Recurrent pericarditis is a common and troublesome complication that affects 15%-30% of patients with a previous episode of pericarditis. However, the pathogenesis of these recurrences is not well understood, and most cases remain idiopathic. Recent advances in medical therapy, including the use of colchicine and anti-interleukin-1 agents like anakinra and rilonacept, have suggested an autoinflammatory rather than an autoimmune mechanism for recurrences with an inflammatory phenotype. As a result, a more personalized approach to treatment is now recommended. Patients with an inflammatory phenotype (fever and elevated C-reactive protein level) should receive colchicine and anti-interleukin-1 agents as first-line therapy, whereas those without systemic inflammation should receive low to moderate doses of corticosteroids (eg, prednisone 0.2-0.5 mg/kg/d as an initial dose) and consider azathioprine and intravenous human immunoglobulins in the case of corticosteroid failure. Tapering of corticosteroids should be slow after achieving clinical remission. In this article, we review the new developments in the management of recurrent pericarditis.
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http://dx.doi.org/10.1016/j.cjca.2023.04.008 | DOI Listing |
ACR Open Rheumatol
January 2025
University of Udine and University Hospital Santa Maria della Misericordia, Udine, Italy.
Objective: We aimed to investigate the remission rate and disease duration in idiopathic or post-cardiac injury pericarditis and risk factors for disease duration and anti-interleukin-1 (IL-1) agent discontinuation.
Methods: This was a multicenter, longitudinal, observational study including 370 patients (51.4% female).
Int J Cardiol
January 2025
Cardiology and Cardiothoracic Department, University Hospital "Santa Maria della Misericordia" (ASUFC) Udine, Italy.
Background: Patients with pericarditis may show elevation of C-reactive protein (CRP) and pericardial effusion at presentation. There are limited data on the prognostic implications of this inflammatory phenotype.
Objectives: Aim of the present study is to evaluate the outcome of the inflammatory phenotype in a cohort of patients with acute pericarditis.
S D Med
October 2024
Department of Internal Medicine, University of South Dakota Sanford School of Medicine, Sioux Falls, South Dakota.
Acute pericarditis, the predominant pericardial disease, often lacks a clear etiology, with 15-30% of patients experiencing recurrence, rising to 20-50% in those with prior relapses. Autoimmune mechanisms significantly contribute to recurrence, with interleukin-1 identified as a pivotal inflammatory mediator. While NSAIDs, colchicine, and steroids remain staples for acute cases, the spotlight in recurrent pericarditis management has shifted toward immunosuppressive medications.
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January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Purpose Of Review: This review provides a contemporary, evidence-based update on the pathophysiological mechanisms and rapidly evolving therapeutic options for recurrent pericarditis.
Recent Findings: Recent studies have elucidated the pathogenesis of recurrent pericarditis, identifying autoinflammation as a key mechanism and interleukin-1 (IL-1) as a central modulator of the inflammatory cascade. Multiple clinical trials have investigated novel therapeutic approaches, particularly focusing on IL-1 inhibition.
Curr Cardiol Rep
January 2025
Division of Internal Medicine, Fatebenefratelli Hospital, ASST Fatebenefratelli Sacco, University of Milan, Piazzale Principessa Clotilde, 3, Milan, 20121, Italy.
Purpose Of Review: To outline the latest discoveries regarding the utility and reliability of serum biomarkers in idiopathic recurrent acute pericarditis (IRAP), considering recent findings on its pathogenesis. The study highlights the predictive role of these biomarkers in potential short- (cardiac tamponade, recurrences) and long-term complications (constrictive pericarditis, death).
Recent Findings: The pathogenesis of pericarditis has been better defined in recent years, focusing on the autoinflammatory pathway.
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