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

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 following⁴⁵⁶: (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,⁴⁵⁹ 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

Finally, some infarcts and cases of infarct-simulating myocarditis appear to be precipitated by systemic (eg, respiratory) infections with a continuing inflammatory myocardial immunopathy that could involve the pericardium.⁹ While at least some postpericardiotomy syndromes require a “permissive” viral infection, studies of tissues and fluid in PMIS have not found infectious agents or their residua.⁴⁵¹⁰

The apparent decline or disappearance of the PMIS predated the current era of reperfusion, multiple thrombolytic agents, aggressive β-adrenergic blockade, and angiotensin-converting enzyme inhibition, as well as prompt coronary bypass—all of which have reduced the size of infarcts and aborted their progress—so that it is not clear which if any of these factors have contributed to the apparent disappearance or near-disappearance of PMIS. However, an intriguing possibility arises, particularly because of the latent period. Occasional patients during MI will develop the classic ECG changes of acute (ie, stage 1) pericarditis,¹¹ therefore implying a generalized lesion. However, transmural infarcts are pyramidal with their base on the endocardium and apex at the epicardium, so that epistenocardiac pericarditis is confined to the relatively small zone of eruption of the infarct on the visceral pericardium and should not produce a generalized ECG change.¹¹ Thus, typical pericarditic ECG changes should represent generalized pericarditis as in PMIS.¹¹ Since approximately one third of infarcts in the Framingham Study¹² have no clinical counterpart, only being discovered by new Q-waves in a routine 2-year examination cycle, and since PMIS has many clinical features in common with idiopathic or viral pericarditis, cases of idiopathic pericarditis in adults with or without diagnosed coronary disease could well be PMIS following a silent infarct.

Some cases of PMIS could indeed occur coincident with the apparent MI onset. We know from investigations of cardiac rupture in which the time of death is clear that tissue dating of infarction may put the actual onset a week to 10 days before symptoms have brought the patient to the hospital; some initially painless MIs may also contribute to the frequent nonspecific symptoms occurring on the days before the clinical onset of some infarcts.⁹ Finally, some unrecognized factors other than those mentioned, perhaps environmental, may have changed or disappeared since Dressler’s era, thereby contributing to apparent disappearance or near-disappearance of this syndrome.