This case series describes the radiologic, etiologic, and pathologic features of surgically proven constrictive pericarditis, highlighting that while tuberculosis is a known cause, many cases have no clear antecedent history.
Etiology often remains idiopathic in surgically confirmed constrictive pericarditis; leaves open questions on pathogenesis and diagnostic strategies.
In previous publications, the radiologic aspects of operable congenital anomalies have been stressed (1–3). One relatively rare acquired lesion in which significant surgical relief may be afforded is constrictive pericarditis. Because recognition of this disease is sometimes difficult, a review of proved cases was undertaken, in order to evaluate the usefulness and consistency of the roentgenologic features. Methods and Material Twenty-one cases, all proved at surgery and all studied intensively, both clinically and radiologically, were analyzed. The clinical, laboratory, and pathologic data for each case were summarized, and the conventional roentgenograms and kymographic studies were re-examined, with careful attention to previous fluoroscopic findings. Notations were made as to overall heart size, cardiothoracic ratio, individual chamber size, central and peripheral pulmonary artery size, the presence or absence of pulmonary engorgement, the prominence of the superior vena cava and aorta, the presence, extent, and location of pericardial calcification, and the cardiac pulsations as noted at fluoroscopy and in kymograms. Results 1. Etiology: In 5 cases, tuberculosis was undoubtedly the cause of the pericardial disease. A sixth patient gave a history of an acute illness, characterized by chest pain and fever, twelve years earlier. The diagnosis of rheumatic fever was made at the time, but no signs of valvular disease were present on admission and calcified hilar nodes were demonstrable roentgenographically. In 14 cases there was no history of tuberculosis, chest injury or acute pericarditis. The tuberculin skin test was performed in 9 of this number and was positive in only 1 instance. One patient had associated congenital pulmonic stenosis. In his case, the development of acute pericarditis, subsequent effusion, and finally of a constrictive pericarditis could be clearly traced over a period of about a year (Fig. 1). Two patients had well documented histories of rheumatic fever and had rheumatic valvular disease. In 1 case, a substernal abscess had been drained ten years prior to the onset of signs and symptoms of constrictive pericarditis. This patient had no evidence of tuberculosis, and a pyogenic pericarditis was presumed to be the cause of the pericardial thickening and constriction. 2. Pathology: The specimens of surgically removed pericardial tissue examined microscopically consisted mainly of acellular, dense fibrous tissue with variable degrees of hyalinization. Ten cases showed calcium in the tissue. Except for 5 instances in which acid-fast bacilli and∕or tubercle formation were noted, no variations were observed from which a clue to etiology could be obtained. The thickness of the pericardial tissue was between 2 and 4 mm.
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Heinz et al. (1957) studied this question.
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