Can you provide a comprehensive overview of Dressler syndrome (post‑myocardial infarction pericarditis)?

Dressler Syndrome: Comprehensive Overview

Definition and Pathophysiology

Dressler syndrome is a late post-myocardial infarction pericarditis that develops 1–2 weeks to several months after MI, caused by an autoimmune inflammatory response triggered by myocardial tissue damage and pericardial bleeding. 1, 2

• The syndrome represents one form of post-cardiac injury syndrome (PCIS), which also includes post-pericardiotomy syndrome and post-traumatic pericarditis 1
• The immune-mediated pathogenesis is supported by a latent period of weeks before symptom onset and the response to anti-inflammatory drugs 1
• Even minor bleeding into the pericardium can precipitate the syndrome, with pericardial bleeding serving as the primary trigger for the autoimmune response 3
• The syndrome develops when antigenic material from damaged myocardial tissue provokes an immune response 3

Epidemiology

Dressler syndrome has become extremely rare in the modern era, occurring in less than 1% of patients treated with primary percutaneous coronary intervention. 2

• The dramatic decline in incidence is attributed to early reperfusion therapy of myocardial infarction 1, 2
• When it does occur, it is associated with larger infarct size, delayed reperfusion, or failed reperfusion 2
• The syndrome may also occur after other cardiac interventions including radiofrequency ablation, pacemaker implantation, and percutaneous procedures 4, 5

Clinical Presentation

Patients present with sharp, pleuritic chest pain that worsens with inspiration and improves when sitting forward—this postural and respiratory relationship is the key distinguishing feature from recurrent ischemia. 2

• Fever without alternative causes is a cardinal feature 1
• A pericardial friction rub may be audible on auscultation, though it can be absent 2
• Pleuritic chest pain and pleural rubs may occur due to concomitant pleuropericardial involvement 1
• Malaise and systemic symptoms are common 6

Diagnostic Criteria

The diagnosis requires at least two of five criteria: (i) fever without alternative causes, (ii) pericarditic or pleuritic chest pain, (iii) pericardial or pleural rubs, (iv) pericardial effusion, and (v) pleural effusion with elevated CRP. 1

Diagnostic Workup

• Physical examination should focus on detecting pericardial friction rub, fever, and signs of tamponade 1
• ECG often shows persistent ST-segment elevation with upright T waves, though these changes are frequently masked by primary infarction-related abnormalities 2
• Transthoracic echocardiography is mandatory to detect pericardial effusion and assess for tamponade 1, 2
• Thoracic echography and/or chest X-ray to evaluate for pleural effusion and pulmonary infiltrates 1
• Elevated CRP confirms inflammatory activity and is essential to establish the diagnosis 1

Macroscopic Findings

• The pericardial effusion is characteristically serosanguinous to hemorrhagic on macroscopic examination, distinguishing it from the clear or straw-colored fluid of other causes 3
• Anticoagulant use, particularly warfarin, significantly increases the risk of hemorrhagic pericardial effusion 3

Critical Diagnostic Pitfalls

Do not misinterpret pericarditic chest pain for recurrent myocardial infarction or unstable angina—careful history focusing on sharp quality, postural change, and respiratory variation is essential. 2

• Pericardial effusions exceeding 10 mm require urgent investigation for possible subacute ventricular rupture, as two-thirds of these patients may progress to tamponade or free-wall rupture 3, 2, 7
• Urgent echocardiography is mandatory when Dressler syndrome is suspected, as tamponade can occur even without anticoagulation 3
• The clinical context (recent MI, latent period of weeks, fever, pleuritic pain) combined with hemorrhagic fluid appearance establishes the diagnosis 3

Management

First-Line Treatment

The treatment of choice is aspirin (500–1,000 mg every 6–8 hours, total 1.5–4 g/day) plus colchicine (0.5–0.6 mg once or twice daily) for 3 months. 2, 7

• Aspirin is the preferred NSAID because it improves coronary flow and provides antiplatelet effects at doses up to 1.5 g/day 2
• Colchicine reduces recurrence rates by approximately 50% 7
• Colchicine dosing should be 0.5 mg twice daily if ≥70 kg or 0.5 mg once daily if <70 kg 7
• The same therapeutic scheme used for other forms of pericarditis is efficacious for Dressler syndrome 1

Treatment Tapering

Decrease aspirin doses gradually (by 250–500 mg every 1–2 weeks) and taper one drug at a time before gradually discontinuing colchicine over several months. 7

• Serial CRP measurements can guide treatment duration and assess therapeutic response 2

Refractory Cases

For refractory cases, short-term corticosteroid therapy (3–6 months) may be used with caution, or intrapericardial triamcinolone (≈300 mg/m²) can be administered via pericardiocentesis. 2, 7

• Systemic corticosteroids should be avoided or reserved for refractory cases given the risk of delayed myocardial healing 2, 7
• Other NSAIDs (except ibuprofen) should be avoided because they may thin the infarct zone 2
• Ibuprofen is acceptable only when aspirin cannot be used, as it also enhances coronary flow 2

Hospitalization

Hospital admission is mandatory to monitor for tamponade and to adjust treatment. 2, 7

Prognosis

Although Dressler syndrome signals a larger infarct size, in-hospital and 1-year mortality rates are comparable between patients with and without post-MI pericarditis. 2

• The syndrome does not independently affect prognosis 2
• Rare but serious complications include hemopericardium, cardiac tamponade (occurring in <2% of cases), and constrictive pericarditis (approximately 3% of cases) 2
• The syndrome can follow a relapsing course but carries a favorable prognosis overall 5