Dressler's syndrome

Associate Editor-In-Chief: Mohammed A. Sbeih, M.D.[mailto:msbeih@perfuse.org] Phone:617-849-2629 ,

Synonyms and keywords: Postmyocardial infarction syndrome, post MI pericarditis, PMIS

Overview
Dressler's syndrome or post myocardial infarction syndrome is a form of pericarditis that occurs in the setting of injury to the heart as a result of myocardial infarction. Dressler's syndrome typically occurs 2 to 10 weeks after myocardial infarctionit's. This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis which occurs between days 2 and 4 after myocardial infarction.

Historical Perspective
It was first characterized by William Dressler in 1956. .

It should not be confused with the Dressler's syndrome of haemoglobinuria named for Lucas Dressler, who characterized it in 1854.

Risk Factors
Dressler's syndrome is associated with myocardial infarction (heart attack). It can also be observed after pulmonary embolism.

Pathophysiology
Dressler's syndrome is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens. It usually occurs within weeks or months of the Infarction due to antiheart antibodies, this begins with myocardial injury that releases cardiac antigens and stimulates antibody formation. The immune complexes that are generated then deposit onto the pericardium and causes the inflamation. The autoimmune response and syndrome may also appear after pulmonary embolism.

Epidemiology and Demographics
In the setting of myocardial infarction, Dressler's syndrome occurs in about 7% of cases. Dressler's syndrome was more commonly seen in the era prior to reperfusion, but its incidence has markedly decreased in the reperfusion era, presumably because of smaller infarct sizes.

Conditions that Dressler's Syndrome should be Differentiated From
Dressler's syndrome typically occurs 2 to 10 weeks after a myocardial infarction has occurred. This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis that occurs in 17 to 25% of cases of acute myocardial infarction between days 2 and 4 after the myocardial infarction. Dressler's syndrome also needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.

Symptoms
The syndrome consists of a persistent low-grade fever, and chest pain which is usually pleuritic in nature. The symptoms tend to occur after a few weeks or even months after myocardial infarction and tend to subside in a few days.

Cardiovascular Examination
A pericardial friction rub, and /or a pericardial effusion is present.

Laboratory Findings
Elevated ESR.

Treatment
Dressler's syndrome is typically treated with high dose (up to 650 mg PO q 4 to 6 hours) enteric-coated aspirin. Acetominophen can be added for pain management as this does not affect the coagulation system. Anticoagulants should be discontinued if the patient develops a pericardial effusion.

NSAIDs such as ibuprofen should be avoided in the peri-infarct period as they:
 * 1) Increase the risk of reinfarction
 * 2) Adversely impact left ventricular remodeling.
 * 3) Block the effectiveness of aspirin

===ACC/AHA Treatment Guidelines (DO NOT EDIT) ===

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Class I
1. Aspirin is recommended for treatment of pericarditis after STEMI. Doses as high as 650 mg orally (entericcoated) every 4 to 6 hours may be needed. (Level of Evidence: B)

2. Anticoagulation should be immediately discontinued if pericardial effusion develops or increases. (Level of Evidence: C)

Class IIa
1. For episodes of pericarditis after STEMI that are not adequately controlled with aspirin, it is reasonable to administer 1 or more of the following:
 * a. Colchicine 0.6 mg orally every 12 hours (Level of Evidence: B)
 * b. Acetaminophen 500 mg orally every 6 hours. (Level of Evidence: C)

Class IIb
1. Corticosteroids might be considered only as a last resort in patients with pericarditis refractory to aspirin or NSAIDs. Although corticosteroids are effective for pain relief, their use is associated with an increased risk of scar thinning and myocardial rupture. (Level of Evidence: C)

2. Nonsteroidal anti-inflammatory drugs may be considered for pain relief; however, they should not be used for extended periods because of their effect on platelet function, an increased risk of myocardial scar thinning, and infarct expansion. (Level of Evidence: B)

Class III
1. Ibuprofen should not be used for pain relief because it blocks the antiplatelet effect of aspirin and it can cause myocardial scar thinning and infarct expansion. (Level of Evidence: B) }}