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CRP in Acute Pericarditis
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, University of California, San Francisco; Lucie Stern Chair in Cardiology, Chief of Clinical Cardiology, University of California, San Francisco Medical Center. Dr. Crawford serves on the speakers bureau for AstraZeneca. This article originally appeared in the May issue of Clinical Cardiology Alert. At that time it was peer reviewed by Ethan Weiss, MD, Associate Professor of Medicine, Division of Cardiology, University of California, San Francisco, CA. Dr. Weiss is an advisory board member for Bionovo.
Synopsis: High sensitivity C-reactive protein may be useful in acute viral or idiopathic pericarditis for establishing the diagnosis, determining the duration of therapy, and suggesting when to escalate therapy.
Source: Imazio M, et al. Prevalence of C-reactive protein elevation and time course of normalization in acute pericarditis. Implication for the diagnosis, therapy and prognosis of pericarditis. Circulation 2011;123:1092-1097.
The utility of inflammatory markers in acute pericarditis is not well understood. Thus, these investigators from Italy prospectively evaluated serial high sensitivity C-reactive protein (hs-CRP) serum levels in patients with acute pericarditis followed for 24 months on average. Of the 240 cases diagnosed as acute pericarditis, 200 had idiopathic (152) or viral (48) pericarditis and are the subjects of this report. Hs-CRP testing was done at presentation and every week until normalization. Values > 3.0 mg/L were considered elevated. All patients received empirical anti-inflammatory therapy: aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) in 170; colchicine in 100; and corticosteroids in 30. Drug therapy was usually tapered in 3 to 4 weeks. Symptom persistence at 1 week, recurrent cardiac tamponade, and constrictive pericarditis were considered adverse events. Patients ranged in age from 18 to 90 years old (mean 53) and about 50% were female. All presented with chest pain, about 85% had diagnostic ECG changes, about one-third had pericardial rubs, and about 50% had pericardial effusions. At presentation, 78% had elevated hs-CRP, which steadily declined to 5% at 3 weeks and none at 4 weeks. Negative hs-CRP values on presentation may have been due to early presentation (15 of 44) or previous anti-inflammatory therapy (22 of 44). A normal hs-CRP value at 1 week was highly predictive of a recurrence free survival (P < 0.001). An incomplete response to initial anti-inflammatory therapy and the use of corticosteroids also were independent predictors of recurrence. The authors concluded that hs-CRP is elevated in three quarters of patients with acute pericarditis and serial measurements identify patients at higher risk of recurrence.
This prospective observational study of patients with acute idiopathic or viral pericarditis is an important contribution because it suggests a procedure for managing these patients. They clearly identify acute pericarditis clinically as patients who have two of the following four criteria: chest pain consistent with pericarditis; a friction rub; diagnostic ECG changes; or a pericardial effusion on echocardiography. They find that hs-CRP is elevated in three-fourths of them and persistently negative in 3.5%. However, there is no control group of patients with chest pain, but no evidence of pericarditis to determine the false-positive rate. Thus, it is not an absolute diagnostic criterion, but if elevated does support the diagnosis.
Current therapy for acute idiopathic or viral pericarditis is empiric. Acute inflammatory agents are currently given until the pain resolves or for some predetermined interval. Hs-CRP offers a more informed approach. The authors suggest weekly values with full dose initial therapy continuing until hs-CRP is < 3.0 mg/L; then tapering therapy off. Of course this would be modified if the patient does not improve symptomatically or there is evidence of recurrence.
Their experience supports previous observational results on the course of treated acute pericarditis. About one-third had persistent symptoms at one week and about one-third had a recurrence during follow up. Only 2% developed pericardial tamponade and none developed constriction over a 2 year average follow-up. These data confirm the relatively benign prognosis of idiopathic or viral acute pericarditis with the biggest problem being recurrence. In this study there were three independent predictors of recurrence: incomplete response to therapy at one week, use of corticosteroids, and an elevated hs-CRP at one week. These observations confirm that corticosteroids should not be used as first-line therapy, but reserved for refractory cases. In my experience, using colchicine for those who do not improve quickly on NSAIDs has almost eliminated the need for corticosteroids. In the future, I will use hs-CRP to tailor the duration of therapy.