Introduction

The clinical table of chronic constrictive pericarditis (CCP) was first described in 1842 by Cheever in his Observations on the Diseases of the Orifice and Valves of the Aorta,in which he reported that dangerous symptoms arose chiefly from the compression of muscle tissue by sticky material that surrounded the heart(1,2). Tuberculosis (TBC) remains a leading cause of pericarditis in some nonindustrialized countries(3). Today, pericardiectomy is a safe procedure with available techniques(2).

Case Presentation

A 44 years old man admitted to our Institute for dyspnea and chest pain. Patient was diagnosed as tuberculosis 18 months ago and he comleted to use the triple therapy regularly. Laboratory parameters were normal. His past medical history was significant for Type II diabetes mellitus that was regulated with oral antidiabetics. Chest radiography was very specific for chronic tuberculous pericarditis and it showed massive pericardial calcific deposits visible. Two-dimensional,color-flow Doppler echocardiography revealed massive pericardial calcification,decreases ejection fraction significantly(40%). Thorax CT showed massive and diffuse pericardial calcific deposits. Diffuse thickening of pericardium was prominent (Figures 1,2 and 3).

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Preoperatively his functional capacity was in New York Heart Association(NYHA) functional class III-IV.

He went under operation.We approached via median sternotomy. We freed the pericardium in this order: first from the aorta and pulmonary artery, including the left ventricular outflow tract; then from the left and right ventricles and the left pulmonary vein orifices; and finally from the superior and inferior venae cavae. To avoid damage to the phrenic nerves, we surgically resected the entire anterior pericardium, within 3 or 4 cm of the phrenic nerves, then completed the dissection of the pericardium from the diaphragm. Constricting layers of epicardium were removed if possible. There were multipl caseification necrosis areas (Figures 4&5).

Figure 4

Figure 4

Figure 5

Figure 5

There was no evidence of phrenic nerve injury either perioperatively or postoperatively.We left large plaques that did not permit the development of a cleavage plane. We performed wedge incisions that reached the epicardium, which reduced the size of the plaques and relieved myocardial constriction. The ventilation time was 6 hours. We didn’t used an inotropic drug for prophylaxis against low-output syndrome in our case.The stay in the intensive care unit was 2 days. The hospital stay was 7 days. Postoperative improvements in hemodynamic results are optimal. Postoperative diagnosis was made in a histologic section of the pericardium. During the 1st postoperative month, the functional capacity of our patient improved dramatically and he was in NYHA functional class I.

Discussion

Diseases of the pericardium can be indolent or have a sudden onset. They may be primary, but more often are secondary to a systemic disease or previous therapy(4). Effective management of pericardial diseases requires an understanding of the pathophysiology and natural history of each disease entity, knowledge of the individual patient, and realistic application of therapy(4).

Tuberculous pericarditis affects 1% to 2% of all patients with TBC by direct extension from the mediastinal lymph nodes and, occasionally, by hematogenous spread or by contiguous spread from the myocardium(5). Tuberculosis is responsible for approximately 4% of cases of acute pericarditis, 7% of cases of cardiac tamponade, and, in older studies, 6% of instances of constrictive pericarditis(5,6).

The occurrence of calcific deposits in pericardia constitutes calcific pericardial heart disease. The calcific deposits may vary in size from microscopic, visible only by histologic examination, to massive, encircling all or most of the heart and readily visible by radiographic examination. Pericardial diseases imitate more common cardiac diseases and therefore can be difficult to diagnose(4). Echocardiography, thoracic computed tomography, and magnetic resonance imaging are three valuable imaging techniques for the management and pathophysiological understanding of cardiac tamponade and constrictive pericarditis. However, these techniques should not be used independently from clinical findings(7).Calcific deposits appear to represent the end stage of organization of a pericardial process and in themselves are not indicative of any specific etiology. Histologic examination of calcified pericardia rarely provides specific diagnoses. Tuberculosis is the classic cause of constrictive pericarditis.

For myocardial constriction to occur, the calcific deposits must encircle both ventricles . Localized bands of calcium, however, may cause cardiac dysfunction(8). Thickened and calcified pericardium frequently comes into direct contact with the myocardium, decreasing the heart muscle's contractility and disrupting the coordination of diastolic filling of the ventricles(2,9).

Median sternotomy incision enables exploration of the left ventricle and right part of the heart and direct vision of the great vessels. It is possible to perform an extensive pericardiectomy with minimal cardiac manipulation. The left ventricle can be decorticated easily via sternotomy, and better cardiac hemodynamics can be achieved through a sternotomy than through a thoracotomy(2,10). Further advantages of the median sternotomy are the ease and comfort of this approach for the surgeon, the ability to initiate CPB if necessary, and the postoperative comfort of the patient; for these reasons, we used this technique. Generally,early death risk postoperatively is more than 2% in many constrictive pericarditis cases. In patients with cardiac function, surgery is the only effective long-term treatment (5).