POST-INFARCTION PERICARDITIS

Acute myocardial infarction (MI) can lead to various forms of pericarditis, classified based on timing and underlying pathophysiology.

Aside from cardiac rupture leading to acute pericardial hemorrhage and cardiac tamponade, the main types of post-infarction pericarditis are:

• Epistenocardial pericarditis: an early-onset inflammatory reaction to myocardial necrosis, occurring between days 2 and 4 post-infarction. It has an incidence of 5-10% in MI patients and presents with mild fibrinous pericardial effusion, usually without clinical significance.
• Dressler's syndrome: a late autoimmune pericarditis developing 2 to 6 weeks after MI. It may be associated with pleuritis and is characterized by exudative effusion, fever, malaise, leukocytosis, and elevated inflammatory markers. It often presents with pleuritic chest pain and transient pulmonary infiltrates.

Diagnosis:

Both forms can be identified via ECG, which may show diffuse ST-segment changes overlapping those of MI, and echocardiography, which is useful for assessing pericardial effusion.

Treatment:

Management includes NSAIDs (ibuprofen or aspirin) and colchicine to reduce the risk of recurrence. Corticosteroids are reserved for refractory or recurrent cases.

TRAUMATIC PERICARDITIS

Traumatic pericarditis occurs due to direct or indirect pericardial injury, most commonly hemorrhagic.

Main Causes:

• Penetrating thoracic trauma: gunshot or stab wounds, with a high risk of hemopericardium and cardiac tamponade.
• Blunt thoracic trauma: car accidents (steering wheel impact), falls from heights, explosions.
• Abdominal trauma: sudden increase in intra-abdominal pressure transmitted to the pericardium.
• Iatrogenic causes: surgical pericardiotomy, cardiac catheterization, external cardiac massage, thoracic radiotherapy (radiation-induced pericarditis).

Clinical Presentation:

Traumatic pericarditis typically presents with delayed chest pain (3-4 weeks after trauma), accompanied by high fever, leukocytosis, and elevated inflammatory markers. Severe cases may progress to constrictive pericarditis.

Diagnosis:

• ECG: ST-segment and T-wave abnormalities, with low voltage in hemopericardium.
• Chest X-ray: useful for detecting rib fractures and indirect signs of pericardial effusion.
• Echocardiography: gold standard for detecting pericardial fluid accumulation.

Treatment:

• Observation and anti-inflammatory therapy (NSAIDs, colchicine) in mild cases.
• Pericardiocentesis in large effusions or suspected cardiac tamponade.
• Pericardiectomy in rare cases of secondary constrictive pericarditis.

DRUG-INDUCED PERICARDITIS

Certain medications can cause pericarditis as an adverse effect, either through an immune hypersensitivity mechanism or direct pericardial toxicity.

Most Commonly Implicated Drugs:

• Procainamide (antiarrhythmic) → associated with lupus-like drug-induced pericarditis.
• Hydralazine (antihypertensive) → may cause immune-mediated pericarditis similar to systemic lupus erythematosus (SLE).
• Penicillin (antibiotic) → hypersensitivity reaction leading to pericardial inflammation.
• Phenylbutazone (NSAID) → withdrawn from many markets due to high systemic toxicity.

Clinical Presentation:

Symptoms vary depending on the drug and pathophysiological mechanism. The autoimmune form (procainamide, hydralazine) is often insidious and chronic, whereas acute toxic reactions (penicillin, phenylbutazone) typically present with fever and serous or hemorrhagic pericardial effusion.

Diagnosis:

• ECG: ST-segment and T-wave abnormalities.
• Echocardiography: pericardial effusion assessment.
• Autoimmune testing: ANA, anti-DNA in suspected drug-induced lupus pericarditis.

Treatment:

• Immediate discontinuation of the offending drug.
• NSAIDs and colchicine to control inflammation.
• Glucocorticoids for severe immune-mediated cases.

References
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