Incidence of Constrictive Pericarditis
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco. Dr. Crawford reports no financial relationships relevant to this field of study.
This article originally appeared in the November 2011 issue of Clinical Cardiology Alert. It was peer reviewed by Ethan Weiss, MD. Dr. Weiss is Assistant Professor of Medicine, Division of Cardiology and CVRI, University of California, San Francisco. Dr. Weiss is a scientific advisory board member for Bionovo.
Source: Imazio M, et al. Risk of constrictive pericarditis after acute pericarditis. Circulation 2011;124:1270-1275.
Since there is a lack of prospective data on the frequency of which constrictive pericarditis (CP) develops after acute pericarditis (AP), this group of investigators from Torino, Italy, conducted such a study. From 2000 until 2008 all cases of first AP were followed and evaluated for the development of CP at 1 month, 3 months, and every 6 months thereafter for a median follow-up of 72 months (range, 24-120). Follow-up evaluation included ECG, blood tests, and echocardiograms. The study included 500 consecutive patients with AP; 416 (83%) had viral or idiopathic AP; 36 (7%) had pericardial injury (e.g., surgery) or connective tissue disease; 25 (5%) had neoplastic; 20 (4%) had tuberculosis; and three (0.6%) had purulent. Recurrent AP was the most frequent subsequent adverse event (30%), followed by tamponade (4%). Transient CP was detected by echocardiography in 15% with resolution in 3 months. Effusive CP was seen in 1%. CP developed in nine (1.8%): two had viral or idiopathic AP and seven had other etiologies of AP. Purulent and tuberculosis patients had the highest incidence of CP. All the patients with permanent CP were confirmed by surgery. Pathology showed normal pericardial thickness in 11% of the permanent CP patients. Those who developed CP were more likely than those who did not to have fever (67% vs 15%), incessant course (56% vs 7%), non-idiopathic/viral etiology (78% vs 16%), large pericardial effusion (67% vs 9%), tamponade (44% vs 4%), and nonsteroidal anti-inflammatory drug failure (67% vs 19%), all P < 0.002. There was a trend toward more steroid use and a lower use of colchicine in those who developed CP, but these differences were not statistically significant. The authors concluded that CP is a rare complication of viral or idiopathic AP, but is more common with other etiologies such as bacterial pericarditis.
The important message of this prospective study is that we can reassure patients with viral or idiopathic pericarditis that the likelihood of them developing CP is very low. Thus, intense follow-up after the first 6 months is unwarranted in these patients. Also, recurrent AP in viral/idiopathic patients has a good prognosis.
Other etiologies are another matter. Tuberculosis has a higher rate of CP ranging from 5%-60% depending on the study and the stage of the disease. The relatively low rate of CP in tuberculosis in this study may be because it was infrequent or the follow-up was not long enough. Other etiologies, such as uremic and neoplastic, may have low rates because the patients do not survive long enough to develop CP. The described risk factors for CP may be a guide for whom to follow more closely. Most useful would be an incessant course, a large effusion, tamponade, or failure of anti-inflammatory therapy. Also of interest clinically was the observation that about 10% of those who developed CP had normal pericardial thickness on pathology and imaging. Thus, normal pericardial thickness does not exclude CP. Another interesting finding was that effusive CP was unusual, occurring in about 1% of the AP patients. Finally, transient CP was observed in 15% and it resolved in 3 months. Thus, surgery should not be considered until 3 months have passed with CP.
The study did not address drug therapy, although there was a trend for more CP in those treated with steroids. Also, the study confirms the use of colchicine as first-line therapy since lower colchicine use correlated with development of CP.