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Background: Aspirin and nonsteroidal anti-inflammatory drugs (A/NSAIDs) are the mainstay treatments for acute pericarditis. We sought to identify factors predicting failure of A/NSAIDs and switch to corticosteroid treatment (STCT) as well as the impact of STCT on pericarditis recurrence., Methods: We enrolled 148 patients with acute pericarditis receiving A/NSAIDs (n=110) or corticosteroids (n=38) as first-line treatment according to clinical indications. In case of poor response to A/NSAIDs (n=37), STCT was performed and factors contributing to such failure were explored. All patients were followed-up prospectively for 18 months for pericarditis recurrence., Results: In multivariate analysis, female sex (odds ratio [OR] =3.57, 95% confidence interval [CI]: 1.00-12.5), age (per decade, OR=0.75, 95% CI: 0.57-0.99), PR-segment depression (OR=4.43, 95% CI: 1.02-19.34), and a secondary cause of pericarditis (OR=13.52, 95% CI: 1.51-117.8) were independent predictors of poor response to A/NSAIDs and STCT. In cox regression analysis, the risk of recurrence was higher in patients requiring STCT (hazards ratio [HR] =3.22, 95% CI: 1.70-6.13) and in those initially treated with corticosteroids (H=2.06, 95% CI: 1.01-4.21) than in patients receiving A/NSAIDs only., Conclusions: Treatment failure with A/NSAIDs in acute pericarditis can be anticipated by certain patient characteristics. STCT identifies patients who are at the highest risk for recurrences, a risk that is approximately threefold higher than that of A/NSAIDs and 1.5-fold higher than that of corticosteroids as first-line treatment., (Copyright © 2018 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.)

The clinical significance of pleural effusions (PLEs) in the setting of acute pericarditis remains poorly investigated. We sought to identify predictive factors for PLEs and their association with the short- and long-term prognosis of patients with acute pericarditis. We enrolled 177 patients hospitalized with a first episode of acute pericarditis. In all cases an extensive clinical, biochemical, and diagnostic work-up to detect PLEs and establish etiological diagnosis was performed. All patients included were prospectively followed for a maximum of 18 months (median 12, range 1-18) and complications were recorded. PLEs were detected in n = 94 cases (53.1% of the cohort; bilateral 53.2%, left-sided 28.7%, right-sided 18.1%) and were strongly associated with c-reactive protein (CRP) levels at admission (rho = 0.328, p < 0.001). In multivariate logistic regression, independent predictors for PLEs were female gender (OR = 2.46, 95% CI 1.03-5.83), age (per 1-year increment OR = 1.030, 95% CI 1.005-1.056), CRP levels (per 1 mg/L increment OR = 1.012, 95% CI 1.006-1.019) and size of pericardial effusion (per 1 cm increment, OR = 1.899, 95% CI 1.228-2.935). Bilateral PLEs were associated with increased risk for in-hospital cardiac tamponade (OR = 7.52, 95% CI 2.16-26.21). There was no association of PLEs with new onset atrial fibrillation or pericarditis recurrence during long-term follow-up (χ 2  = 0.003, p = 0.958). We conclude that PLEs are common in patients hospitalized with a first episode of acute pericarditis. They are related to the intensity of inflammatory reaction, and they should not be considered necessarily as a marker of secondary etiology. Bilateral PLEs are associated with increased risk of in-hospital cardiac tamponade, but do not affect the long-term risk of pericarditis recurrence.