Dressler syndrome

Description

Dressler syndrome: Fibrinous or fibrinohaemorrhagic secondary pericarditis that occurs as a result of injury to the heart or pericardium, either from myocardial infarction (MI) or cardiac surgery. Also known as post myocardial infarction syndrome

Initially described by William Dressler (1890-1969) as a condition developing as early as 2-3 days after a transmural infarct, due to underlying myocardial inflammation

Exact cause is unknown but appears to be an immune-mediated response to injury to pericardial cells with subsequent immune complex deposition in the pericardium causing an inflammatory response

Although an uncommon condition it should be considered in patients with persistent fatigue or malaise following MI or cardiac surgery

History of Dressler syndrome

1929 – Pericarditis was usually considered as a sign rather than as a complication of myocardial infarction. Samuel Albert Levine (1891-1966) described the pericardial reaction which was thought to occur when infarction extends to the epicardial surface. According to Levine, a pericardial friction rub is the sole manifestation of pericarditis which accompanies myocardial infarction.

1936 – George Blumer (1872-1962) reviewed a series of patients post myocardial infarction. He found that a pericardial friction rub becomes audible in most instances between the second and fourth day of the illness and disappears after a day or two. Occasionally, however, it may not appear until the 5th or 10th day and may persist for one or two weeks.

In 109 patients whom I saw at some period during the ten days immediately following an acute coronary occlusion, thirty-two, or 22%, showed pericarditis. The clinical reports, like the pathologic reports, do not, as yet, cover a number of cases sufficiently large for statistical purposes.

Blumer G, 1936

Formerly pericardial friction rub as sign of “pericarditis epistenscardica” represented the most important evidence of recent myocardial infarction, but with increasing knowledge of other clinical and laboratory features of coronary thrombosis this sign was reduced to minor significance

1938 – Charles F. Stewart and Kenneth B. Turner found localized fibrinous pericarditis in postmortem studies of recent myocardial infarctions in 25 – 32% of cases. William Bennett Bean (1909-1989) in a study of postmortem cases of myocardial infarction, frequently observed pleural effusion, which he attributed to congestive heart failure. In seven cases of our series there was roentgenologic evidence of pleural effusion, which was left-sided in four and bilateral in three instances. Only one of these cases showed gross signs of congestive heart failure. In three patients pleural effusion was copious enough to require paracentesis.

1956 – In his initial study, William Dressler suggested an incidence rate of 3-4% in patients with myocardial infarction. With modern management these rates now appear to be much lower

Myocardial infarction was followed in 10 instances by a febrile complication resembling idiopathic pericarditis with pleuritis and/or pneumonitis. A pericardial friction rub was heard in eight cases. Roentgenologic evidence of pericardial effusion was found in two cases. Pleural effusion occurred in seven.

Associated with the signs of pericarditis was a peculiar temperature curve that showed protracted periods of low-grade fever between high peaks of fever and flare-ups of pain. Leukocytosis, occasionally giving counts as high as 35,000 cells per cubic millimeter, was present in 7 of the 10 cases. Frequent relapses prolonged the febrile course to weeks or months, but in all cases the outcome was favorable

Dressler, 1956

Associated Persons

• Samuel Albert Levine (1891-1966)
• George Blumer (1872-1962)
• William Bennett Bean (1909-1989)
• William (Wilhelm) Dressler (1890-1969)

Alternative names

• Post myocardial infarction syndrome (PMIS)

References

Historical reports

• Levine SA. Coronary Thrombosis: Its Various Clinical Features. Medicine 1929; 8: 245-418
• Blumer G. Pericarditis Epistenocardica: Frank Billings Lecture, JAMA 1936; 107: 178
• Stewart CF, Turner KB. A Note on Pericardial Involvement in Coronary Thrombosis, Am. Heart J. 1938; 15: 232-234.
• Bean WB. Infarction of the heart. III. Clinical course and morphological findings. Annals of Internal Medicine. 1938; 12: 71-94.
• Dressler W. Post-Myocardial Infarction Syndrome: Preliminary Report of a Complication Resembling Idiopathic, Recurrent, Benign Pericarditis. JAMA. 1956;160(16):1379-1383.
• Dressler W. The post-myocardial-infarction syndrome: a report on forty-four cases. AMA Arch Intern Med. 1959 Jan;103(1):28-42
• Dressler W, Leavitt SS. Pericarditis after acute myocardial infarction. Relapses over period of twenty-eight months. JAMA. 1960 Jul 16;173:1225-6.

Reviews

• Bendjelid K, Pugin J. Is Dressler syndrome dead? Chest. 2004 Nov;126(5):1680-2
• Jaworska-Wilczynska M, Abramczuk E, Hryniewiecki T. Postcardiac injury syndrome. Med Sci Monit. 2011; 17(11): CQ13-14.
• Imazio M et al. Contemporary features, risk factors, and prognosis of the post-pericardiotomy syndrome. Am J Cardiol. 2011; 108(8): 1183-7.
• Kumar V, Abbas A, Aster J. Robbins and Cotran Pathologic Basis of Disease. 9e. 2014

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