Dressler syndrome is a delayed inflammatory pericarditis that typically develops 2 to 10 weeks following myocardial infarction (MI) or cardiac surgery 1. It is considered a type of postcardiac injury syndrome (PCIS) 1,2. The condition is characterised by inflammation of the pericardium, often accompanied by pleural effusion, and is believed to arise from an autoimmune reaction to myocardial or pericardial neo-antigens released after cardiac injury 1. Prompt recognition and management are crucial to prevent complications like cardiac tamponade or constrictive pericarditis 1.

Epidemiology

The incidence of Dressler syndrome has significantly decreased in the modern era of reperfusion therapy for MI 1. While historically reported in up to 5% of MI patients, current estimates suggest a much lower prevalence, potentially less than 1% 1. It can occur after any form of cardiac injury, including MI, coronary artery bypass grafting (CABG), percutaneous coronary intervention (PCI), and even cardiac trauma 1,2.

Aetiology

  • primary causes / triggers: The primary triggers are cardiac injury events, most commonly acute myocardial infarction (especially large anterior MIs) 1 and open-heart cardiac surgery (like CABG) 1,2. Less common triggers include PCI, cardiac implantable electronic device placement, and blunt cardiac trauma 1,2.

  • secondary associations / risk factors: While the exact predisposition is not fully understood, factors increasing the risk might include the extent of myocardial necrosis after MI or the degree of surgical trauma 1. There is no strong association with specific patient demographics like age or sex, although it can occur in any patient following a qualifying cardiac event 1.

Pathophysiology

Dressler syndrome is thought to be an autoimmune phenomenon 1,2. Following cardiac injury, myocardial antigens (like actin and myosin) are released and may trigger an immune response 1,2. This leads to inflammation of the pericardium and often the pleura, resulting in pericarditis and pericardial/pleural effusions 1,2. The inflammatory response involves T-cell mediated immunity and the production of autoantibodies 1,2.

Clinical presentation

  • presenting symptoms: The classic presentation occurs weeks after the inciting cardiac event 1. Key symptoms include fever (often low-grade), sharp, pleuritic chest pain that is typically relieved by sitting up and leaning forward 1. The pain may radiate to the left shoulder or arm 1. Some patients may experience symptoms similar to acute MI, such as dyspnoea or palpitations 1.

  • physical examination signs: A pericardial friction rub may be heard, although it can be transient 1. Signs of pericardial effusion, such as pulsus paradoxus or Kussmaul's sign (distended neck veins with paradoxical fall in blood pressure during inspiration), may be present if the effusion is large enough 1. Signs of right ventricular failure, such as dependent oedema, can occur if the effusion causes significant cardiac compression 1.

Investigations

Bedside & Laboratory

  • laboratory / bedside studies: Blood tests typically show elevated inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) 1. Cardiac enzymes (troponin) are usually normal, distinguishing it from recurrent MI 1. A complete blood count may show leukocytosis 1.

Imaging & Special Investigations

  • imaging / specialist studies: Electrocardiogram (ECG) may show diffuse ST-segment elevation and PR-segment depression, similar to acute pericarditis, but without reciprocal changes 1. Chest radiography may show globular cardiac enlargement due to pericardial effusion 1. Echocardiography is the key investigation, confirming the presence and size of a pericardial effusion and assessing for signs of cardiac tamponade 1.

Management

  • acute / first-line management: Initial management focuses on symptomatic relief and reducing inflammation 1,2. First-line treatment involves non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin (high dose) or indomethacin 1,2. Colchicine is often added to NSAIDs as it accelerates symptom resolution and reduces recurrence rates 1,2.

  • definitive / long-term management: If symptoms are severe, refractory to NSAIDs, or if there is recurrent effusion requiring repeated drainage, corticosteroids (e.g., prednisone) may be indicated, provided infection has been excluded 1,2. In rare, refractory cases, other immunosuppressants like anakinra (an IL-1 inhibitor) might be considered 1. Prophylactic colchicine may be considered in high-risk individuals after cardiac surgery 1,2.

Differential diagnosis

  • Acute Myocardial Infarction: Differentiating features include the timing (weeks post-MI vs. acute event), ECG changes (diffuse ST elevation vs. localized changes with reciprocal depression), and cardiac enzyme levels (usually normal in Dressler's vs. elevated in MI) 1.

  • Acute Pericarditis: While sharing similar symptoms (chest pain, friction rub, ECG changes), Dressler syndrome occurs specifically after cardiac injury, often with a larger effusion and associated pleural effusion, and typically later in its course 1.

  • Cardiac Tamponade: This is a potential complication of Dressler syndrome (due to large effusion), not a differential diagnosis itself. However, other causes of tamponade (e.g., post-MI ventricular rupture, malignancy) need consideration if tamponade is present 1.

Prognosis & complications

With appropriate treatment, the prognosis for Dressler syndrome is generally good 1,2. Potential complications include recurrent pericarditis, progression to constrictive pericarditis (rare), and cardiac tamponade (if effusion is large) 1,2. Long-term follow-up may be needed, especially if corticosteroids are used 1,2.

See also