Dressler syndrome

Dressler syndrome is a delayed form of pericarditis thought to result from an autoimmune reaction against cardiac neoantigens exposed during myocardial necrosis (post-MI) or pericardial injury (post-cardiotomy). Unlike the early, fibrinous pericarditis that occurs within days of a transmural MI (due to direct inflammatory extension), Dressler syndrome develops weeks to months later, reflecting a type III/IV hypersensitivity-like immune response with anti-myocardial antibodies. Clinically, patients present with fever, malaise, pleuritic chest pain that improves with sitting forward, and a pericardial friction rub on auscultation. ECG may show diffuse ST elevations and PR depressions; echocardiography may reveal pericardial effusion. Labs often show elevated ESR/CRP and leukocytosis. It can lead to complications such as pericardial effusion, cardiac tamponade, or constrictive pericarditis if untreated. Diagnosis is largely clinical, supported by history of recent cardiac injury, characteristic exam findings, and imaging. Treatment mirrors that of other pericarditis: NSAIDs (e.g., aspirin, preferred post-MI to avoid impairing infarct healing) plus colchicine to reduce recurrence; corticosteroids are used in refractory or severe cases but avoided early post-MI due to risk of impaired myocardial healing. It's important to differentiate Dressler syndrome from early post-MI pericarditis (occurs within 1-3 days, due to direct inflammation) and from reinfarction or pulmonary embolism, which can also cause chest pain in this population.