Dressler syndrome and post-cardiac injury syndrome: an autoinflammatory framework for reappraising a seventy-year-old diagnosis: a state-of-the-art review

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.