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Decreased Recognition of the Post-Myocardial Infarction (Dressler) Syndrome in the Postinfarct Setting : Does It Masquerade as “Idiopathic Pericarditis” Following Silent Infarcts?

David H. Spodick, MD, DSc, FCCP
Author and Funding Information

Affiliations: Worcester, MA
 ,  Dr. Spodick is Professor of Medicine, Cardiovascular Division, University of Massachusetts Medical School.

Correspondence to: David H. Spodick, MD, DSc, FCCP, Department of Medicine, Division of Cardiovascular Medicine, Univer sity Campus, 55 Lake Avenue North, Worcester, MA 01655; e-mail: spodickd@ummhc.org



Chest. 2004;126(5):1410-1411. doi:10.1378/chest.126.5.1410
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In this issue of CHEST (see page 1680), Bendjelid and Pugin have called attention to the current scarcity of Dressler syndrome. The post-myocardial infarction syndrome (PMIS) [Dressler syndrome] indeed appears to be disappearing in the last quarter century.1 Although there is some dissent,2 investigators who see large numbers of patients with myocardial infarction (MI), including infarction pericarditis (epistenocardiac pericarditis), have not recognized a case of PMIS in many years.3 PMIS differs dramatically from the common epistenocardiac pericarditis, since the latter is generally paucisymptomatic with few objective manifestations, and thereby is often missed because of infrequent auscultation, usual absence of new systemic symptoms and signs (occasional slight rise in temperature), and diagnostic ECG changes, although a transmural infarction is necessary, since only transmural MIs directly injure the visceral pericardium.45 Classic PMIS differs markedly in that it does not require a transmural infarction and is distinguished by high sedimentation rate, considerable “pericardial” pain, frequent pericardial effusions, pleuritis, and sometimes pneumonitis.5 It usually appears between 1 week and several months after the onset of symptoms and signs of infarction, whereas epistenocardiac pericarditis is almost coincident with the onset of the MI (usually from the first to the third day).4 Both are more frequent after larger infarctions, particularly anterior infarcts, inferior infarcts accompanied by right ventricular infarction, and infarctions with complicated in-hospital courses. PMIS appears to occur somewhat more often in patients who have had epistenocardiac pericarditis and even as an exacerbation of it.5 PMIS has been considered an autoimmune process, with factors in common with other pericardial injury syndromes, notably the postpericardiotomy syndrome. Evidence for autoimmunity includes the following46: (1) latent period; (2) antiheart antibodies; (3) preceding pericardial injury in many cases; (4) occurrence in patients with anatomatically nontransmural infarctions, therefore without the direct visceral pericardial injury that causes epistenocardiac pericarditis; (5) frequent recurrences; (6) prompt response to anti-inflammatory agents; (7) frequent associated pleuritis with or without pneumonitis; (8) changes in cellular immunity suggested by altered lymphocyte subsets compared to control patients78; and (9) evidence favoring immune complex formation incorporating antibody combined with myocardial antigen, complement pathway activation,45,9 and evidence of cellular as well as humoral immunopathic responses. Antibodies—antiheart, antiactin, and antimyosin—are provoked by both cardiac surgery and infarction; surgery is more immunostimulating than infarction, evoking much greater quantities of them.4 (Antipericardial antibodies have not been identified). Ancillary evidence includes occasional occurrence of PMIS with the Sweet syndrome, an acute febrile neutrophilic dermatosis sometimes associated with inflammatory bowel disease, a notorious cause of pericarditis.5

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