patient was taken to the operating room for presumed constrictive pericarditis. A reoperative median sternotomy was performed. The pericardium, which was left open at the original operation, was minimally thickened. On cardiopulmonary bypass the heart was freed from the surrounding pericardium, which was then resected anteriorly from phrenic to phrenic. The epicardium, in contrast to the pericardium, was globally thickened. As the epicardium was sharply incised, there was notable expansion of the underlying myocardium. This process was repeated along the diaphragmatic and lateral surfaces of the heart creating a crosshatch or waffle pattern (Fig 1). At the conclusion of the case, hemodynamic measurements were improved with central venous pressure decreasing from 19 to 9 mm Hg, and his cardiac index increased to 3.5 L/min–1/m–2. The fibrous pericardium submitted to pathology was read as mild chronic inflammation and was measured to be approximately 1-mm thick. Since being discharged, the patient has resumed normal activity, including jogging.

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Fig 1. Diaphragmatic surface of the heart showing thickened epicardium that has been sharply incised. This process encapsulated a large portion of the left and right ventricles.
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Comment
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Constrictive pericarditis classically involves a thickened, noncompliant pericardium. Early filling is normal, but abruptly ceases when the volume limitation imposed by the pericardium is reached. Impaired filling causes symptoms of heart failure despite normal myocardial contraction. This disease may be idiopathic, but it is also related to a diverse list of conditions including uremia, radiation exposure, tuberculosis, and prior cardiac surgery. Postoperative constrictive pericarditis is increasingly prevalent in more recent series [1, 2].
Surgery offers the only definitive treatment and traditionally involves resection of pericardium anterior to the phrenic nerves. Some very experienced centers advocate a more aggressive resection to include pericardium posterior to the left phrenic and along the diaphragm [3]. This can frequently be accomplished without cardiopulmonary bypass, as is our standard practice. In this case, we elected to use cardiopulmonary bypass because of the early postoperative state and anticipated dense adhesions. The response to pericardiectomy can be immediate and dramatic, but a small subset of patients fails to improve [4]. An obvious cause of poor surgical outcomes is failure to correctly identify a restrictive or myocardial element. This distinction is critical as patients with primary myocardial impairment will not benefit from nor tolerate a lengthy operation to remove the pericardium. Once constrictive physiology is correctly identified, surgical success depends on recognition and removal of all constrictive layers, which may notably include the epicardium.
The contribution of the epicardium to the constrictive process is variable. Most often, it occurs concurrently to some degree with pericardial constriction. Isolated cases of epicarditis have been reported, and are predominately in patients who have previously undergone cardiac surgery [5–7]. In this patient, epicardial constriction occurred very early after routine coronary bypass surgery. Crosshatching of the epicardial surface with sharp dissection was necessary to relieve myocardial constriction. This technique has been previously described as the "turtle cage" and "waffle" operation by others [7, 8]. In these cases the long-term outcome was also good with complete resolution of symptoms. Although the anterior pericardium did not seem to be abnormal, it was removed to ensure that no constrictive element was left behind.
In summary, constrictive pericarditis may occur very early after cardiac surgery. A classically thickened pericardium is not always present and should not dissuade cardiac catheterization. Successful surgical management requires release of all constrictive layers. The epicardium may be the primary constrictive element, and therefore it must be carefully scrutinized at the time of operation, especially if the remaining pericardium is normal. Crosshatching provides safe and effective relief of pericardial constriction when surgical planes are believed to be prohibitive.
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References
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