# Preventing Postpericardiotomy Syndrome: Current Evidence and Future Directions

**Authors:** Christos E. Ballas, Thomas Theologou, Evangelia Samara, Fotios Barkas, Theodora Bampali, Kyriakos Kintzoglanakis, Christos Diamantis, Petros Tzimas, Christos S. Katsouras, Christos Alexiou

PMC · DOI: 10.3390/jcdd13020063 · 2026-01-24

## TL;DR

This paper reviews current and future strategies to prevent postpericardiotomy syndrome, a common inflammatory complication after heart surgery, focusing on drugs, surgical techniques, and biomarkers.

## Contribution

The paper systematically evaluates evidence-based prevention strategies and highlights novel approaches like anti–interleukin-1 therapies and biomarker-based risk stratification.

## Key findings

- Colchicine is the most effective pharmacologic intervention for preventing PPS.
- Anti–interleukin-1 therapies show promise for high-risk patients.
- Biomarkers like neutrophil-to-lymphocyte ratios and cytokines help identify high-risk patients.

## Abstract

Postpericardiotomy syndrome (PPS) is the most frequent inflammatory after-effect of cardiac surgery and is characterized by high morbidity, delayed hospitalization, and increased long-term mortality rates. Although PPS is common, empirical anti-inflammatory therapy has historically been employed for its prevention, and mechanism-based approaches have not yet been standardized. In this literature review, which was conducted on the basis of randomized controlled trials, meta-analyses, cohort studies, and mechanistic research regarding pharmacologic interventions, surgical modalities, and biomarker-based preventive strategies, the deficiencies of a critical synthesis of existing preventive strategies and emerging risk stratification instruments for PPS are addressed. The review affirms that the most evidence-based pharmacologic intervention is colchicine, which demonstrates a consistent reduction in PPS incidence across a range of randomized trials. Nonsteroidal anti-inflammatory drugs show variable responses, whereas corticosteroids are no longer recommended for routine prophylaxis due to relapse. Specific anti–interleukin-1 therapies represent a promising novel approach for high-risk patients. Surgical interventions, such as pericardial closure using biomaterials and posterior pericardiotomy, are important and do not lead to increased hemodynamic complications, while postoperative effusions, atrial fibrillation, and tamponade are reduced. Less invasive methods may also be employed to mitigate inflammatory causes, particularly in valve-sparing procedures and congenital operations. Emerging biomarker data, including postoperative neutrophil-to-lymphocyte ratios, C-reactive protein levels, and pericardial fluid cytokines, enable the identification of high-risk patients and form the basis for a personalized prevention approach. In summary, pharmacologic prophylaxis, innovative surgical techniques, and biomarker-based risk stratification represent a pathway toward reducing the incidence and burden of PPS in modern cardiac surgery.

## Linked entities

- **Chemicals:** colchicine (PubChem CID 2833)

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, MPO (myeloperoxidase) [NCBI Gene 4353], NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, NPPA (natriuretic peptide A) [NCBI Gene 4878] {aka ANF, ANP, ATFB6, ATRST2, CDD, CDD-ANF}
- **Diseases:** myocardial swelling (MESH:D004487), surgical (MESH:D007431), ASD (MESH:D001321), renal insufficiency (MESH:D051437), corticosteroid (MESH:C565152), injury to (MESH:D014947), Atrial Septal Defect (MESH:D006344), Inflammatory (MESH:D007249), pericardial effusion (MESH:D010490), fever (MESH:D005334), diarrhea (MESH:D003967), myocardial strain (MESH:D013180), chest pain (MESH:D002637), myocardial injury (MESH:D009202), autoimmune (MESH:D001327), arrhythmia (MESH:D001145), bleeding (MESH:D006470), impaired left ventricular functioning (MESH:D018487), pleural effusion (MESH:D010996), congenital heart defects (MESH:D006330), pericardial (MESH:D008476), toxicity (MESH:D064420), gastrointestinal adverse effects (MESH:D005767), pericardial thickening (MESH:D013585), Atrial Fibrillation (MESH:D001281), effusion (MESH:D000080324), infection (MESH:D007239), Supraventricular Tachycardia (MESH:D013617), death (MESH:D003643), constrictive pericarditis (MESH:D010494), Pericarditis (MESH:D010493), cardiac tamponade (MESH:D002305), immune dysregulation (OMIM:614878), systemic (MESH:D015619), cardiac injury (MESH:D006331), Postoperative (MESH:D019106), PPS (MESH:D011185), renal dysfunction (MESH:D007674)
- **Chemicals:** ibuprofen (MESH:D007052), Colchicine (MESH:D003078), Diclofenac (MESH:D004008), indomethacin (MESH:D007213), anti- (-), canakinumab (MESH:C541220)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942030/full.md

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Source: https://tomesphere.com/paper/PMC12942030