Constrictive epicarditis as a cause of delayed or absent response to pericardiectomy: a clinicopathological study.

It is widely held that constrictive pericarditis is curable by pericardiectomy, and failure to respond reflects an underlying myocardial disease. Fibrous epicarditis could account for residual cardiac constriction, and delayed hemodynamic response in some patients is an alternative explanation. To examine this, we studied the 12 consecutive patients with otherwise normal hearts treated with extensive pericardiectomy for constrictive pericarditis over the past 7 years. Three hemodynamic responses to pericardiectomy were observed: (1) rapid response, where central venous pressure (CVP) fell below 10 cm H2O by 24 hours in two patients; (2) delayed response, where CVP fell below 10 cm H2O by 48 hours in six patients; and (3) no response of CVP in four patients. The CVPs remained critically elevated (greater than 25 cm H2O) in three patients with delayed response until a sclerotic epicardial peel was resected. Another patient whose CVP of 30 cm H2O showed no change after parietal pericardiectomy was thought to have amyloid cardiomyopathy but instead at autopsy had constrictive epicardial sclerosis not recognized at parietal pericardiectomy. Histologic features of parietal pericardium had no correlation with hemodynamic response, whereas epicardial histology did correlate with hemodynamic response in four patients. The data showed a spectrum of postpericardiectomy delayed hemodynamic responses, which in some patients may be due to a slowly resolving or fixed component of fibrous epicarditis that may be clinically misconstrued as a cardiomyopathy. Interruption of visceral pericardial tissue may be as important as resection of the parietal pericardium in patients with epicardial sclerosis.