Dressler Syndrome: Autoimmune Pathogenesis
Dressler syndrome is an autoimmune reaction, not a viral inflammation. The condition represents a post-cardiac injury syndrome with a presumed immune-mediated pathogenesis triggered by myocardial necrosis, not by direct viral infection of the pericardium 1, 2.
Pathophysiological Mechanism
The autoimmune nature of Dressler syndrome is supported by several key features:
Latent period: The syndrome develops 1-2 weeks to several months after myocardial infarction, not immediately as would be expected with direct viral inflammation 1, 2. This delay reflects the time required for the immune system to mount an antibody response against cardiac antigens.
Antigenic trigger: Initial myocardial necrosis releases cardiac antigens that provoke autoantibody formation, particularly antiheart antibodies 2, 3. The extent of the antibody response correlates with the amount of antigenic material released from damaged myocardium 2.
Response to anti-inflammatory therapy: The condition responds to immunomodulatory drugs including NSAIDs, corticosteroids, and colchicine, which target immune-mediated inflammation rather than viral pathogens 1, 4, 2.
Recurrence pattern: The possibility of recurrences despite initial treatment resolution supports an ongoing immune dysregulation rather than persistent viral infection 1.
Clinical Distinction from Viral Pericarditis
Dressler syndrome differs fundamentally from viral pericarditis:
Timing: Occurs specifically after cardiac injury (MI, surgery, trauma), not as a primary infectious process 1.
Hemorrhagic effusion: The pericardial fluid is characteristically serosanguinous to hemorrhagic, reflecting immune-mediated inflammation triggered by pericardial bleeding, not the serous effusion typical of viral pericarditis 2, 5.
Systemic autoimmune features: Patients develop fever, elevated inflammatory markers (CRP), and pleuropericardial involvement consistent with systemic immune activation 1, 4.
Important Clinical Caveat
While viral infections can cause myocarditis and pericarditis as primary conditions, Dressler syndrome specifically refers to the post-injury autoimmune phenomenon 1. The dramatic decrease in incidence (now <0.5-1%) with modern reperfusion therapy supports the autoimmune mechanism—early restoration of blood flow limits myocardial necrosis and thus reduces antigenic release 2, 6.
The classification as a post-cardiac injury syndrome alongside post-pericardiotomy syndrome and post-traumatic pericarditis further emphasizes the shared autoimmune pathogenesis triggered by tissue injury rather than infectious agents 1, 3.