What is the etiology of Dressler syndrome?

Etiology of Dressler Syndrome

Dressler syndrome is primarily caused by an autoimmune response triggered by initial damage to pericardial and/or pleural tissues following myocardial injury, most commonly myocardial infarction. 1

Pathophysiological Mechanism

Dressler syndrome, also known as late post-myocardial infarction pericarditis, is part of a broader category called post-cardiac injury syndromes (PCIS). The underlying pathophysiology involves:

• Autoimmune mechanism: The syndrome is presumed to have an autoimmune pathogenesis 1

  • Triggered by initial damage to pericardial and/or pleural tissues
  • Primarily caused by myocardial necrosis in the case of post-MI Dressler syndrome
  • Characterized by a greater antiheart antibody response (antisarcolemmal and antifibrillary) compared to other post-cardiac injury syndromes 1

• Temporal relationship: Typically occurs 1-6 weeks after the initial cardiac injury 2

  • Characterized by a latent period between the initial injury and symptom onset
  • This latency period supports the immune-mediated pathogenesis theory 1

• Inflammatory response: Involves pericardial inflammation with potential pleural involvement

  • Often includes pericardial effusion, which may be bloody 1
  • Frequently accompanied by systemic inflammatory markers

Triggering Events

Dressler syndrome can be triggered by various cardiac injuries:

1. Myocardial infarction: Most common historical cause

   • Particularly associated with transmural infarctions
   • Has become rare (<1%) in the era of primary percutaneous coronary intervention 1
   • May reflect larger infarct size and/or late reperfusion 1

2. Other cardiac injuries: Can also occur following:

   • Cardiac surgery (as part of post-pericardiotomy syndrome)
   • Traumatic cardiac injury
   • Percutaneous coronary interventions
   • Pulmonary vein isolation procedures for atrial fibrillation 3
   • Even minor pericardial bleeding can trigger the syndrome 1

Clinical Significance and Evolution

The incidence of Dressler syndrome has significantly decreased in the modern era of early reperfusion therapy for myocardial infarction 1, 4. However, it remains clinically important as:

• It can still occur despite modern interventions 5, 2
• It can lead to significant morbidity if not properly diagnosed and treated
• It requires differentiation from other causes of post-MI chest pain, particularly recurrent ischemia

Diagnostic Considerations

The diagnosis of Dressler syndrome is based on clinical criteria following cardiac injury:

1. Fever without alternative causes
2. Pericarditic or pleuritic chest pain
3. Pericardial or pleural rubs
4. Evidence of pericardial effusion
5. Pleural effusion with elevated CRP 1

At least two of these five criteria should be fulfilled for diagnosis, with demonstration of inflammatory activity being essential.

Treatment Implications

Understanding the autoimmune etiology of Dressler syndrome guides treatment approaches:

• Anti-inflammatory therapy is the cornerstone of management
• Aspirin is recommended as first-line treatment 1
• Colchicine may be effective, particularly in patients with recent coronary stenting 4
• Glucocorticoids and some NSAIDs are potentially harmful for treatment of post-MI pericarditis 1

The autoimmune nature of the condition explains why it responds to anti-inflammatory medications and may recur if treatment is discontinued prematurely.