Dressler syndrome and post-cardiac injury syndrome: an autoinflammatory framework for reappraising a seventy-year-old diagnosis: a state-of-the-art review
9 affiliations
- 1Department of Cardiometabolic Sciences, Nexoria Institute of Cardiometabolic Excellence (NICE), Vigyaved Healthcare
- 2Department of Cardiology, PearResearch
- 3Department of Medicine, Subharti Medical College, Swami Vivekanand Subharti University
- 4Department of Physiology, Shri Guru Ram Rai Institute of Medical Sciences
- 5Department of Cardiology, Himachal Heart Institute
- 6Department of Cardiology, Subharti Medical College, Swami Vivekanand Subharti University
- 7Department of Cardiology, Northshore Heart, Lutheran General Hospital
- 8Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome
- 9IRCCS Maria Cecilia Hospital – GVM Care & Research
Abstract
Dressler syndrome, the delayed pericarditis after myocardial infarction remains firmly established in cardiological teaching, yet contemporary direct evidence specific to it is sparse. Its reported incidence has fallen markedly in the reperfusion era, while post-cardiac injury syndrome (PCIS) is now encountered chiefly after cardiac surgery and catheter-based procedures. These trends reflect a change in the clinical settings in which delayed post-injury pericardial inflammation is recognised, rather than evidence of a transfer of the same biological disease burden; incidence estimates across eras and procedures are not directly comparable. The historical anti-heart antibody framework does not, on its own, account for current observations. Randomised trials in predominantly idiopathic recurrent pericarditis show that colchicine and interleukin-1 (IL-1)–directed agents (anakinra, rilonacept, goflikicept) reduce recurrence, and experimental and human pericardial tissue data implicate the NLRP3 inflammasome. These data support an important role for innate immune signalling in pericarditis, but they do not establish IL-1 dependency in late post-infarction Dressler syndrome, and they do not exclude a contribution of adaptive immunity to amplification, persistence or recurrence. We grade the evidence at three levels—direct human PCIS data, data from other human pericarditis phenotypes, and experimental data—and stratify therapeutic evidence by phenotype and drug class, distinguishing colchicine, for which randomised prevention data exist in post-pericardiotomy syndrome, from IL-1 blockade, for which no PCIS-specific trial exists. We propose a pericardial injury-threshold model as a testable hypothesis in which clinical expression reflects the interaction of damage-associated molecular pattern load, the directness of pericardial and mesothelial exposure, and host inflammatory susceptibility, with adaptive responses acting as potential amplifiers. The model yields falsifiable predictions and identifies a key unanswered question: whether IL-1 inhibition during infarct healing is safe and effective. We outline a staged research programme, including a candidate two-tier research case definition requiring prospective validation, registry-based ascertainment, pericardial fluid immunophenotyping, inflammasome genetics, and phenotype-specific trials, including of emerging direct NLRP3 inhibitors.
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BibTeX
@article{sethi2026dressler,
title = {{Dressler syndrome and post-cardiac injury syndrome: an autoinflammatory framework for reappraising a seventy-year-old diagnosis: a state-of-the-art review}},
author = {Yashendra Sethi and Arsalan Moinuddin and Kunal Mahajan and Amit Sharma and Chris Pavlovic and Thomas Pavlovic and Giuseppe Biondi-Zoccai},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1977374},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1977374/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dressler syndrome and post-cardiac injury syndrome: an autoinflammatory framework for reappraising a seventy-year-old diagnosis: a state-of-the-art review
AU - Yashendra Sethi
AU - Arsalan Moinuddin
AU - Kunal Mahajan
AU - Amit Sharma
AU - Chris Pavlovic
AU - Thomas Pavlovic
AU - Giuseppe Biondi-Zoccai
PY - 2026
DA - 2026/10/20
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1977374
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1977374/full
AB - Dressler syndrome, the delayed pericarditis after myocardial infarction remains firmly established in cardiological teaching, yet contemporary direct evidence specific to it is sparse. Its reported incidence has fallen markedly in the reperfusion era, while post-cardiac injury syndrome (PCIS) is now encountered chiefly after cardiac surgery and catheter-based procedures. These trends reflect a change in the clinical settings in which delayed post-injury pericardial inflammation is recognised, rather than evidence of a transfer of the same biological disease burden; incidence estimates across eras and procedures are not directly comparable. The historical anti-heart antibody framework does not, on its own, account for current observations. Randomised trials in predominantly idiopathic recurrent pericarditis show that colchicine and interleukin-1 (IL-1)–directed agents (anakinra, rilonacept, goflikicept) reduce recurrence, and experimental and human pericardial tissue data implicate the NLRP3 inflammasome. These data support an important role for innate immune signalling in pericarditis, but they do not establish IL-1 dependency in late post-infarction Dressler syndrome, and they do not exclude a contribution of adaptive immunity to amplification, persistence or recurrence. We grade the evidence at three levels—direct human PCIS data, data from other human pericarditis phenotypes, and experimental data—and stratify therapeutic evidence by phenotype and drug class, distinguishing colchicine, for which randomised prevention data exist in post-pericardiotomy syndrome, from IL-1 blockade, for which no PCIS-specific trial exists. We propose a pericardial injury-threshold model as a testable hypothesis in which clinical expression reflects the interaction of damage-associated molecular pattern load, the directness of pericardial and mesothelial exposure, and host inflammatory susceptibility, with adaptive responses acting as potential amplifiers. The model yields falsifiable predictions and identifies a key unanswered question: whether IL-1 inhibition during infarct healing is safe and effective. We outline a staged research programme, including a candidate two-tier research case definition requiring prospective validation, registry-based ascertainment, pericardial fluid immunophenotyping, inflammasome genetics, and phenotype-specific trials, including of emerging direct NLRP3 inhibitors.
SN - 1664-3224
ER -