What is post-infarction pericarditis?

It is a type of pericarditis that arises after an acute myocardial infarction, usually within days or weeks, and may present as early epistenocardial pericarditis or as late autoimmune Dressler's syndrome.

What are the main causes of traumatic pericarditis?

Traumatic pericarditis is caused by penetrating or blunt chest trauma, abdominal trauma, invasive cardiac procedures, thoracic radiotherapy, or surgical interventions involving the pericardium.

Which drugs can induce pericarditis?

The main drugs involved are procainamide, hydralazine, penicillin and phenylbutazone. They can act through immunological or direct toxic mechanisms on the pericardium.

What are the most common symptoms?

Pleuritic chest pain, fever, dyspnea, pericardial friction rub, pericardial effusion and, in severe cases, cardiac tamponade.

What is the treatment for non-infectious pericarditis?

NSAIDs and colchicine are the first choice; corticosteroids are reserved for refractory or immune-mediated cases. In the presence of large effusions or tamponade, pericardiocentesis is indicated.

What are the main complications?

Cardiac tamponade, constrictive pericarditis and recurrences, especially in patients with autoimmune forms or significant trauma.

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POST-INFARCTION PERICARDITIS

Article written and reviewed by Dr Luca Moretti

Acute myocardial infarction (AMI) can be complicated by several forms of pericarditis, distinguished by their timing and pathogenetic mechanism.

In addition to cardiac rupture with acute pericardial hemorrhage and cardiac tamponade, the main types of post-infarction pericarditis are:

Epistenocardial pericarditis: occurs early, between the 2nd and 4th day after infarction, as an inflammatory reaction to myocardial necrosis. It has an incidence of 5-10% in infarcted patients and presents with a mild fibrinous effusion, generally of little clinical significance.
Dressler's syndrome: a late autoimmune pericarditis, arising between the 2nd and 6th week post-infarction. It may be associated with pleuritis and is characterized by exudative effusion, fever, malaise, leukocytosis and elevated inflammatory markers. It is often accompanied by pleuritic chest pain and transient pulmonary infiltrates.

Diagnosis:

both forms are identified by ECG, which may show diffuse ST-segment changes (superimposed on those of AMI), and by echocardiography, which is useful for assessing the presence of pericardial effusion.

Treatment:

management is based on NSAIDs (ibuprofen or aspirin) and colchicine to reduce the risk of recurrence. Corticosteroids are reserved for resistant cases or those with multiple recurrences.

TRAUMATIC PERICARDITIS

Traumatic pericarditis develops following trauma involving the pericardium, predominantly of hemorrhagic type.

Main causes:

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

Clinical manifestations:

Traumatic pericarditis generally presents with late-onset chest pain (3-4 weeks after trauma), associated with high fever, leukocytosis and elevated ESR. In severe cases, it may progress to constrictive pericarditis.

Diagnosis:

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

Treatment:

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

DRUG-INDUCED PERICARDITIS

Certain drugs can induce pericarditis as an adverse effect, either through a hypersensitivity mechanism or a direct toxic effect on the pericardium.

Most frequently implicated drugs:

Procainamide (antiarrhythmic) → associated with pericarditis within the spectrum of drug-induced lupus syndrome.
Hydralazine (antihypertensive) → can cause an immune-mediated pericarditis similar to SLE.
Penicillin (antibiotic) → hypersensitivity reaction with pericardial inflammation.
Phenylbutazone (NSAID) → withdrawn from the market in many countries due to high systemic toxicity.

Clinical manifestations:

Symptoms vary depending on the drug and pathogenetic mechanism. The autoimmune form (procainamide, hydralazine) may be insidious and chronic, while acute toxic reactions (penicillin, phenylbutazone) tend to present with fever and serous or hemorrhagic pericardial effusion.

Diagnosis:

ECG: ST-segment and T-wave changes.
Echocardiography: assessment of effusion.
Autoimmune tests: ANA, anti-DNA for suspected drug-induced lupus.

Treatment:

Withdrawal of the causative drug.
NSAIDs and colchicine to control inflammation.
Glucocorticoids in severe immune-mediated cases.

References

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